The ichnovirus TrIV, transmitted by the endoparasitic wasp Tranosema rostrale to its lepidopteran host during oviposition, replicates asymptomatically in wasp ovaries and causes physiological dysfunctions in parasitiz...The ichnovirus TrIV, transmitted by the endoparasitic wasp Tranosema rostrale to its lepidopteran host during oviposition, replicates asymptomatically in wasp ovaries and causes physiological dysfunctions in parasitized caterpillars. The need to identify ichnoviral genes responsible for disturbances induced in lepidopteran hosts has provided the impetus for the sequencing and annotation of ichnovirus genomes, including that of TrIV. In the latter, 86 putative genes were identified, including 35 that could be assigned to recognized ichnoviral gene families. With the aim of assessing the relative importance of each TrIV gene, as inferred from its level of expression, and evaluating the accuracy of the gene predictions made during genome annotation, the present study builds on an earlier qPCR quantification of transcript abundance of TrIV rep ORFs, in both lepidopteran and wasp hosts, extending it to other gene families as well as to a sample of unassigned ORFs. We show that the majority (91%) of putative ORFs assigned to known gene families are expressed in infected larvae, while this proportion is lower (67%) for a sample taken among the remaining ORFs. Selected members of the TrV and rep gene families are shown to be transcribed in infected larvae at much higher levels than genes from any other TrIV gene family, pointing to their likely involvement in host subjugation. In wasp ovaries, the transcriptional profile is dominated by a rep gene and a member of a newly described gene family encoding secreted proteins displaying a novel cysteine motif, which we identified among previously unassigned ORFs.展开更多
ObjectiveTo observe the effects of pretreatment with electroacupuncture (EA) on neuron activity in the rostral ventrolateral medulla (RVLM) of rats with myocardial ischemia-reperfusion injury (MIRI) and explore the ce...ObjectiveTo observe the effects of pretreatment with electroacupuncture (EA) on neuron activity in the rostral ventrolateral medulla (RVLM) of rats with myocardial ischemia-reperfusion injury (MIRI) and explore the central regulatory mechanism of EA in attenuating MIRI.MethodsOf 72 SD rats, 12 were randomly allocated into the group of EA pretreatment + RVLM nucleus damage (EA + RVLM lesion group). The other 60 rats were randomized (20 rats each) into a sham-operation group, a model group, and an EA pretreatment group (EA group). Except for the rats in the sham-operation group, the models of MIRI were prepared by ligating the left anterior descending coronary artery in the model, EA, and EA + RVLM lesion groups. The rats of the EA group were intervened with EA at “Shénmén (神门HT7)” and “Tōnglĭ (通里HT5)”, 1 mA in current intensity and 2 Hz in frequency, for 20 min each time per day. Before modeling, the intervention was given for seven consecutive days. In the EA + RVLM lesion group, 3 weeks after microinjection with the neuronal apoptotic virus at bilateral RVLM, the same EA intervention as the EA group was provided. Afterward, the MIRI models were prepared. In the model group, no EA intervention was given. Using Powerlab electrophysiolograph, ST segment displacement value and arrhythmia score were recorded and analyzed before modeling, 30 min after ligation, and 120 min after reperfusion in each group. The concentration of cardiac troponin (cTnl) was detected with an ELISA assay kit. Using immunofluorescence staining, the expression level of c-fos protein of RVLM was detected in the sham-operation, model, and EA groups separately. Plexon multichannel acquisition processor was adopted to record the neuronal firing and field potential of RVLM in the sham-operation, model, and EA groups.ResultsST segment displacement value, arrhythmia score, and cTnl concentration 30 min after ligation and 120 min after reperfusion were all elevated in the model group compared to the sham-operation group (all P < 0.01). ST segment displacement value, arrhythmia score, and cTnl concentration were lower in the EA group compared to the model and EA + RVLM lesion groups (P < 0.01). Compared with the sham-operation group, the expression level of c-fos and the total firing frequency in RVLM were significantly higher in the model group (P < 0.01). However, the expression level of c-fos and the total firing frequency in RVLM were lower in the EA group compared with the model group (P < 0.01).ConclusionElectroacupuncture pretreatment may induce changes in c-fos protein expression and neuronal activity in RVLM to mitigate myocardial lesions. RVLM plays an important role in electroacupuncture pretreatment for alleviating MIRI.展开更多
Objective The rostral anterior cingulate cortex （rACC） is implicated in processing the emotional component of pain. N-methyl-D-aspartate receptors （NMDARs） are highly expressed in the rACC and mediate painrelated ...Objective The rostral anterior cingulate cortex （rACC） is implicated in processing the emotional component of pain. N-methyl-D-aspartate receptors （NMDARs） are highly expressed in the rACC and mediate painrelated affect by activating a signaling pathway that involves cyclic adenosine monophosphate （cAMP）/protein ki- nase A （PKA） and/or extracellular regulated kinase （ERK）/cAMP-response element-binding protein （CREB）. The present study investigated the contributions of the NMDAR glycine site and GluN2B subunit to the activation of ERK and CREB both in vitro and in vivo in rat rACC. Methods Immunohistochemistry and Western blot analy- sis were used to separately assess the expression of phospho-ERK （pERK） and phospho-CREB （pCREB） in vitro and in vivo. Double immunostaining was also used to determine the colocalization of pERK and pCREB. Results Both bath application of NMDA in brain slices in vitro and intraplantar injection of formalin into the rat hindpaw in vivo induced significant up-regulation of pERK and pCREB in the rACC, which was inhibited by the NMDAR antago- nist DL-2-amino-5-phospho-novaleric acid. Selective blockade of the NMDAR GluN2B subunit and the glycine- binding site, or degradation of endogenous D-serine, a co-agonist for the glycine site, significantly decreased the up- regulation of pERK and pCREB expression in the rACC. Further, the activated ERK predominantly colocalized with CREB. Conclusion Either the glycine site or the GluN2B subunit of NMDARs participates in the phosphorylation of ERK and CREB induced by bath application of NMDA in brain slices or hindpaw injection of 5% formalin in rats, and these might be fundamental molecular mechanisms underlying pain affect.展开更多
