Ca2+-channels involved in neostriatal glutamatergic transmission.

The actions of peptidic toxins that work as Ca2+-channel antagonists were investigated on neostriatal glutamatergic transmission. Both intracellularly recorded excitatory postsynaptic potentials (EPSPs) and extracellularly recorded population spikes (PS) evoked by afferent stimulation were evaluated in the presence of 10 microM bicuculline. Percentage of block (mean +/- SEM; n = 4) for these events (EPSP and PS, respectively) was: omega-AgTxIVA (100-200 nM): 35 +/- 2 and 54 +/- 4%; omega-CgTxGVIA (1 microM): 37 +/- 3 and 63 +/- 6%; omega-CgTxMVIIC (500 nM): 40 +/- 4 and 50 +/- 2%; and calciseptine (500 nM): 5 +/- 4 and 9 +/- 6%. When given together, toxins had additive effects. The calciseptine effects were nonsignificant. The toxins were also tested on Ca2+-dependent random synaptic responses induced by 100 microM 4-AP. Each toxin reduced the frequency of spontaneous EPSPs by more than 60% (n = 2). The summed actions of individual toxins yields more than 100% block (superadditivity); suggesting that several terminals may possess more than one channel type. The reduction in frequency was not accompanied by a reduction in amplitude confirming that toxins' actions were presynaptic. It is concluded that at least three different Ca2+-channel subtypes are involved in glutamate release in neostriatal afferents: N-type, P/Q-type, and a type resistant to the toxins used. The L-type Ca2+-channel had little, if any, participation.