The Journal of Neuroscience, July 15, 2001, 21(14):5182-5190
Long-Lasting Enhancement of Glutamatergic Synaptic Transmission
by Acetylcholine Contrasts with Response Adaptation after Exposure to
Low-Level Nicotine
Romain
Girod and
Lorna W.
Role
Department of Anatomy and Cell Biology, Center for Neurobiology and
Behavior, Columbia University, College of Physicians and Surgeons, New
York, New York 10032
Attempts to mimic synaptic delivery of acetylcholine (ACh) with
brief, repetitive pulses of high concentration ACh at synapses of
medial habenula (MHN) and interpeduncular nucleus (IPN) neurons in vitro elicited temporally distinct facilitation and
inhibition of glutamate secretion via nicotinic and muscarinic ACh
receptor-mediated pathways, respectively. ACh-induced nicotinic
facilitation was sustained for up to 2 hr, whereas muscarinic
inhibition was transient. Prolonged exposure to nicotine inactivated
nicotinic receptors selectively, thus decreasing the relative
contribution of the facilitatory versus inhibitory influences of ACh.
The net effect of ACh in modulating glutamatergic transmission at
MHN-IPN synapses may be determined by pre-exposure to nicotine,
because the drug appears to switch the balance between the facilitatory
and inhibitory actions of ACh.
Key words:
neuromodulation; glutamate; acetylcholine; nicotine; presynaptic; nicotinic acetylcholine receptors; medial habenula; interpeduncular nucleus
Copyright © 2001 Society for Neuroscience 0270-6474/01/21145182-09$05.00/0