Trigeminal ganglia neurons significantly affect the amplitude and type of 5-HT receptor gene expression following activation of their axon terminals and sensitisation by painful stimuli. Moreover, these neurons signif...Trigeminal ganglia neurons significantly affect the amplitude and type of 5-HT receptor gene expression following activation of their axon terminals and sensitisation by painful stimuli. Moreover, these neurons significantly alter gene expression in cytoskeletal proteins following injury. The aim of the present study was to determine whether peripheral and/or central deafferenting lesions affect gene expression in serotonergic receptors that are involved in pain transmission. Adult rats were subjected to unilateral ablation of the facial sensory and motor cortices. Fifteen days after the surgery, degeneration of the cortico-trigeminal pathway was observed. Presynaptic deafferentation of the primary trigeminal neurons and central afferents of the contralateral ganglia was conducted. As a consequence of the excision of the meninges covering the ablated cortices, the peripheral axotomy of the trigeminal-vascular primary neurons of the ipsi-lateral side was induced. Serotonergic receptor (5-HT5A/5B/1B/1D/1F) gene expression was analysed in both sides of the trigeminal ganglia neurons. The results of the present study showed a significant increase in 5-HT5A/5B/1B/1D receptor gene expression in the primary sensory neurons of both ganglia, with the highest levels of expression noted in the ganglia contralateral to the lesion. 5-HT1F receptor expression, however, was more strongly expressed in the ganglia ipsilateral to the lesion. Our results also confirm that the adaptive response of primary trigeminal neurons to injury involves anatomical remodelling, as well as changes in receptor gene expression involved in sensory transmission. This may explain the distortion of sensory signals observed in trigeminal neuropathic states, and may lead to the development of novel pharmacological interventions.展开更多
Background Muscles present different responses to muscle relaxants, a mechanism of importance in surgeries requiring facial nerve evoked electromyography under general anaesthesia. The non-depolarizing muscle relaxant...Background Muscles present different responses to muscle relaxants, a mechanism of importance in surgeries requiring facial nerve evoked electromyography under general anaesthesia. The non-depolarizing muscle relaxants have multiple reaction formats in the neuromuscular junction, in which pre-synaptic quantal release of acetylcholine was one of the important mechanisms. This study was to compare the pre-synaptic quantal release of acetylcholine from the neuromuscular junctions innervated by normal/damaged facial nerves and somatic nerve under the effect of rocuronium in rats in vitro. Methods Acute right-sided facial nerve injury was induced by nerve crush axotomies. Both sided facial nerve connected orbicularis oris strips and tibial nerve connected gastrocnemius strips were isolated to measure endplate potentials （EPP） and miniature endplate potentials （MEPP） using an intracellular microelectrode gauge under different rocuronium concentrations. Then, the pre-synaptic quantal releases of acetylcholine were calculated by the ratios of the EPPs and the MEPPs, and compared among the damaged or normal facial nerve innervated orbicularis oris and tibial nerve innervated gastrocnemius. Results The EPP/MEPP ratios of the three neuromuscular junctions decreased in a dose dependent manner with the increase of the rocuronium concentration. With the concentrations of rocuronium being 5 pg/ml, 7.5 IJg/ml and 10 pg/ml, the decrease of the EPP/MEPP ratio in the damaged facial nerve group was greater than that in the normal facial nerve group. The decrease in the somatic nerve group was the biggest, with significant differences. Conclusions Rocuronium presented different levels of inhibition on the pre-synaptic quantal release of acetylcholine in the three groups of neuromuscular junctions. The levels of the inhibition showed the following sequence： somatic nerve 〉 damaged facial nerve 〉 normal facial nerve. The difference may be one of the reasons causing the different sensitivities to rocuronium among the muscles innervated by the normal/injured facial nerves and the somatic nerve. The results may provide some information for the proper usage of muscle relaxants in surgeries requiring electromyographic monitoring for the pre-surgically impaired facial nerves.展开更多
文摘Trigeminal ganglia neurons significantly affect the amplitude and type of 5-HT receptor gene expression following activation of their axon terminals and sensitisation by painful stimuli. Moreover, these neurons significantly alter gene expression in cytoskeletal proteins following injury. The aim of the present study was to determine whether peripheral and/or central deafferenting lesions affect gene expression in serotonergic receptors that are involved in pain transmission. Adult rats were subjected to unilateral ablation of the facial sensory and motor cortices. Fifteen days after the surgery, degeneration of the cortico-trigeminal pathway was observed. Presynaptic deafferentation of the primary trigeminal neurons and central afferents of the contralateral ganglia was conducted. As a consequence of the excision of the meninges covering the ablated cortices, the peripheral axotomy of the trigeminal-vascular primary neurons of the ipsi-lateral side was induced. Serotonergic receptor (5-HT5A/5B/1B/1D/1F) gene expression was analysed in both sides of the trigeminal ganglia neurons. The results of the present study showed a significant increase in 5-HT5A/5B/1B/1D receptor gene expression in the primary sensory neurons of both ganglia, with the highest levels of expression noted in the ganglia contralateral to the lesion. 5-HT1F receptor expression, however, was more strongly expressed in the ganglia ipsilateral to the lesion. Our results also confirm that the adaptive response of primary trigeminal neurons to injury involves anatomical remodelling, as well as changes in receptor gene expression involved in sensory transmission. This may explain the distortion of sensory signals observed in trigeminal neuropathic states, and may lead to the development of novel pharmacological interventions.
基金The study was supported by a grant from tt（e National Natural Science Foundation of China （No. 30872428）.
文摘Background Muscles present different responses to muscle relaxants, a mechanism of importance in surgeries requiring facial nerve evoked electromyography under general anaesthesia. The non-depolarizing muscle relaxants have multiple reaction formats in the neuromuscular junction, in which pre-synaptic quantal release of acetylcholine was one of the important mechanisms. This study was to compare the pre-synaptic quantal release of acetylcholine from the neuromuscular junctions innervated by normal/damaged facial nerves and somatic nerve under the effect of rocuronium in rats in vitro. Methods Acute right-sided facial nerve injury was induced by nerve crush axotomies. Both sided facial nerve connected orbicularis oris strips and tibial nerve connected gastrocnemius strips were isolated to measure endplate potentials （EPP） and miniature endplate potentials （MEPP） using an intracellular microelectrode gauge under different rocuronium concentrations. Then, the pre-synaptic quantal releases of acetylcholine were calculated by the ratios of the EPPs and the MEPPs, and compared among the damaged or normal facial nerve innervated orbicularis oris and tibial nerve innervated gastrocnemius. Results The EPP/MEPP ratios of the three neuromuscular junctions decreased in a dose dependent manner with the increase of the rocuronium concentration. With the concentrations of rocuronium being 5 pg/ml, 7.5 IJg/ml and 10 pg/ml, the decrease of the EPP/MEPP ratio in the damaged facial nerve group was greater than that in the normal facial nerve group. The decrease in the somatic nerve group was the biggest, with significant differences. Conclusions Rocuronium presented different levels of inhibition on the pre-synaptic quantal release of acetylcholine in the three groups of neuromuscular junctions. The levels of the inhibition showed the following sequence： somatic nerve 〉 damaged facial nerve 〉 normal facial nerve. The difference may be one of the reasons causing the different sensitivities to rocuronium among the muscles innervated by the normal/injured facial nerves and the somatic nerve. The results may provide some information for the proper usage of muscle relaxants in surgeries requiring electromyographic monitoring for the pre-surgically impaired facial nerves.
