Canonical organization of opioid modulation of nociceptive circuits. Focus on 'mu opioid receptor activation inhibits GABAergic inputs to basolateral amygdala neurons through Kv1.1/Kv1.2 channels'.

摘要

Opioids are powerful analgesics that produce their effects at both spinal and supraspinal levels. These effects are largely mediated by actions at mu type opioid receptors (MORs). Using whole cell recordings from neurons in the basolateral amygdala (BLA) in acute brain slices, Finnegan et al. (2006) in this issue of the Journal of Neurophysiology (p. 2032-2041) show that activation of mu opioid receptors reduces GABAergic inhibition to these cells. This inhibition arises from local circuit interneu-rons that act as feedforward and -back neurons. With a combination of pharmacological manipulations and immunohisto-chemistry, the authors go on to show that these actions of mu opioid receptors are due to modulation of Kvl.l and Kvl.2 voltage-dependent potassium channels. Reduction of inhibition to these projection neurons leads to an increase in their activity thus potentiating excitatory inputs to the central amygdala. Finnegan and colleagues suggest that this modulation of GABAergic inhibition in the BLAmay underlie the amygdala-dependent antinociceptive action of opioids.