Nicotinic acetylcholine receptor-mediated synaptic potentials in rat neocortex

• Published in: Brain research 2000-12, Vol.887 (2), p.399-405
• Main Authors: Chu, Z.G., Zhou, F.M., Hablitz, J.J.
• Format: Article
• Language: English
• Subjects: 2-Amino-5-phosphonovalerate - pharmacology; 6-Cyano-7-nitroquinoxaline-2,3-dione - pharmacology; Acetylcholine; Acetylcholinesterase - metabolism; amino acids (excitatory); Animals; Bicuculline - pharmacology; Biological and medical sciences; Central nervous system; Dihydro-beta-Erythroidine - pharmacology; Electrophysiology; EPSP; Excitatory Amino Acid Antagonists - pharmacology; Excitatory Postsynaptic Potentials - drug effects; Excitatory Postsynaptic Potentials - physiology; Fundamental and applied biological sciences. Psychology; Kynurenic Acid - pharmacology; Mecamylamine - pharmacology; Neocortex; Neocortex - drug effects; Neocortex - physiology; Neostigmine - pharmacology; Nicotine; Nicotinic Antagonists - pharmacology; Pyramidal Cells - drug effects; Pyramidal Cells - physiology; Rat; Rats; Rats, Sprague-Dawley; Receptors, Nicotinic - physiology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/S0006-8993(00)03076-6

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 μM D-APV+20 μM CNQX, or 5 mM kynurenic acid) plus the GABA A-receptor antagonist bicuculline (BIC, 20 μM). This EAA-antagonist resistant EPSC was observed in about 70% of neurons tested. It had a duration of approximately 20 ms and an amplitude of 61.5±6.8 pA at −70 mV ( n=35). The EAA-antagonist resistant EPSC current–voltage relation was linear and reversed near 0 mV ( n=23). The nonselective nicotinic acetylcholine receptor (nAChR) antagonists dihydro-β-erythroidine (DHβE, 100 μM) or mecamylamine (50 μM) reduced EPSC amplitudes by 42 ( n=20) and 33% ( n=9), respectively. EPSC kinetics were not significantly changed by either antagonist. Bath application of 10 μM 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 3) and purinergic (P2) receptors. The EAA-antagonist resistant EPSC appears 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.