Calcium channels involved in synaptic transmission from reticulospinal axons in lamprey

The pharmacology of calcium channels involved in glutamatergic synaptic tra nsmission from reticulospinal axons in the lamprey spinal cord was analyzed with specific agonists and antagonists of different high-voltage activated calcium channels. The N-type calcium channel blocker omega-cono-toxin GVIA (omega-CgTx) induced a large decrease of the amplitude of reticulospinal-e voked excitatory postsynaptic potentials (EPSPs). The P/Q-type calcium chan nel blocker omega-agatoxin IVA (omega-Aga) also reduced the amplitude of th e reticulospinal EPSPs, but to a lesser extent than omega-CgTx. The dihydro pyridine agonist Bay K and antagonist nimodipine had no effect on the ampli tude of the reticulospinal EPSP. Combined application of omega-CgTx and ome ga-Aga strongly decreased the amplitude the EPSPs but was never able to com pletely block them, indicating that calcium channels insensitive to these t oxins (R-type) are also involved in synaptic transmission from reticulospin al axons. We have previously shown that the group III metabotropic glutamat e receptor agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4) mediates pr esynaptic inhibition at the reticulospinal synapse. To test if this presyna ptic effect is mediated through inhibition of calcium influx, the effect of L-AP4 on reticulospinal transmission was tested before and after blockade of N-type channels, which contribute predominantly to transmitter release a t this synapse. Blocking the N-type channels with omega-CgTx did not preven t inhibition of reticulospinal synaptic transmission by L-AP4. In addition, L-AP4 had no affect on the calcium current recorded in the somata of retic ulospinal neurons or on the calcium component of action potentials in retic ulospinal axons. These results show that synaptic transmission from reticul ospinal axons in the lamprey is mediated by calcium influx through N-. P/Q- and R-type channels, with N-type channels playing the major role. Furtherm ore, presynaptic inhibition of reticulospinal transmission by L-AP4 appears not to be mediated through inhibition of presynaptic calcium channels.