Research report Nicotinic acetylcholine receptor-mediated synaptic potentials in rat

In the neocortex, fast excitatory synaptic transmission can typically be blocked by using excitatory amino acid (EAA) receptor antagonists. In recordings from layer II / III neocortical pyramidal neurons, we observed an evoked excitatory postsynaptic potential (EPSP) or current (EPSC) in the presence of EAA receptor antagonists (40‐100 mM D-APV120 mM CNQX, or 5 mM kynurenic acid) plus the GABA -receptor antagonist bicuculline (BIC, 20 mM). This EAA-antagonist resistant EPSC was observed in about 70% of A neurons tested. It had a duration of approximately 20 ms and an amplitude of 61.566.8 pA at 270 mV (n535). The EAA-antagonist resistant EPSC current‐voltage relation was linear and reversed near 0 mV (n523). The nonselective nicotinic acetylcholine receptor (nAChR) antagonists dihydro-b-erythroidine (DHbE, 100 mM) or mecamylamine (50 mM) reduced EPSC amplitudes by 42 (n520) and 33% (n59), respectively. EPSC kinetics were not significantly changed by either antagonist. Bath application of 10 mM neostigmine, a potent acetylcholinesterase inhibitor, prolonged the EPSC decay time. EAA-antagonist resistant EPSCs were observed in the presence of antagonists of metabotropic glutamate, serotonergic (5-HT ) and purinergic (P2) receptors. The EAA-antagonist resistant EPSC appears 3 to be due in part to activation of postsynaptic nAChRs. These results suggest the existence of functional synaptic nAChRs on pyramidal neurons in rat neocortex. © 2000 Elsevier Science B.V. All rights reserved. Theme: Neurotransmitters, modulators, transporters, and receptors Topic: Acetycholine receptors: nicotinic