Objective Despite accumulating evidence on a role of immune cells and their associated chemicals in mecha- nisms of pain, few studies have addressed the potential role of chemokines in the descending facilitation of p...Objective Despite accumulating evidence on a role of immune cells and their associated chemicals in mecha- nisms of pain, few studies have addressed the potential role of chemokines in the descending facilitation of persistent pain. The present study was undertaken to test the hypothesis that the chemokine （C-C motif） ligand 2 （CCL2） （commonly known as monocyte chemoattractant protein-1） signaling in the rostral ventromedial medulla （RVM）, a pivotal structure in brainstem pain modulatory circuitry, is involved in descending pain facilitation in rats. Methods An L5 spinal nerve ligation （SNL） was produced in rats under pentobarbital anesthesia. Western blot and immunohistochemistry were used to detect the expression levels of CCL2 and CCL2 receptor （CCR2）, and examine their distributions compared with the neuronal marker NeuN as well as glial markers glial fibrillary acidic protein （GFAP, astroglial） and CD 11 b （microglial）, respectively. Results SNL induced an increase in CCL2 expression in the RVM, and this returned to the control level at 4 weeks after injury. The induced CCL2 colocalized with NeuN, but not with GFAP and CD1 lb. CCR2 was also upregu- lated by SNL in the RVM, and this increase lasted for at least 4 weeks. CCR2 was colocalized with CD1 lb but not GFAP. Few RVM neurons also exhibited CCR2 staining. Neutralizing CCL2 with an anti-CCL2 antibody （0.2-20 ng） or injecting RS-102895 （0.1-10 pmol）, a CCR2b chemokine receptor antagonist, into the RVM on day 1 after SNL, significantly at- tenuated the established thermal and mechanical hypersensitivity. In addition, injection of recombinant rat CCL2 （0.03-3 pmol） into the RVM induced dose-dependent hyperalgesia, which was prevented by pretreatment with RS-102895 （10 pmol）. Interleukin-β （IL-1]3）, a potent inducer of neuronal CCL2, was also selectively upregulated in RVM reactive as- trocytes. Injection of IL-1 ]3 （120 fmol） into the RVM induced behavioral hyperalgesia, which was blocked by RS-102895 （10 pmol）. However, an IL-1 receptor antagonist （3 pmol） did not prevent CCL2 （3 pmol）-induced hyperalgesia. These results suggest that the effect of CCL2 is downstream to IL-113 signaling. Conclusion The IL-1 β and CCL2-CCR2 signaling cascades play a role in neuron-glia-cytokine interactions and the descending facilitation of neuropathic pain.展开更多
Cross-sectional and longitudinal studies have identified widespread and progressive grey matter volume （GMV） reductions in schizophrenia, especially in the frontal lobe. In this study, we found a progressive GMV dec...Cross-sectional and longitudinal studies have identified widespread and progressive grey matter volume （GMV） reductions in schizophrenia, especially in the frontal lobe. In this study, we found a progressive GMV decrease in the rostral medial frontal cortex （rMFC, including the anterior cingulate cortex） in the patient group during a 6-week follow-up of 40 patients with schizophrenia and 31 healthy controls well-matched for age, gender, and education. The higher baseline GMV in the rMFC predicted better improvement in the positive score on the Positive and Negative Syndrome Scale （PANSS）, and this might be related to the improved reality-monitoring. Besides, a higher baseline GMV in the posterior rMFC predicted better remission of general symptoms, and a lesser GMV reduction in this region was correlated with better remission of negative symptoms, probably associated with ameliorated self-referential pro- cessing and social cognition. Besides, a shorter disease course and higher educational level contributed to better improvement in the general psychopathological PANSS score, and a family history was negatively associated with improvement of the negative and total PANSS scores. These phenomena might be important for understanding the neuropathological mechanisms underlying the symp- toms of schizophrenia and for making clinical decisions.展开更多
The rostral ventromedial medulla （RVM） is a prominent component of the descending modulatory system involved in the control of spinal nociceptive transmission. In the current study, we investigated melanocortin-4 re...The rostral ventromedial medulla （RVM） is a prominent component of the descending modulatory system involved in the control of spinal nociceptive transmission. In the current study, we investigated melanocortin-4 receptor （MC4R） expression in the RVM, where the neurons involved in modulation of nociception reside. Using a line of mice expressing green fluorescent protein （GFP） under the control of the MC4R promoter, we found a large number of GFP-positive neurons in the RVM [nucleus raphe magnus （NRM） and nucleus gigantocellularis pars a （NGCa）]. Fluorescence immunohisto- chemistry revealed that approximately 10% of MC4R-GFP-positive neurons coexpressed tyrosine hydroxylase, indicating that they were catecholaminergic, whereas 50%-75% of those coexpressed tryp- tophan hydroxylase, indicating that they were serotonergic. Our findings support the hypothesis that MC4R signaling in RVM may modulate the activity of serotonergic sympathetic outflow sensitive to nociceptive signals, and that MC4R signaling in RVM may contribute to the descending modulation of nociceptive transmission.展开更多
Neuro myelitis optica spectrum disorder(NMOSD) is an inflammatory demyelinating disease of the central nervous system.However,whether and how cortical changes occur in NMOSD with normal-appearing brain tissue,or wheth...Neuro myelitis optica spectrum disorder(NMOSD) is an inflammatory demyelinating disease of the central nervous system.However,whether and how cortical changes occur in NMOSD with normal-appearing brain tissue,or whether any cortical changes correlate with clinical chara cteristics,is not completely clear.The current study recruited 43 patients with NMOSD who had normal-appearing brain tissue and 45 healthy controls matched for age,sex,and educational background from December 2020 to February 2022.A surface-based morphological analysis of high-resolution T1-weighted structural magnetic resonance images was used to calculate the cortical thickness,sulcal depth,and gyrification index.Analysis showed that cortical thickness in the bilate ral rostral middle frontal gyrus and left superior frontal gyrus was lower in the patients with NMOSD than in the control participants.Subgroup analysis of the patients with NMOSD indicated that compared with those who did not have any optic neuritis episodes,those who did have such episodes exhibited noticeably thinner cortex in the bilateral cuneus,superior parietal co rtex,and pericalcarine co rtex.Correlation analysis indicated that co rtical thickness in the bilateral rostral middle frontal gyrus was positively correlated with scores on the Digit Symbol Substitution Test and negatively correlated with scores on the Trail Making Test and the Expanded Disability Status Scale.These results are evidence that cortical thinning of the bilateral regional frontal cortex occurs in patients with NMOSD who have normal-appearing brain tissue,and that the degree of thinning is correlated with clinical disability and cognitive function.These findings will help im prove our understanding of the imaging chara cteristics in NMOSD and their potential clinical significance.展开更多
Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP). Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facili...Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP). Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facilitation circuitry, but so far the mechanisms are poorly known. In this study, we investigated the role of RVM glial activation in the descending nociceptive facilitation circuitry in a CIBP rat model. CIBP rats showed significant activation of microglia and astrocytes, and also up-regulation of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and pro-inflammatory mediators released by glial cells (IL-1β, IL-6, TNF-α and brain-derived neurotrophic factor) in the RVM. Stereotaxic microinjection of the glial inhibitors (minocycline and fluorocitrate) into CIBP rats’ RVM could reverse the glial activation and significantly attenuate mechanical allodynia in a time-dependent manner. RVM microinjection of p38 MAPK inhibitor (SB203580) abolished the activation of microglia, reversed the associated up-regulation of proinflammatory mediators and significantly attenuated mechanical allodynia. Taken together, these results suggest that RVM glial activation is involved in the pathogenesis of CIBP. RVM microglial p38 MAPK signaling pathway is activated and leads to the release of downstream pro-inflammatory mediators, which contribute to the descending facilitation of CIBP.展开更多
