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Abstract

Immunohistochemical and hybridization studies have revealed the presence of μ-, but not k- and δ-opioid receptors in the medial geniculate body. Using whole-cell patch clamp techniques, I examined the effects of opioid agonists on gerbil MGB neurons (P9-P16) in vitro. The opioid effects were concentration-dependent. Opioids produced different actions on the input conductance (G[sub i]) when applied in low, compared with high concentrations. The increase in G[sub i] might be due to increase in K⁺ conductance whereas the decrease in G[sub i] might be due to l[sub H] inactivation. When Gi was increased, the reversal potential was —65 mV; this implicates opioid actions on K+ , among other ion channels. In the case of decreased G[sub i], the opioid currents did not reverse from -100 mV to -50 mV, implying the involvement of cationic channels, other than K⁺ . DAMGO, a μ-selective opioid agonist, had a reversal potential that was similar to that observed when morphine increased G[sub i], implying that opioids activate u-opioid receptors in MGB neurons. Tetrodotoxin altered the concentration-dependent action of morphine. Here, the suggestion is morphine's actions involve neurons that presynaptic to the patch clamped neuron. Morphine application blocked spike-frequency adaptation and reduced firing rates in response to depolarizing current pulse injection. Morphine application may block Ca²⁺-mediated K⁺ channels that inhibited spike-frequency adaptation. Such blockade may be expected to increase the spike frequency. However, the increased conductance due to morphine would shunt the Na⁺ current, resulting in a lower spike frequency. The results of this study have revealed that opioids have both excitatory and inhibitory effects on MGB neurons.