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.