New neurons are integrated into the circuitry of the olfactory bulb throughout the lifespan in the mamma- lian brain--including in humans. These new neurons are born in the subventricular zone and subsequently mature ...New neurons are integrated into the circuitry of the olfactory bulb throughout the lifespan in the mamma- lian brain--including in humans. These new neurons are born in the subventricular zone and subsequently mature as they are guided over long distances via the rostral migratory stream through mechanisms we are only just beginning to understand. Regeneration after brain injury is very limited, and although some neuroblasts from the rostral migratory stream will leave the path and migrate toward cortical lesion sites, this neuronal replacement is generally not sustained and therefore does not provide enough new neurons to alleviate functional deficits. Using newly discovered microtissue engineering techniques, we have built the first self-contained, implantable constructs that mimic the architecture and function of the rostral migratory stream. This engineered microtissue emulates the dense cord-like bundles of astrocytic somata and processes that are the hallmark anatomical feature of the glial tube. As such, our living microtissue-en- gineered rostral migratory stream can serve as an in vitro test bed for unlocking the secrets of neuroblast migration and maturation, and may potentially serve as a living transplantable construct derived from a patient＇s own cells that can redirect their own neuroblasts into lesion sites for sustained neuronal replace- ment following brain injury or neurodegenerative disease. In this paper, we summarize the development of fabrication methods for this microtissue-engineered rostral migratory stream and provide proof-of-princi- ple evidence that it promotes and directs migration of immature neurons.展开更多
Objective: The present study was designed to investigate the effect of microinfusion angiotensin Ⅱ(Ang Ⅱ),Ang Ⅱ type 1(AT_1)receptor antagonist losartan into the rostral ventrolateral medulla(RVLM)on the barorecept...Objective: The present study was designed to investigate the effect of microinfusion angiotensin Ⅱ(Ang Ⅱ),Ang Ⅱ type 1(AT_1)receptor antagonist losartan into the rostral ventrolateral medulla(RVLM)on the baroreceptor reflex sensitivity(BRS)in urethane-anesthetized rats. Methods: Reflex changes in heart rate(HR)were elicited by bolus intravenous injection of phenylephrine before and during RVLM microinfusion of saline(0.5 μl/h),Ang Ⅱ (1.5 nmol/h),losartan(250 nmol/h),and Ang Ⅱ(1.5 nmol/h)pretreated with microinjection of losartan (50 nmol/0.51 μl)into the RVLM.The average ratio between changes in HR in beats per minute(beats·min -1)and changes in mean arterial pressure [MAP,mmHg(1 mmHg=0.133 kPa)] was used as an index of BRS. Results: Ang Ⅱ resulted in a significant decrease in the BRS for reflex bradycardia compared with control(-2.1±0.1 vs-3.9±0.4 beats·min -1·mmHg -1).Microinfusion of losartan had no significant effect on BRS for reflex bradycardia.The effect of Ang Ⅱ was almost completely abolished by pretreatment with microinjection of losartan. Conclusion:These results showed that the exogenous Ang Ⅱ in the RVLM produces inhibitory modulation of BRS,which is mediated by AT_1 receptor.However,AT_1 receptor in the RVLM is not involved in the tonic control of BRS.展开更多
The rostral agranular insular cortex(RAIC)has been associated with pain modulation.Although the endogenous cannabinoid system(eCB)has been shown to regulate chronic pain,the roles of eCBs in the RAIC remain elusive un...The rostral agranular insular cortex(RAIC)has been associated with pain modulation.Although the endogenous cannabinoid system(eCB)has been shown to regulate chronic pain,the roles of eCBs in the RAIC remain elusive under the neuropathic pain state.Neuropathic pain was induced in C57BL/6 mice by common peroneal nerve(CPN)ligation.The roles of the eCB were tested in the RAIC of ligated CPN C57BL/6J mice,glutamatergic,or GABAergic neuron cannabinoid receptor 1(CB1R)knockdown mice with the whole-cell patch-clamp and pain behavioral methods.The E/I ratio(amplitude ratio between mEPSCs and mIPSCs)was significantly increased in layer V pyramidal neurons of the RAIC in CPN-ligated mice.Depolarization-induced suppression of inhibition but not depolarization-induced suppression of excitation in RAIC layer V pyramidal neurons were significantly increased in CPN-ligated mice.The analgesic effect of ACEA(a CB1R agonist)was alleviated along with bilateral dorsolateral funiculus lesions,with the administration of AM251(a CB1R antagonist),and in CB1R knockdown mice in GABAergic neurons,but not glutamatergic neurons of the RAIC.Our results suggest that CB1R activation reinforces the function of the descending pain inhibitory pathway via reducing the inhibition of glutamatergic layer V neurons by GABAergic neurons in the RAIC to induce an analgesic effect in neuropathic pain.展开更多
The initial mechanical damage of a spinal cord injury(SCI)triggers a progressive secondary injury cascade,which is a complicated process integrating multiple systems and cells.It is crucial to explore the molecular an...The initial mechanical damage of a spinal cord injury(SCI)triggers a progressive secondary injury cascade,which is a complicated process integrating multiple systems and cells.It is crucial to explore the molecular and biological process alterations that occur after SCI for therapy development.The differences between the rostral and caudal regions around an SCI lesion have received little attention.Here,we analyzed the differentially expressed genes between rostral and caudal sites after injury to determine the biological processes in these two segments after SCI.We identified a set of differentially expressed genes,including Col3a1,Col1a1,Dcn,Fn1,Kcnk3,and Nrg1,between rostral and caudal regions at different time points following SCI.Functional enrichment analysis indicated that these genes were involved in response to mechanical stimulus,blood vessel development,and brain development.We then chose Col3a1,Col1a1,Dcn,Fn1,Kcnk3,and Nrg1 for quantitative real-time PCR and Fn1 for immunostaining validation.Our results indicate alterations in different biological events enriched in the rostral and caudal lesion areas,providing new insights into the pathology of SCI.展开更多
Neurogenesis is the process by which cells divide, migrate, and subsequently differentiate into a neuronal phenotype. Significant rates of neurogenesis persist into adulthood in two brain regions, the subgranular zone...Neurogenesis is the process by which cells divide, migrate, and subsequently differentiate into a neuronal phenotype. Significant rates of neurogenesis persist into adulthood in two brain regions, the subgranular zone of the dentate gyrus and the subventricular zone of the lateral ventricles. Cells of the subventricular zone divide and migrate via the rostral migratory stream to the olfactory bulb where they differentiate into granule and pefiglomerular cells. With the discovery of large-sca^e neurogenesis in the adult brain, there have been significant efforts to identify the mechanisms that control this process as well as the role of these cells in neuronal functioning. Although many questions remain unanswered, new insights appear daily about adult neurogenesis, regulatory mechanisms, and the fates of the progeny. In this review we highlight the main studies investigating factors that regulate neurogenesis in the subventricular zone, neuronal migration to the olfactory bulb, neuronal integration into the existing bulbar network and shortly discuss the functional meaning of this process.展开更多
