Opioid receptor activation attenuates nicotinic enhancement of spontaneous GABA release in lateral spiriform nucleus of the chick.

We examined the effects of opioids on the nicotinic enhancement of spontaneous GABA release from presynaptic terminals in the lateral spiriform nucleus (SpL) of the chick. Whole cell recordings from SpL neurons in brain slices were used to monitor spontaneous GABA release. Nicotine (1 microM) produced an 8-fold increase in the frequency of GABA events without changing their amplitude, consistent with an increase of GABA release from presynaptic terminals. L-enkephalin (1 microM) blocked these effects of nicotine on presynaptic GABA release, and the opioid antagonist naloxone (100 nM) antagonized the actions of L-enkephalin. The selective mu agonist DAMGO (300 nM) also attenuated the nicotine-mediated enhancement of GABA release, and the mu selective antagonist CTOP (1 microM) blocked the actions of DAMGO. In contrast, the kappa opioid agonist U50488 (3 microM) and the delta opioid agonist DPDPE (1 microM) had no effect. The results demonstrate that presynaptic release of GABA in the SpL can be regulated by both nicotinic agonists and mu opioids. While mu opioids have little effect on GABA release by themselves, they are able to block the marked enhancement of GABA release normally produced by nicotine. Since both cholinergic and enkephalinergic nerves are present in the SpL, the interactions of these two neurotransmitter systems may serve to precisely regulate GABA release in this brain region.