Simmons M L, Chavkin C
Department of Pharmacology, University of Washington, Seattle 98195, USA.
Int Rev Neurobiol. 1996;39:145-96. doi: 10.1016/s0074-7742(08)60666-2.
Endogenous opioid peptides modulate neural transmission in the hippocampus. Procnkephalin-derived peptides have been demonstrated to act at mu and delta opioid receptors to inhibit GABA release from inhibitory interneurons, resulting in increased excitability of hippocampal pyramidal cells and dentate gyrus granule cells. Prodynorphin-derived peptides primarily act at presynaptic kappa opioid receptors to inhibit excitatory amino acid release from perforant path and mossy fiber terminals. Opioid receptors reduce membrane excitability by modulating ion conductances, and in this way they may decrease voltage-dependent calcium influx and transmitter release. Synaptic plasticity in the hippocampus also is modulated by endogenous opioids. Enkephalins facilitate long-term potentiation, whereas dynorphins inhibit the induction of this type of neuroplasticity. Further, opioids may play important roles in hippocampal epilepsy. Recurrent seizures induce changes in the expression of opioid peptides and receptors. Also, enkephalins have proconvulsant effects in the epileptic hippocampus, whereas dynorphins may function as endogenous anticonvulsants.
内源性阿片肽调节海马体中的神经传递。已证明源自前脑啡肽原的肽作用于μ和δ阿片受体，以抑制抑制性中间神经元释放γ-氨基丁酸（GABA），从而导致海马锥体细胞和齿状回颗粒细胞的兴奋性增加。源自强啡肽原的肽主要作用于突触前κ阿片受体，以抑制来自穿通通路和苔藓纤维终末的兴奋性氨基酸释放。阿片受体通过调节离子电导来降低膜兴奋性，并且通过这种方式它们可能减少电压依赖性钙内流和递质释放。海马体中的突触可塑性也受内源性阿片类物质调节。脑啡肽促进长时程增强，而强啡肽抑制这种类型的神经可塑性的诱导。此外，阿片类物质可能在海马癫痫中起重要作用。反复癫痫发作会引起阿片肽和受体表达的变化。而且，脑啡肽在癫痫海马体中具有促惊厥作用，而强啡肽可能作为内源性抗惊厥剂发挥作用。
