Endogenously released ACh and exogenous nicotine differentially facilitate long-term potentiation induction in the hippocampal CA1 region of mice.
about
Gating of long-term potentiation by nicotinic acetylcholine receptors at the cerebellum input stageCellular, molecular, and genetic substrates underlying the impact of nicotine on learning.How cigarette smoking may increase the risk of anxiety symptoms and anxiety disorders: a critical review of biological pathways.α7nAchR/NMDAR coupling affects NMDAR function and object recognition.Endogenous ACh suppresses LTD induction and nicotine relieves the suppression via different nicotinic ACh receptor subtypes in the mouse hippocampusHippocampal changes produced by overexpression of the human CHRNA5/A3/B4 gene cluster may underlie cognitive deficits rescued by nicotine in transgenic mice.Neonatal nicotine exposure increases excitatory synaptic transmission and attenuates nicotine-stimulated GABA release in the adult rat hippocampus.Extended access nicotine self-administration with periodic deprivation increases immature neurons in the hippocampusNicotine elicits prolonged calcium signaling along ventral hippocampal axons.Early postnatal nicotine exposure causes hippocampus-dependent memory impairments in adolescent mice: Association with altered nicotinic cholinergic modulation of LTP, but not impaired LTP.Nicotine Administration Attenuates Methamphetamine-Induced Novel Object Recognition Deficits.Early postnatal nicotine exposure disrupts the α2* nicotinic acetylcholine receptor-mediated control of oriens-lacunosum moleculare cells during adolescence in rats.Effects of M1 and M4 activation on excitatory synaptic transmission in CA1.Genetic knockout of the α7 nicotinic acetylcholine receptor gene alters hippocampal long-term potentiation in a background strain-dependent manner.Coexistence of Multiple Types of Synaptic Plasticity in Individual Hippocampal CA1 Pyramidal Neurons.Impaired function of α2-containing nicotinic acetylcholine receptors on oriens-lacunosum moleculare cells causes hippocampus-dependent memory impairments.Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition.
P2860
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P2860
Endogenously released ACh and exogenous nicotine differentially facilitate long-term potentiation induction in the hippocampal CA1 region of mice.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@ast
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@en
type
label
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@ast
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@en
prefLabel
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@ast
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@en
P2860
P1476
Endogenously released ACh and ...... ippocampal CA1 region of mice.
@en
P2093
Katumi Sumikawa
Sakura Nakauchi
P2860
P304
P356
10.1111/J.1460-9568.2012.08056.X
P407
P577
2012-03-30T00:00:00Z