TY - JOUR
T1 - Nicotine-mediated plasticity in robust nucleus of the archistriatum of the adult zebra finch
AU - Salgado-Commissariat, Delanthi
AU - Rosenfield, David B.
AU - Helekar, Santosh
N1 - Funding Information:
This work was supported by the M.R. Bauer Foundation and the National Institute on Deafness and Other Communication Disorders.
Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2004/8/20
Y1 - 2004/8/20
N2 - Activation of neuronal nicotinic acetylcholine receptors (nAChRs) modulates the induction of long-term potentiation (LTP), a possible cellular mechanism for learning. This study was undertaken to determine the effects of activation of nAChRs by nicotine on long-term plasticity in the songbird zebra finch, which is a valuable model to study synaptic plasticity and its implications to behavioral learning. Electrophysiological recordings in the robust nucleus of the archistriatum (RA) in adult zebra finch brain slices reveal that tetanic stimulation alone does not produce LTP. However, LTP is induced by such stimulation in the presence of nicotine. The nicotine-mediated LTP is blocked by dihydro-β-erythroidine (DHβE, 1 μM), an antagonist having a greater effect against nAChRs containing the alpha 4 subunit. In the presence of methyllcaconitine (MLA, 10 nM), an antagonist of nAChRs containing the alpha 7 subunit, a long-term depression (LTD) is unmasked, implicating a bi-directional type of plasticity in the zebra finch RA, which is modulated by differential activation of nAChR subtypes. Intracellular recordings from single neurons show a depression of the afterhyperpolarization (AHP) and an increase in frequency of evoked and spontaneous action potentials in the presence of nicotine. These results suggest that nicotinic cholinergic mechanisms may play a critical role in synaptic plasticity in the zebra finch song system and thereby influence song learning and plasticity.
AB - Activation of neuronal nicotinic acetylcholine receptors (nAChRs) modulates the induction of long-term potentiation (LTP), a possible cellular mechanism for learning. This study was undertaken to determine the effects of activation of nAChRs by nicotine on long-term plasticity in the songbird zebra finch, which is a valuable model to study synaptic plasticity and its implications to behavioral learning. Electrophysiological recordings in the robust nucleus of the archistriatum (RA) in adult zebra finch brain slices reveal that tetanic stimulation alone does not produce LTP. However, LTP is induced by such stimulation in the presence of nicotine. The nicotine-mediated LTP is blocked by dihydro-β-erythroidine (DHβE, 1 μM), an antagonist having a greater effect against nAChRs containing the alpha 4 subunit. In the presence of methyllcaconitine (MLA, 10 nM), an antagonist of nAChRs containing the alpha 7 subunit, a long-term depression (LTD) is unmasked, implicating a bi-directional type of plasticity in the zebra finch RA, which is modulated by differential activation of nAChR subtypes. Intracellular recordings from single neurons show a depression of the afterhyperpolarization (AHP) and an increase in frequency of evoked and spontaneous action potentials in the presence of nicotine. These results suggest that nicotinic cholinergic mechanisms may play a critical role in synaptic plasticity in the zebra finch song system and thereby influence song learning and plasticity.
KW - acetylcholine
KW - ACh
KW - long-term depression
KW - long-term potentiation
KW - LTD
KW - LTP
KW - nAChR
KW - Neural basis of behavior
KW - Neural plasticity
KW - Nicotine
KW - nicotinic acetylcholine receptor
KW - Plasticity
KW - RA
KW - robust nucleus of the archistriatum
KW - Song nucleus
KW - Songbird
KW - Zebra finch
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U2 - 10.1016/j.brainres.2004.05.051
DO - 10.1016/j.brainres.2004.05.051
M3 - Article
C2 - 15262210
AN - SCOPUS:3242721426
SN - 0006-8993
VL - 1018
SP - 97
EP - 105
JO - Brain Research
JF - Brain Research
IS - 1
ER -