Nicotinic receptors modulate the function of presynaptic AMPA receptors on glutamatergic nerve terminals in the trigeminal caudal nucleus.

In this study, we demonstrate the existence on trigeminal caudal nucleus (TCN) glutamatergic terminals of α4β2 nicotinic receptors (nAChRs) capable of enhancing the terminals' spontaneous release of [(3)H]d-aspartate ([(3)H]D-Asp). In rat TCN synaptosomes, spontaneous [(3)H]D-Asp release was increased by nicotine and the nicotinic receptor agonists (±)epibatidine and RJR2403. The increase was potentiated by the positive allosteric modulator of nAChRs LY2087101, inhibited by the nicotinic antagonists mecamylamine (MEC) and dihydro-β-erythroidine hydrobromide (DHβE), and unaffected by α-bungarotoxin (α-BgTx) and methyllycaconitine (MLA).

Co-application of the GABAB receptor agonist, baclofen, and the mGlu receptor agonist, L-CCG-I, facilitates [(3)H]GABA release from rat cortical nerve endings.

Interaction between different transmitter receptor systems is an emerging feature of neurotransmission at central synapses. G protein-coupled receptors' ability to form dimers or larger hetero-oligomers probably serves to facilitate the integration of diverse signals within the cell. We found that, in nerve terminals isolated from the cerebral cortices of rats, co-application of the GABAB agonist, baclofen, and of the non-selective mGlu agonist, L-CCG-I, potentiates the basal and depolarization-evoked release of [(3)H]GABA via a mechanism that involves mobilization of intracellular Ca(2+) ions.