Nicotine activates immature "silent" connections in the developing hippocampus.
In the hippocampus at birth, most glutamatergic synapses are immature and functionally "silent" either because the neurotransmitter is released in insufficient amount to activate low-affinity alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors or because the appropriate receptor system is missing or nonfunctional. Here we show that, in the newborn rat, a brief application of nicotine at immature Schaffer collateral-CA1 connections strongly enhances neurotransmitter release and converts presynaptically silent synapses into conductive ones. This effect is persistent and can be mimicked by endogenous acetylcholine released from cholinergic fibers. Thus, during a critical period of postnatal development, activation of nicotinic acetylcholine receptors contributes to the maturation of functional synaptic contacts and the wiring of adult hippocampal circuitry.
Maggi
Laura
L
Neuroscience Program and Istituto Nazionale di Fisica della Materia Unit, International School for Advanced Studies, Via Beirut 2-4, 34014 Trieste, Italy.
Le Magueresse
Corentin
C
Changeux
Jean-Pierre
JP
Cherubini
Enrico
E
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn; D002118:Calcium / Q000378:metabolism; D019706:Excitatory Postsynaptic Potentials; D006624:Hippocampus / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism / Q000502:physiology; D066298:In Vitro Techniques; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D011978:Receptors, Nicotinic / Q000378:metabolism; D013569:Synapses / Q000378:metabolism*
D011978:Receptors, Nicotinic; D009538:Nicotine; D000109:Acetylcholine; D002118:Calcium