Predatory hunting is an important type of innate behavior evolutionarily conserved across the animal king-dom.It is typically composed of a set of sequential actions,including prey search,pursuit,attack,and consumptio...Predatory hunting is an important type of innate behavior evolutionarily conserved across the animal king-dom.It is typically composed of a set of sequential actions,including prey search,pursuit,attack,and consumption.This behavior is subject to control by the nervous system.Early studies used toads as a model to probe the neuroethology of hunting,which led to the proposal of a sensory-triggered release mechanism for hunting actions.More recent stud-ies have used genetically-trackable zebrafish and rodents and have made breakthrough discoveries in the neuroethol-ogy and neurocircuits underlying this behavior.Here,we review the sophisticated neurocircuitry involved in hunting and summarize the detailed mechanism for the circuitry to encode various aspects of hunting neuroethology,including sensory processing,sensorimotor transformation,motivation,and sequential encoding of hunting actions.We also discuss the overlapping brain circuits for hunting and feeding and point out the limitations of current studies.We propose that hunting is an ideal behavioral paradigm in which to study the neuroethology of motivated behaviors,which may shed new light on epidemic disorders,including bingeeating,obesity,and obsessive-compulsive disorders.展开更多
In 2012,we published the first special issue on the mechanisms of pain and itch in Neuroscience Bulletin[1],covering peripheral[2,3],central[4],and glial[5]mechanisms.In 2018,the second special issue expanded on these...In 2012,we published the first special issue on the mechanisms of pain and itch in Neuroscience Bulletin[1],covering peripheral[2,3],central[4],and glial[5]mechanisms.In 2018,the second special issue expanded on these topics[6],featuring single-cell profiling and in vivo Ca2+imaging of primary sensory neurons[7,8],and illustrating how nociceptors regulate pain,itch,and infection[9].It also highlighted spinal neurocircuits of pain[10]and itch[11],glial contributions[12],sex differences[13],and supraspinal mechanisms underlying pain and empathy[14,15].Over the past seven years,significant advances have been made in neuroglial and neuroimmune interactions and supraspinal circuits.Thus,this third special issue—comprising one review,eleven original articles,and one research highlight[16,17,18,19,20,21,22,23,24,25,26,27,28]—timely summarizes recent progress in pain and itch research.展开更多
Chronic pain is a common clinical condition that is frequently linked to negative emotions such as anxiety and depression.Electroacupuncture(EA) has been shown to have beneficial therapeutic effects in analgesia and t...Chronic pain is a common clinical condition that is frequently linked to negative emotions such as anxiety and depression.Electroacupuncture(EA) has been shown to have beneficial therapeutic effects in analgesia and the reduction of pain-induced negative emotions,and promising results have been obtained in the study of its neural circuit mechanism.Optogenetics,chemogenetics,neurocircuit tracing,functional magnetic resonance imaging(fMRI),and conditional gene knockdown experiments have shown that EA activates parvalbumin(PV) interneurons in the anterior cingulate cortex(ACC),inhibits Protein kinase Mzeta-glutamate receptor(PKMzeta-GluR1) signaling pathway in ACC,and upregulates the expression of the neuropeptide S/neuropeptide S receptor(NPS/NPSR) system in ACC to alleviate pain and pain-induced anxiety.EA activates endogenous cannabinoid receptors 1(CB1Rs),inhibits y-aminobutyric acid(^(GABA))-ergic neurons and activates glutamatergic neurons in the ventrolateral periaqueductal gray(vlPAG) to exert an analgesic effect,while EA exerts an anxiolytic effect by downregulating CB1R in ^(GABA)ergic neurons in the ventral hippocampus(vHPC).EA relieves only pain-induced anxiety but not pain through inhibiting the rostral anterior cingulate cortex(rACC)Glu-thalamus circuit.By inhibiting the medial prefrontal cortex(mPFC)Glu-vlPAC^(GABA)circuit,EA relieves only pain but not pain-induced anxiety.EA activated dopamine receptor D1(DRD1) or inhibited dopamine receptor D2(DRD2) in the basolateral amygdala(BLA) to alleviate anxiety-like behaviors.Taken together,these findings would offer a novel theoretical framework for a thorough investigation of theoretical studies and clinical promotion of EA analgesic mechanisms.展开更多