The nucleus tractus solitarii(NTS)is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity.Phenotypically-characterized NTS neurons have been im...The nucleus tractus solitarii(NTS)is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity.Phenotypically-characterized NTS neurons have been implicated in the differential regulation of blood pressure(BP).Here,we investigated whether phenylethanolamine N-methyltransferase(PNMT)-expressing NTS(NTS^(PNMT))neurons contribute to the control of BP.We demonstrate that photostimulation of NTS^(PNMT)neurons has variable effects on BP.A depressor response was produced during optogenetic stimulation of NTS^(PNMT)neurons projecting to the paraventricular nucleus of the hypothalamus,lateral parabrachial nucleus,and caudal ventrolateral medulla.Conversely,photostimulation of NTS^(PNMT)neurons projecting to the rostral ventrolateral medulla produced a robust pressor response and bradycardia.In addition,genetic ablation of both NTS^(PNMT)neurons and those projecting to the rostral ventrolateral medulla impaired the arterial baroreflex.Overall,we revealed the neuronal phenotype-and circuit-specific mechanisms underlying the contribution of NTS^(PNMT)neurons to the regulation of BP.展开更多
The brainstem is a major site in the central nervous system involved in the processing of the cardiovascular reflexes such as the baroreflex and the peripheral chemoreflex. The nucleus tractus solitarius and the rostr...The brainstem is a major site in the central nervous system involved in the processing of the cardiovascular reflexes such as the baroreflex and the peripheral chemoreflex. The nucleus tractus solitarius and the rostral ventrolateral medulla are 2 important brainstem nuclei, and they play pivotal roles in autonomic cardiovascular regulation. Angiotensin II is one of the neurotransmitters involved in the processing of the known that one of the mechanisms by which angiotensin II exerts cardiovascular reflexes within the brainstem. It is well- its effect is via the activation of pathways that generate reactive oxygen species （ROS）. In the central nervous system, ROS are reported to be involved in several pathological dis- eases such as hypertension, heart failure and sleep apnea. However, little is known about the role of ROS in the processing of the cardiovascular reflexes within the brainstem. The present review mainly discussed some recent findings documenting a role for ROS in the processing of the baroreflex and the peripheral chemoreflex in the brainstem.展开更多
Objective: To study the characteristics of the postsynaptic potentials in thoracic sympatheticpreganglionic neurons (SPNs) evoked by electrical stimulation of the rostral ventrolateral medulla (RVLM ) incats. Methods:...Objective: To study the characteristics of the postsynaptic potentials in thoracic sympatheticpreganglionic neurons (SPNs) evoked by electrical stimulation of the rostral ventrolateral medulla (RVLM ) incats. Methods: In 11 α--chloralose/urethane anesthetized, artificially ventilated cats, intracellular recordings weremade from T, spinal cord with microelectrodes filled with 3 mol/L KCl. SPNs were identified by antidromicstimulation of the T3 white ramus. Results: Twenty--four SPNs were recorded, the resting membrane potentials ofwhich ranged between -- 45 -- -- 90 mV. The onset latency and threshold of the antidromic action potentialsaveraged (6. 48 + 0. 89) ms and (2. 86 + 0. 37) V respectively. Single pulse (0. 2 ms. 50-- 300 PA) electricalstimulation of RVLM evoked fast excitatory postsynaptic potentials (eEPSPs) with short latencies (4--47 ms) inall the 24 SPNs. In 11 of the SPNs, EPSPs with longer latencies (IEPSPs, 70-- 140 ms) were also recorded. Mostof the eEPSPs and some of the IEPSPs were typical monosynaptic EPSPs as they were of constant onset latency.Conclusion: The results provided direct physiological evidence for that some RVLM sympathoexcitatory neuronsproject monosynaptically to thoracic SPNs. The descending pathways from RVLM may consist of two distinctgroups of fibers, the conduction velocities were calculated to be 5--25 m/s and 0. 78-- 1. 6 m/s respectively.展开更多
The impact of the gustatory stimuli on the rostral portion of the nucleus of the solitary tract (rNST) was investigated in developing rats, by using c-fos immunohistochemical staining. Wistar male rats of 5, 15, and 2...The impact of the gustatory stimuli on the rostral portion of the nucleus of the solitary tract (rNST) was investigated in developing rats, by using c-fos immunohistochemical staining. Wistar male rats of 5, 15, and 25 days of age were isolated from the mother for 12 h, then stimulated via the intraoral route with quinine, sucrose, or NaCl, and sacrificed 90 min later. The water-stimulated group showed minimal c-fos-like immunoreactivity (FLI) compared with taste-stimulated groups that exhibited different FLI in the rNST at the different ages. At all ages the quinine-stimulated group induced FLI in the medial subfield, while sucrose induced FLI in the lateral subfield of the rNST. The intensity of FLI was highest at P15, and it declined at P25. These findings provide detailed insight into the anatomical basis of rNST activation that is involved in early food intake and the learning capacity of the newborn.展开更多
基金Grants from the Canadian Forest Service(CFS) and a Discovery grant from the Natural Sciences and Engineering Research Council of Canada to MC
文摘The ichnovirus TrIV, transmitted by the endoparasitic wasp Tranosema rostrale to its lepidopteran host during oviposition, replicates asymptomatically in wasp ovaries and causes physiological dysfunctions in parasitized caterpillars. The need to identify ichnoviral genes responsible for disturbances induced in lepidopteran hosts has provided the impetus for the sequencing and annotation of ichnovirus genomes, including that of TrIV. In the latter, 86 putative genes were identified, including 35 that could be assigned to recognized ichnoviral gene families. With the aim of assessing the relative importance of each TrIV gene, as inferred from its level of expression, and evaluating the accuracy of the gene predictions made during genome annotation, the present study builds on an earlier qPCR quantification of transcript abundance of TrIV rep ORFs, in both lepidopteran and wasp hosts, extending it to other gene families as well as to a sample of unassigned ORFs. We show that the majority (91%) of putative ORFs assigned to known gene families are expressed in infected larvae, while this proportion is lower (67%) for a sample taken among the remaining ORFs. Selected members of the TrV and rep gene families are shown to be transcribed in infected larvae at much higher levels than genes from any other TrIV gene family, pointing to their likely involvement in host subjugation. In wasp ovaries, the transcriptional profile is dominated by a rep gene and a member of a newly described gene family encoding secreted proteins displaying a novel cysteine motif, which we identified among previously unassigned ORFs.
