Nicotinic modulation of [3H]D-aspartate outflow from cultured cerebellar granule cells

• Published in: Synapse (New York, N.Y.) Vol. 36; no. 4; pp. 307 - 313
• Main Authors: Bianchi, Clementina, Tomasini, Maria Cristina, Antonelli, Tiziana, Marani, Luca, Beani, Lorenzo
• Format: Journal Article
• Language: English
• Published: New York John Wiley & Sons, Inc 15.06.2000
• Subjects: Acetylcholine - pharmacology; Animals; Aspartic Acid - metabolism; Bungarotoxins - pharmacology; Cells, Cultured; cerebellar granule cells; Cerebellum - cytology; Cerebellum - drug effects; Cerebellum - metabolism; Cerebellum - physiology; Electric Stimulation; mecamylamine; Mecamylamine - pharmacology; Neurons - drug effects; Neurons - metabolism; Neurons - physiology; nicotine; Nicotine - pharmacology; Nicotinic Antagonists - pharmacology; Rats; transmitter release; Tritium; α-bugarotoxin
• ISSN: 0887-4476; 1098-2396
• DOI: 10.1002/(SICI)1098-2396(20000615)36:4<307::AID-SYN7>3.0.CO;2-P

The effect of nicotine on basal and electrically evoked (20 Hz for 20 sec) [3H]D‐aspartate efflux (assumed as an index of transmitter release) was studied in rat cerebellar granule primary cultures. Nicotine (10–100 nM) increased the basal efflux two to three times and concentration‐dependently enhanced the electrically evoked efflux up to ten times. Higher drug concentration (1 μM) underwent rapid desensitization. Facilitation of the efflux was similarly reduced by the nicotinic acetylcholine receptor antagonists, α‐bungarotoxin and mecamylamine, suggesting the involvement of at least two receptor subtypes containing and lacking α7 subunits, respectively. Since the increased efflux induced by nicotine in granule cells kept at rest or depolarized by KCl 15 mM was antagonized by tetrodotoxin, the involvement of sodium channels by receptors located at preterminal sites was suggested. Taken together, these findings emphasize the role of the cholinergic input in granule cell function and in glutamatergic signaling. Synapse 36:307–313, 2000. © 2000 Wiley‐Liss, Inc.