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Using whole-cell patch clamp recording from neurones in an in vitro slice preparation, we have examined opioid- and orphanin FQ (OFQ)-mediated modulation of synaptic transmission in the rat arcuate nucleus and ventromedial hypothalamus (VMH).
Application of OFQ activated a Ba2+-sensitive and inwardly rectifying K+ conductance in ~50 % of arcuate nucleus neurones and ~95 % of VMH neurones. The OFQ-activated current was blocked by the nociceptin antagonist [Phe1
(CH2NH)Gly2]-nociceptin(1-13) NH2 (NCA), a peptide that on its own exhibited only weak agonist activity at high concentrations (> 1 µM). Similar current activation was observed with the µ agonist DAMGO but not 
(DPDPE) or 
(U69593) agonists.
In arcuate nucleus neurones, DAMGO (1 µM), U69593 (1 µM) and OFQ (100 nM to 1 µM) but not DPDPE (1 µM) were found to depress the amplitude of electrically evoked glutamatergic postsynaptic currents (EPSCs) and decrease the magnitude of paired-pulse depression, indicating that opioid receptors were located presynaptically.
In VMH neurones, DAMGO strongly depressed the EPSC amplitude in all cells examined. DAMGO decreased the magnitude of paired-pulse depression, indicating that µ receptors were located presynaptically. U69593 weakly depressed the EPSC while OFQ and DPDPE had no effect.
In VMH neurones, DAMGO depressed the frequency of miniature EPSCs (-58 %) in the presence of tetrodotoxin and Cd2+ (100 µM), suggesting that the actions of µ receptors could be mediated by an inhibition of the synaptic vesicle release process downstream of Ca2+ entry.
The data presented show that presynaptic modulation of excitatory neurotransmission in the arcuate nucleus occurs through µ, and the orphan opioid ORL-1 receptors while in the VMH presynaptic modulation only occurs through µ opioid receptors. Additionally, postsynaptic µ and ORL-1 receptors in both the arcuate nucleus and VMH modulate neuronal excitability through activation of a K+ conductance.
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