基金Supported by National Natural Science Foundation of China:8197375,82074536,82104999Cultivation of Outstanding and Top Talents in Universities of Anhui Province:gxgwfx2019025Nature Science Research Project of Anhui province:2108085Y30,2108085QH36。
文摘ObjectiveTo observe the effects of pretreatment with electroacupuncture (EA) on neuron activity in the rostral ventrolateral medulla (RVLM) of rats with myocardial ischemia-reperfusion injury (MIRI) and explore the central regulatory mechanism of EA in attenuating MIRI.MethodsOf 72 SD rats, 12 were randomly allocated into the group of EA pretreatment + RVLM nucleus damage (EA + RVLM lesion group). The other 60 rats were randomized (20 rats each) into a sham-operation group, a model group, and an EA pretreatment group (EA group). Except for the rats in the sham-operation group, the models of MIRI were prepared by ligating the left anterior descending coronary artery in the model, EA, and EA + RVLM lesion groups. The rats of the EA group were intervened with EA at “Shénmén (神门HT7)” and “Tōnglĭ (通里HT5)”, 1 mA in current intensity and 2 Hz in frequency, for 20 min each time per day. Before modeling, the intervention was given for seven consecutive days. In the EA + RVLM lesion group, 3 weeks after microinjection with the neuronal apoptotic virus at bilateral RVLM, the same EA intervention as the EA group was provided. Afterward, the MIRI models were prepared. In the model group, no EA intervention was given. Using Powerlab electrophysiolograph, ST segment displacement value and arrhythmia score were recorded and analyzed before modeling, 30 min after ligation, and 120 min after reperfusion in each group. The concentration of cardiac troponin (cTnl) was detected with an ELISA assay kit. Using immunofluorescence staining, the expression level of c-fos protein of RVLM was detected in the sham-operation, model, and EA groups separately. Plexon multichannel acquisition processor was adopted to record the neuronal firing and field potential of RVLM in the sham-operation, model, and EA groups.ResultsST segment displacement value, arrhythmia score, and cTnl concentration 30 min after ligation and 120 min after reperfusion were all elevated in the model group compared to the sham-operation group (all P < 0.01). ST segment displacement value, arrhythmia score, and cTnl concentration were lower in the EA group compared to the model and EA + RVLM lesion groups (P < 0.01). Compared with the sham-operation group, the expression level of c-fos and the total firing frequency in RVLM were significantly higher in the model group (P < 0.01). However, the expression level of c-fos and the total firing frequency in RVLM were lower in the EA group compared with the model group (P < 0.01).ConclusionElectroacupuncture pretreatment may induce changes in c-fos protein expression and neuronal activity in RVLM to mitigate myocardial lesions. RVLM plays an important role in electroacupuncture pretreatment for alleviating MIRI.
基金supported by the National Natural Science Foundation of China (30900444,31070973,30870835,31121061 and 30830044)
文摘Objective The rostral anterior cingulate cortex （rACC） is implicated in processing the emotional component of pain. N-methyl-D-aspartate receptors （NMDARs） are highly expressed in the rACC and mediate painrelated affect by activating a signaling pathway that involves cyclic adenosine monophosphate （cAMP）/protein ki- nase A （PKA） and/or extracellular regulated kinase （ERK）/cAMP-response element-binding protein （CREB）. The present study investigated the contributions of the NMDAR glycine site and GluN2B subunit to the activation of ERK and CREB both in vitro and in vivo in rat rACC. Methods Immunohistochemistry and Western blot analy- sis were used to separately assess the expression of phospho-ERK （pERK） and phospho-CREB （pCREB） in vitro and in vivo. Double immunostaining was also used to determine the colocalization of pERK and pCREB. Results Both bath application of NMDA in brain slices in vitro and intraplantar injection of formalin into the rat hindpaw in vivo induced significant up-regulation of pERK and pCREB in the rACC, which was inhibited by the NMDAR antago- nist DL-2-amino-5-phospho-novaleric acid. Selective blockade of the NMDAR GluN2B subunit and the glycine- binding site, or degradation of endogenous D-serine, a co-agonist for the glycine site, significantly decreased the up- regulation of pERK and pCREB expression in the rACC. Further, the activated ERK predominantly colocalized with CREB. Conclusion Either the glycine site or the GluN2B subunit of NMDARs participates in the phosphorylation of ERK and CREB induced by bath application of NMDA in brain slices or hindpaw injection of 5% formalin in rats, and these might be fundamental molecular mechanisms underlying pain affect.
