CALCIUM INFLUX IN RAT THALAMIC RELAY NEURONS THROUGH VOLTAGE-DEPENDENT CALCIUM CHANNELS IS INHIBITED BY ENKEPHALIN

High and low voltage-activated, transient (HVA and LVA,T) Ca2+ current s are crucial in determining the characteristic thalamic firing patter n, during the oscillatory mode. The modulatory effects induced by D-al a(2)-D-leu(5)-enkephalin (DADLE) on voltage-dependent Ca2+ channels ha ve been investigated on acutely dissociated neurons from rat ventro-ba sal (VB) thalamus, by means of whole cell patch-clamp technique. DADLE (400 nM) reduced HVA Ca2+ channel currents in 37 out of 44 cells test ed (-53 +/- 5.3% to 0 mV test potential, n = 24,). In 50% of the cases DADLE induced an effect which was persistent at all the potentials te sted, i.e. a voltage-independent one. In the remaining neurons, the in hibition partially or totally disappeared on the currents evoked at th e highest potentials. DADLE was also able to inhibit LVA Ca2+ channels (-40% in five out of 12 cells). In conclusion, thalamic relay neurons present opioid receptors negatively coupled to both HVA and LVA Ca2channels. The presence of two inhibitory effects of DADLE on the total HVA Ca2+ channels has been observed, and they are distinguishable on the basis of their sensitivity to voltage. It is suggested that Ca2+ c urrent modulation may play a role in the production and tuning of the rhythmic burst discharge in these neurons.