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5-HT_(2A) receptor mediates the ventrolateral orbital cortex-evoked antiallodynia in a neuropathic pain model of rats:A possible presynaptic facilitatory effect

【摘要】:正Previous studies have indicated that the ventrolateral orbital cortex(VLO),as a high center,is involved in an endogenous analgesic system consisting of a spinal cord-thalamic nucleus submedius-VLO-periaqueductal gray(PAG)-spinal cord loop.Behavioral study has showed that 5-HT_(2A) receptor is involved in the VLO mediated descending antinociception in the tail flick test.However,it is unknown,under neuropathic pain state,whether the VLO 5-HT_2 receptor is also involved.Since the 5-HT_(2A) receptor is an excitatory G-protein coupled receptor and is distributed not only in the postsynaptic neurons,but also in presynaptic neurons or terminals.Therefore,we suppose that activation of 5-HT_(2A) receptor induced anti-neuropathic pain in VLO may be produced,except for by postsynaptic direct activation of the VLO neurons projecting to PAG,also probably through a presynaptic facilitatory effect on the excitatory glutamate synapse transmission,leading to activation of the VLO-PAG brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal level.To provide support for this hypothesis,the current study was designed to examine whether 5-HT_(2A) receptor activation-induced anti-allodynia could be blocked by glutamate receptor antagonist and enhanced by its agonist.Paw withdrawal threshold(PWT) as an index of nociceptive response was measured in response to mechanical stimulation(von Frey filaments) in the spared nerve injury(SNI) rats.The effect of microinjection of drugs into the VLO on the PWT was observed.The results showed that microinjection of DOI(2,4,8,16 nmol/0.5μL),a selective 5-HT_(2A) receptor agonist,into VLO attenuated SNI-induced mechanical allodynia in a dose-dependent manner.This effect was completely blocked by the selective 5-HT_(2A) receptor antagonist ketanserin tartrate salt(10 nmol/0.5μL) or significantly attenuated by premicroinjection of a non-selective glutamate receptor antagonist kynurenic acid(KA,2 nmol/0.5μL) into VLO.A small dose(25 nmol/0.5μL) of glutamate administrated into the VLO significantly enhanced the DOI(2 nmol/0.5μL)-induced inhibition.However,microinjection of KA alone into VLO had no effect on the allodynia.These results provide support for above-mentioned hypothesis that 5-HT_(2A) receptor activation-induced anti-allodynia in VLO in the neuropathic pain rats is produced at least partially through a pre-synaptic facilitatory effect on excitatory glutamate synapse transmission leading to activation of the VLO-PAG brainstem descending inhibitory system and depression of the nociceptive inputs at the spinal level.

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