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⁺ currents are crucial in determining the characteristic thalamic firing pattern, during the oscillatory mode. The modulatory effects induced by d-ala²-d-leu⁵-enkephalin (DADLE) on voltage-dependent Ca²⁺ channels have been investigated on acutely dissociated neurons from rat ventro-basal (VB) thalamus, by means of whole cell patch-clamp technique. DADLE (400 nM) reduced HVA Cat+ channel currents in 37 out of 44 cells tested (-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 tested, i.e. a voltage-independent one. In the remaining neurons, the inhibition partially or totally disappeared on the currents evoked at the 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 Ca²⁺ channels. 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⁺ current modulation may play a role in the production and tuning of the rhythmic burst discharge in these neurons.