基金supported by grants from the National Institutes of Health (NS059028,NS060735, DE011964, DE021804, and DE018573)
文摘Objective Despite accumulating evidence on a role of immune cells and their associated chemicals in mecha- nisms of pain, few studies have addressed the potential role of chemokines in the descending facilitation of persistent pain. The present study was undertaken to test the hypothesis that the chemokine （C-C motif） ligand 2 （CCL2） （commonly known as monocyte chemoattractant protein-1） signaling in the rostral ventromedial medulla （RVM）, a pivotal structure in brainstem pain modulatory circuitry, is involved in descending pain facilitation in rats. Methods An L5 spinal nerve ligation （SNL） was produced in rats under pentobarbital anesthesia. Western blot and immunohistochemistry were used to detect the expression levels of CCL2 and CCL2 receptor （CCR2）, and examine their distributions compared with the neuronal marker NeuN as well as glial markers glial fibrillary acidic protein （GFAP, astroglial） and CD 11 b （microglial）, respectively. Results SNL induced an increase in CCL2 expression in the RVM, and this returned to the control level at 4 weeks after injury. The induced CCL2 colocalized with NeuN, but not with GFAP and CD1 lb. CCR2 was also upregu- lated by SNL in the RVM, and this increase lasted for at least 4 weeks. CCR2 was colocalized with CD1 lb but not GFAP. Few RVM neurons also exhibited CCR2 staining. Neutralizing CCL2 with an anti-CCL2 antibody （0.2-20 ng） or injecting RS-102895 （0.1-10 pmol）, a CCR2b chemokine receptor antagonist, into the RVM on day 1 after SNL, significantly at- tenuated the established thermal and mechanical hypersensitivity. In addition, injection of recombinant rat CCL2 （0.03-3 pmol） into the RVM induced dose-dependent hyperalgesia, which was prevented by pretreatment with RS-102895 （10 pmol）. Interleukin-β （IL-1]3）, a potent inducer of neuronal CCL2, was also selectively upregulated in RVM reactive as- trocytes. Injection of IL-1 ]3 （120 fmol） into the RVM induced behavioral hyperalgesia, which was blocked by RS-102895 （10 pmol）. However, an IL-1 receptor antagonist （3 pmol） did not prevent CCL2 （3 pmol）-induced hyperalgesia. These results suggest that the effect of CCL2 is downstream to IL-113 signaling. Conclusion The IL-1 β and CCL2-CCR2 signaling cascades play a role in neuron-glia-cytokine interactions and the descending facilitation of neuropathic pain.
基金supported by the National Basic Research Development Program of China(2011CB707805)the National Natural Science Foundation of China(91232305,81361120395,91432304,81370032,and 81601171)the National Key Technology R&D Program of China(2015BAI13B01)
文摘Cross-sectional and longitudinal studies have identified widespread and progressive grey matter volume （GMV） reductions in schizophrenia, especially in the frontal lobe. In this study, we found a progressive GMV decrease in the rostral medial frontal cortex （rMFC, including the anterior cingulate cortex） in the patient group during a 6-week follow-up of 40 patients with schizophrenia and 31 healthy controls well-matched for age, gender, and education. The higher baseline GMV in the rMFC predicted better improvement in the positive score on the Positive and Negative Syndrome Scale （PANSS）, and this might be related to the improved reality-monitoring. Besides, a higher baseline GMV in the posterior rMFC predicted better remission of general symptoms, and a lesser GMV reduction in this region was correlated with better remission of negative symptoms, probably associated with ameliorated self-referential pro- cessing and social cognition. Besides, a shorter disease course and higher educational level contributed to better improvement in the general psychopathological PANSS score, and a family history was negatively associated with improvement of the negative and total PANSS scores. These phenomena might be important for understanding the neuropathological mechanisms underlying the symp- toms of schizophrenia and for making clinical decisions.
基金supported by grants from National Natural Science Foundation of China(No.81071307,No.81271766,and No.81673964)Special Fund of Fundamental Scientific Research Business Expense for Higher School of Central Government(No.2012TS060)
文摘The rostral ventromedial medulla （RVM） is a prominent component of the descending modulatory system involved in the control of spinal nociceptive transmission. In the current study, we investigated melanocortin-4 receptor （MC4R） expression in the RVM, where the neurons involved in modulation of nociception reside. Using a line of mice expressing green fluorescent protein （GFP） under the control of the MC4R promoter, we found a large number of GFP-positive neurons in the RVM [nucleus raphe magnus （NRM） and nucleus gigantocellularis pars a （NGCa）]. Fluorescence immunohisto- chemistry revealed that approximately 10% of MC4R-GFP-positive neurons coexpressed tyrosine hydroxylase, indicating that they were catecholaminergic, whereas 50%-75% of those coexpressed tryp- tophan hydroxylase, indicating that they were serotonergic. Our findings support the hypothesis that MC4R signaling in RVM may modulate the activity of serotonergic sympathetic outflow sensitive to nociceptive signals, and that MC4R signaling in RVM may contribute to the descending modulation of nociceptive transmission.
基金Clinical Research Center for Medical Imaging in Hunan Province,No.2020SK4001Science and Technology Innovation Program of Hunan Province,No.2021RC4016Accurate Localization Study of Mild Traumatic Brain Injury Based on Deep Learning Through Multimodal Image and Neural Network,No.2021gfcx05 (all to JL)。
文摘Neuro myelitis optica spectrum disorder(NMOSD) is an inflammatory demyelinating disease of the central nervous system.However,whether and how cortical changes occur in NMOSD with normal-appearing brain tissue,or whether any cortical changes correlate with clinical chara cteristics,is not completely clear.The current study recruited 43 patients with NMOSD who had normal-appearing brain tissue and 45 healthy controls matched for age,sex,and educational background from December 2020 to February 2022.A surface-based morphological analysis of high-resolution T1-weighted structural magnetic resonance images was used to calculate the cortical thickness,sulcal depth,and gyrification index.Analysis showed that cortical thickness in the bilate ral rostral middle frontal gyrus and left superior frontal gyrus was lower in the patients with NMOSD than in the control participants.Subgroup analysis of the patients with NMOSD indicated that compared with those who did not have any optic neuritis episodes,those who did have such episodes exhibited noticeably thinner cortex in the bilateral cuneus,superior parietal co rtex,and pericalcarine co rtex.Correlation analysis indicated that co rtical thickness in the bilateral rostral middle frontal gyrus was positively correlated with scores on the Digit Symbol Substitution Test and negatively correlated with scores on the Trail Making Test and the Expanded Disability Status Scale.These results are evidence that cortical thinning of the bilateral regional frontal cortex occurs in patients with NMOSD who have normal-appearing brain tissue,and that the degree of thinning is correlated with clinical disability and cognitive function.These findings will help im prove our understanding of the imaging chara cteristics in NMOSD and their potential clinical significance.