文摘Predatory hunting is an important type of innate behavior evolutionarily conserved across the animal king-dom.It is typically composed of a set of sequential actions,including prey search,pursuit,attack,and consumption.This behavior is subject to control by the nervous system.Early studies used toads as a model to probe the neuroethology of hunting,which led to the proposal of a sensory-triggered release mechanism for hunting actions.More recent stud-ies have used genetically-trackable zebrafish and rodents and have made breakthrough discoveries in the neuroethol-ogy and neurocircuits underlying this behavior.Here,we review the sophisticated neurocircuitry involved in hunting and summarize the detailed mechanism for the circuitry to encode various aspects of hunting neuroethology,including sensory processing,sensorimotor transformation,motivation,and sequential encoding of hunting actions.We also discuss the overlapping brain circuits for hunting and feeding and point out the limitations of current studies.We propose that hunting is an ideal behavioral paradigm in which to study the neuroethology of motivated behaviors,which may shed new light on epidemic disorders,including bingeeating,obesity,and obsessive-compulsive disorders.
文摘In 2012,we published the first special issue on the mechanisms of pain and itch in Neuroscience Bulletin[1],covering peripheral[2,3],central[4],and glial[5]mechanisms.In 2018,the second special issue expanded on these topics[6],featuring single-cell profiling and in vivo Ca2+imaging of primary sensory neurons[7,8],and illustrating how nociceptors regulate pain,itch,and infection[9].It also highlighted spinal neurocircuits of pain[10]and itch[11],glial contributions[12],sex differences[13],and supraspinal mechanisms underlying pain and empathy[14,15].Over the past seven years,significant advances have been made in neuroglial and neuroimmune interactions and supraspinal circuits.Thus,this third special issue—comprising one review,eleven original articles,and one research highlight[16,17,18,19,20,21,22,23,24,25,26,27,28]—timely summarizes recent progress in pain and itch research.
基金Sponsored by National Natural Science Foundation of China:No.81973949。
文摘Chronic pain is a common clinical condition that is frequently linked to negative emotions such as anxiety and depression.Electroacupuncture(EA) has been shown to have beneficial therapeutic effects in analgesia and the reduction of pain-induced negative emotions,and promising results have been obtained in the study of its neural circuit mechanism.Optogenetics,chemogenetics,neurocircuit tracing,functional magnetic resonance imaging(fMRI),and conditional gene knockdown experiments have shown that EA activates parvalbumin(PV) interneurons in the anterior cingulate cortex(ACC),inhibits Protein kinase Mzeta-glutamate receptor(PKMzeta-GluR1) signaling pathway in ACC,and upregulates the expression of the neuropeptide S/neuropeptide S receptor(NPS/NPSR) system in ACC to alleviate pain and pain-induced anxiety.EA activates endogenous cannabinoid receptors 1(CB1Rs),inhibits y-aminobutyric acid(^(GABA))-ergic neurons and activates glutamatergic neurons in the ventrolateral periaqueductal gray(vlPAG) to exert an analgesic effect,while EA exerts an anxiolytic effect by downregulating CB1R in ^(GABA)ergic neurons in the ventral hippocampus(vHPC).EA relieves only pain-induced anxiety but not pain through inhibiting the rostral anterior cingulate cortex(rACC)Glu-thalamus circuit.By inhibiting the medial prefrontal cortex(mPFC)Glu-vlPAC^(GABA)circuit,EA relieves only pain but not pain-induced anxiety.EA activated dopamine receptor D1(DRD1) or inhibited dopamine receptor D2(DRD2) in the basolateral amygdala(BLA) to alleviate anxiety-like behaviors.Taken together,these findings would offer a novel theoretical framework for a thorough investigation of theoretical studies and clinical promotion of EA analgesic mechanisms.
