PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 3598770-2 1987 Nicotine enhanced CA1 population spikes (PS) evoked by Schaffer collateral stimulation in a concentration-dependent manner (100 microM to 3.2 mM). Nicotine 0-8 carbonic anhydrase 1 Mus musculus 18-21 2841012-1 1988 Bath-application of nicotine (800 microM) to mouse hippocampal slices resulted in an increase in the amplitude of the population spike and the appearance of multiple population spikes in the CA1 pyramidal cell layer. Nicotine 20-28 carbonic anhydrase 1 Mus musculus 191-194 2841012-5 1988 The results are consistent with the hypothesis that the electrophysiological effects of nicotine on CA1 pyramidal cell excitability is mediated by disruption of GABAergic transmission. Nicotine 88-96 carbonic anhydrase 1 Mus musculus 100-103 34045967-10 2021 We also found that nicotine offspring showed an increase of neurite length in the molecular layer and CA1 by Tuj1 staining, as well as an increase in the expression of synapse associated protein, PSD95, but the expression of NeuroD1 in CA1 and CA3 reduced. Nicotine 19-27 carbonic anhydrase 1 Mus musculus 102-105 33895349-0 2021 Long-term effects of early postnatal nicotine exposure on cholinergic function in the mouse hippocampal CA1 region. Nicotine 37-45 carbonic anhydrase 1 Mus musculus 104-107 34045967-10 2021 We also found that nicotine offspring showed an increase of neurite length in the molecular layer and CA1 by Tuj1 staining, as well as an increase in the expression of synapse associated protein, PSD95, but the expression of NeuroD1 in CA1 and CA3 reduced. Nicotine 19-27 carbonic anhydrase 1 Mus musculus 236-239 31129809-6 2019 When kinase signaling was assessed in the nucleus accumbens and hippocampal CA1 region after repeated nicotine administration, both Ca2+/calmodulin-dependent protein kinase (CaMKII) and extracellular signal-regulated kinase (ERK) were upregulated in WT mice but not in D2RKO mice. Nicotine 102-110 carbonic anhydrase 1 Mus musculus 76-79 28507032-1 2017 The absence of alpha2* nicotinic acetylcholine receptors (nAChRs) in oriens lacunosum moleculare (OLM) GABAergic interneurons ablate the facilitation of nicotine-induced hippocampal CA1 long-term potentiation and impair memory. Nicotine 153-161 carbonic anhydrase 1 Mus musculus 182-185 28549967-9 2017 On the other hand, the activation of the dorsal hippocampal nAChRs by pre-test microinjection of nicotine (0.1-1microg/mouse, intra-CA1) improved amnesia induced by the co-administration of MDMD and ethanol. Nicotine 97-105 carbonic anhydrase 1 Mus musculus 132-135 28549967-10 2017 It is important to note that intra-CA1 microinjection of the same doses of MDMA or nicotine could not affect memory formation by itself. Nicotine 83-91 carbonic anhydrase 1 Mus musculus 35-38 28549967-11 2017 Pre-test intra-CA1 microinjection of nicotine (0.3-0.9microg/mouse) could not reverse amnesia induced by pre-training administration of ethanol while this treatment enhanced MDMA response on ethanol state-dependent learning. Nicotine 37-45 carbonic anhydrase 1 Mus musculus 15-18 28591584-0 2017 Dorsal-CA1 Hippocampal Neuronal Ensembles Encode Nicotine-Reward Contextual Associations. Nicotine 49-57 carbonic anhydrase 1 Mus musculus 7-10 28591584-5 2017 Our findings increase our understanding of CA1 hippocampal function in general and as it relates to reward processing by identifying a critical role for CA1 neuronal ensembles in nicotine place preference. Nicotine 179-187 carbonic anhydrase 1 Mus musculus 43-46 28591584-5 2017 Our findings increase our understanding of CA1 hippocampal function in general and as it relates to reward processing by identifying a critical role for CA1 neuronal ensembles in nicotine place preference. Nicotine 179-187 carbonic anhydrase 1 Mus musculus 153-156 28507032-9 2017 Our results demonstrated that alpha2* nAChRs influenced hippocampus-dependent learning and memory, as well as nicotine-facilitated CA1 hippocampal synaptic plasticity. Nicotine 110-118 carbonic anhydrase 1 Mus musculus 131-134 27737762-9 2017 Mature dendritic spines on CA1 pyramidal hippocampal neurons decreased 4 days after the precipitation of nicotine withdrawal, when the cognitive deficits were still present. Nicotine 105-113 carbonic anhydrase 1 Mus musculus 27-30 25545599-4 2015 Using voltage sensitive dye to visualize hippocampal activity, we found that early postnatal nicotine exposure also results in enhanced CA1 depolarization and