基金supported by grants from the National Natural Science Foundation of China(No.30901396,No.81070890,No.30872441and No.81171259)
文摘Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP). Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facilitation circuitry, but so far the mechanisms are poorly known. In this study, we investigated the role of RVM glial activation in the descending nociceptive facilitation circuitry in a CIBP rat model. CIBP rats showed significant activation of microglia and astrocytes, and also up-regulation of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and pro-inflammatory mediators released by glial cells (IL-1β, IL-6, TNF-α and brain-derived neurotrophic factor) in the RVM. Stereotaxic microinjection of the glial inhibitors (minocycline and fluorocitrate) into CIBP rats’ RVM could reverse the glial activation and significantly attenuate mechanical allodynia in a time-dependent manner. RVM microinjection of p38 MAPK inhibitor (SB203580) abolished the activation of microglia, reversed the associated up-regulation of proinflammatory mediators and significantly attenuated mechanical allodynia. Taken together, these results suggest that RVM glial activation is involved in the pathogenesis of CIBP. RVM microglial p38 MAPK signaling pathway is activated and leads to the release of downstream pro-inflammatory mediators, which contribute to the descending facilitation of CIBP.
基金supported by the National Institutes of Health[U01-NS094340(Cullen),F31-NS090746(Katiyar)&F32-NS103253(O’Donnell)]University of Pennsylvania[Center for Undergraduate Research&Fellowships(Panzer)]+2 种基金Michael J.Fox Foundation[Therapeutic Pipeline Program#9998(Cullen)]Department of Veterans Affairs[RR&D Merit Review I01-RX001097(Cullen)&BLR&D Merit Review I01-BX003748(Cullen)]the U.S.Army Medical Research and Materiel Command[W81XWH-16-1-0796(Cullen)]
文摘New neurons are integrated into the circuitry of the olfactory bulb throughout the lifespan in the mamma- lian brain--including in humans. These new neurons are born in the subventricular zone and subsequently mature as they are guided over long distances via the rostral migratory stream through mechanisms we are only just beginning to understand. Regeneration after brain injury is very limited, and although some neuroblasts from the rostral migratory stream will leave the path and migrate toward cortical lesion sites, this neuronal replacement is generally not sustained and therefore does not provide enough new neurons to alleviate functional deficits. Using newly discovered microtissue engineering techniques, we have built the first self-contained, implantable constructs that mimic the architecture and function of the rostral migratory stream. This engineered microtissue emulates the dense cord-like bundles of astrocytic somata and processes that are the hallmark anatomical feature of the glial tube. As such, our living microtissue-en- gineered rostral migratory stream can serve as an in vitro test bed for unlocking the secrets of neuroblast migration and maturation, and may potentially serve as a living transplantable construct derived from a patient＇s own cells that can redirect their own neuroblasts into lesion sites for sustained neuronal replace- ment following brain injury or neurodegenerative disease. In this paper, we summarize the development of fabrication methods for this microtissue-engineered rostral migratory stream and provide proof-of-princi- ple evidence that it promotes and directs migration of immature neurons.
文摘Objective: The present study was designed to investigate the effect of microinfusion angiotensin Ⅱ(Ang Ⅱ),Ang Ⅱ type 1(AT_1)receptor antagonist losartan into the rostral ventrolateral medulla(RVLM)on the baroreceptor reflex sensitivity(BRS)in urethane-anesthetized rats. Methods: Reflex changes in heart rate(HR)were elicited by bolus intravenous injection of phenylephrine before and during RVLM microinfusion of saline(0.5 μl/h),Ang Ⅱ (1.5 nmol/h),losartan(250 nmol/h),and Ang Ⅱ(1.5 nmol/h)pretreated with microinjection of losartan (50 nmol/0.51 μl)into the RVLM.The average ratio between changes in HR in beats per minute(beats·min -1)and changes in mean arterial pressure [MAP,mmHg(1 mmHg=0.133 kPa)] was used as an index of BRS. Results: Ang Ⅱ resulted in a significant decrease in the BRS for reflex bradycardia compared with control(-2.1±0.1 vs-3.9±0.4 beats·min -1·mmHg -1).Microinfusion of losartan had no significant effect on BRS for reflex bradycardia.The effect of Ang Ⅱ was almost completely abolished by pretreatment with microinjection of losartan. Conclusion:These results showed that the exogenous Ang Ⅱ in the RVLM produces inhibitory modulation of BRS,which is mediated by AT_1 receptor.However,AT_1 receptor in the RVLM is not involved in the tonic control of BRS.
基金This work was supported by the National Natural Science Foundation of China(32271056,81671081,and 81701095)University Science and Technology Fund Planning Projects(2022XC002 and 2019XB006).
文摘The rostral agranular insular cortex(RAIC)has been associated with pain modulation.Although the endogenous cannabinoid system(eCB)has been shown to regulate chronic pain,the roles of eCBs in the RAIC remain elusive under the neuropathic pain state.Neuropathic pain was induced in C57BL/6 mice by common peroneal nerve(CPN)ligation.The roles of the eCB were tested in the RAIC of ligated CPN C57BL/6J mice,glutamatergic,or GABAergic neuron cannabinoid receptor 1(CB1R)knockdown mice with the whole-cell patch-clamp and pain behavioral methods.The E/I ratio(amplitude ratio between mEPSCs and mIPSCs)was significantly increased in layer V pyramidal neurons of the RAIC in CPN-ligated mice.Depolarization-induced suppression of inhibition but not depolarization-induced suppression of excitation in RAIC layer V pyramidal neurons were significantly increased in CPN-ligated mice.The analgesic effect of ACEA(a CB1R agonist)was alleviated along with bilateral dorsolateral funiculus lesions,with the administration of AM251(a CB1R antagonist),and in CB1R knockdown mice in GABAergic neurons,but not glutamatergic neurons of the RAIC.Our results suggest that CB1R activation reinforces the function of the descending pain inhibitory pathway via reducing the inhibition of glutamatergic layer V neurons by GABAergic neurons in the RAIC to induce an analgesic effect in neuropathic pain.
基金supported by Postgraduate Research&Practice Innovation Program of Jiangsu Province,No.KYCX-2065(to XMC).
文摘The initial mechanical damage of a spinal cord injury(SCI)triggers a progressive secondary injury cascade,which is a complicated process integrating multiple systems and cells.It is crucial to explore the molecular and biological process alterations that occur after SCI for therapy development.The differences between the rostral and caudal regions around an SCI lesion have received little attention.Here,we analyzed the differentially expressed genes between rostral and caudal sites after injury to determine the biological processes in these two segments after SCI.We identified a set of differentially expressed genes,including Col3a1,Col1a1,Dcn,Fn1,Kcnk3,and Nrg1,between rostral and caudal regions at different time points following SCI.Functional enrichment analysis indicated that these genes were involved in response to mechanical stimulus,blood vessel development,and brain development.We then chose Col3a1,Col1a1,Dcn,Fn1,Kcnk3,and Nrg1 for quantitative real-time PCR and Fn1 for immunostaining validation.Our results indicate alterations in different biological events enriched in the rostral and caudal lesion areas,providing new insights into the pathology of SCI.
文摘Neurogenesis is the process by which cells divide, migrate, and subsequently differentiate into a neuronal phenotype. Significant rates of neurogenesis persist into adulthood in two brain regions, the subgranular zone of the dentate gyrus and the subventricular zone of the lateral ventricles. Cells of the subventricular zone divide and migrate via the rostral migratory stream to the olfactory bulb where they differentiate into granule and pefiglomerular cells. With the discovery of large-sca^e neurogenesis in the adult brain, there have been significant efforts to identify the mechanisms that control this process as well as the role of these cells in neuronal functioning. Although many questions remain unanswered, new insights appear daily about adult neurogenesis, regulatory mechanisms, and the fates of the progeny. In this review we highlight the main studies investigating factors that regulate neurogenesis in the subventricular zone, neuronal migration to the olfactory bulb, neuronal integration into the existing bulbar network and shortly discuss the functional meaning of this process.
基金supported by the Natural Science Foundation of China(31971050)the Natural Science Foundation of Hebei Province for Distinguished Young Scholars(H2020206509)+1 种基金Hebei Province Innovative Research Project for Postgraduate(2021074)the Natural Science Foundation of Hebei Province for Innovative Research Group Project(H2021206203).
文摘The nucleus tractus solitarii(NTS)is one of the morphologically and functionally defined centers that engage in the autonomic regulation of cardiovascular activity.Phenotypically-characterized NTS neurons have been implicated in the differential regulation of blood pressure(BP).Here,we investigated whether phenylethanolamine N-methyltransferase(PNMT)-expressing NTS(NTS^(PNMT))neurons contribute to the control of BP.We demonstrate that photostimulation of NTS^(PNMT)neurons has variable effects on BP.A depressor response was produced during optogenetic stimulation of NTS^(PNMT)neurons projecting to the paraventricular nucleus of the hypothalamus,lateral parabrachial nucleus,and caudal ventrolateral medulla.Conversely,photostimulation of NTS^(PNMT)neurons projecting to the rostral ventrolateral medulla produced a robust pressor response and bradycardia.In addition,genetic ablation of both NTS^(PNMT)neurons and those projecting to the rostral ventrolateral medulla impaired the arterial baroreflex.Overall,we revealed the neuronal phenotype-and circuit-specific mechanisms underlying the contribution of NTS^(PNMT)neurons to the regulation of BP.
文摘The brainstem is a major site in the central nervous system involved in the processing of the cardiovascular reflexes such as the baroreflex and the peripheral chemoreflex. The nucleus tractus solitarius and the rostral ventrolateral medulla are 2 important brainstem nuclei, and they play pivotal roles in autonomic cardiovascular regulation. Angiotensin II is one of the neurotransmitters involved in the processing of the known that one of the mechanisms by which angiotensin II exerts cardiovascular reflexes within the brainstem. It is well- its effect is via the activation of pathways that generate reactive oxygen species （ROS）. In the central nervous system, ROS are reported to be involved in several pathological dis- eases such as hypertension, heart failure and sleep apnea. However, little is known about the role of ROS in the processing of the cardiovascular reflexes within the brainstem. The present review mainly discussed some recent findings documenting a role for ROS in the processing of the baroreflex and the peripheral chemoreflex in the brainstem.
文摘Objective: To study the characteristics of the postsynaptic potentials in thoracic sympatheticpreganglionic neurons (SPNs) evoked by electrical stimulation of the rostral ventrolateral medulla (RVLM ) incats. Methods: In 11 α--chloralose/urethane anesthetized, artificially ventilated cats, intracellular recordings weremade from T, spinal cord with microelectrodes filled with 3 mol/L KCl. SPNs were identified by antidromicstimulation of the T3 white ramus. Results: Twenty--four SPNs were recorded, the resting membrane potentials ofwhich ranged between -- 45 -- -- 90 mV. The onset latency and threshold of the antidromic action potentialsaveraged (6. 48 + 0. 89) ms and (2. 86 + 0. 37) V respectively. Single pulse (0. 2 ms. 50-- 300 PA) electricalstimulation of RVLM evoked fast excitatory postsynaptic potentials (eEPSPs) with short latencies (4--47 ms) inall the 24 SPNs. In 11 of the SPNs, EPSPs with longer latencies (IEPSPs, 70-- 140 ms) were also recorded. Mostof the eEPSPs and some of the IEPSPs were typical monosynaptic EPSPs as they were of constant onset latency.Conclusion: The results provided direct physiological evidence for that some RVLM sympathoexcitatory neuronsproject monosynaptically to thoracic SPNs. The descending pathways from RVLM may consist of two distinctgroups of fibers, the conduction velocities were calculated to be 5--25 m/s and 0. 78-- 1. 6 m/s respectively.
文摘The impact of the gustatory stimuli on the rostral portion of the nucleus of the solitary tract (rNST) was investigated in developing rats, by using c-fos immunohistochemical staining. Wistar male rats of 5, 15, and 25 days of age were isolated from the mother for 12 h, then stimulated via the intraoral route with quinine, sucrose, or NaCl, and sacrificed 90 min later. The water-stimulated group showed minimal c-fos-like immunoreactivity (FLI) compared with taste-stimulated groups that exhibited different FLI in the rNST at the different ages. At all ages the quinine-stimulated group induced FLI in the medial subfield, while sucrose induced FLI in the lateral subfield of the rNST. The intensity of FLI was highest at P15, and it declined at P25. These findings provide detailed insight into the anatomical basis of rNST activation that is involved in early food intake and the learning capacity of the newborn.