hyperpolarization after SC stimulation. Nicotine 93-101 carbonic anhydrase 1 Mus musculus 136-139 27660076-2 2016 In rodent models of smoking during pregnancy, early postnatal nicotine exposure results in impaired long-term hippocampus-dependent memory, functional loss of alpha2-containing nicotinic acetylcholine receptors (alpha2* nAChRs) in oriens-lacunosum moleculare (OLM) cells, increased CA1 network excitation, and unexpected facilitation of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses. Nicotine 62-70 carbonic anhydrase 1 Mus musculus 282-285 27660076-2 2016 In rodent models of smoking during pregnancy, early postnatal nicotine exposure results in impaired long-term hippocampus-dependent memory, functional loss of alpha2-containing nicotinic acetylcholine receptors (alpha2* nAChRs) in oriens-lacunosum moleculare (OLM) cells, increased CA1 network excitation, and unexpected facilitation of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses. Nicotine 62-70 carbonic anhydrase 1 Mus musculus 389-392 27623427-5 2016 Brains from nicotine- or saline-exposed mice were processed with Golgi stain for whole neuron reconstruction in the CA1 and CA3 regions of the hippocampus. Nicotine 12-20 carbonic anhydrase 1 Mus musculus 116-119 27623427-10 2016 In addition, reduced dendritic length and complexity in the apical CA1 branches in adult mice exposed to nicotine during adolescence were found. Nicotine 105-113 carbonic anhydrase 1 Mus musculus 67-70 25545599-5 2015 Furthermore, we show that postnatal nicotine exposure induces pervasive changes to the nicotinic modulation of CA1 activity: activation of nicotinic receptors no longer increases CA1 network depolarization, acute nicotine inhibits rather than facilitates the induction of LTP at the SC pathway by recruiting an additional nicotinic receptor subtype, and acute nicotine no longer blocks LTP induction at the temporoammonic pathway. Nicotine 36-44 carbonic anhydrase 1 Mus musculus 111-114 25545599-5 2015 Furthermore, we show that postnatal nicotine exposure induces pervasive changes to the nicotinic modulation of CA1 activity: activation of nicotinic receptors no longer increases CA1 network depolarization, acute nicotine inhibits rather than facilitates the induction of LTP at the SC pathway by recruiting an additional nicotinic receptor subtype, and acute nicotine no longer blocks LTP induction at the temporoammonic pathway. Nicotine 213-221 carbonic anhydrase 1 Mus musculus 111-114 25545599-5 2015 Furthermore, we show that postnatal nicotine exposure induces pervasive changes to the nicotinic modulation of CA1 activity: activation of nicotinic receptors no longer increases CA1 network depolarization, acute nicotine inhibits rather than facilitates the induction of LTP at the SC pathway by recruiting an additional nicotinic receptor subtype, and acute nicotine no longer blocks LTP induction at the temporoammonic pathway. Nicotine 213-221 carbonic anhydrase 1 Mus musculus 111-114 22698687-10 2012 Moreover, intra-CA1 microinjection of L-NAME reversed the L-arginine-induced potentiation of the nicotine response. Nicotine 97-105 carbonic anhydrase 1 Mus musculus 16-19 23624371-1 2013 The present study examined whether nicotinic acetylcholine receptors (nAChRs) of the CA1 regions of the dorsal hippocampus and medial septum (MS) are involved in cross state-dependent memory retrieval between WIN55, 212-2 (WIN, a non-selective CB1/CB2 receptor agonist) and nicotine or ethanol. Nicotine 274-282 carbonic anhydrase 1 Mus musculus 85-88 23624371-6 2013 Pre-test intra-CA1 microinjection of nicotine (1 and 2mug/mouse) before systemic administration of an ineffective dose of nicotine (0.5mg/kg, s.c.) or ethanol (0.25g/kg) significantly reversed WIN-induced memory impairment. Nicotine 37-45 carbonic anhydrase 1 Mus musculus 15-18 23624371-7 2013 Pre-test intra-CA1 microinjection of mecamylamine (1 and 3mug/mouse) inhibited cross state-dependent memory between WIN and nicotine or ethanol. Nicotine 124-132 carbonic anhydrase 1 Mus musculus 15-18 21995552-8 2013 However, pre-test intra-CA1 microinjection of AM251 prevented the ethanol (1 g/kg) or nicotine (0.7 mg/kg) response on ethanol-induced amnesia. Nicotine 86-94 carbonic anhydrase 1 Mus musculus 24-27 22698687-11 2012 The results suggest the importance of NO system(s) in the CA1 regions of the dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia. Nicotine 124-132 carbonic anhydrase 1 Mus musculus 58-61 20974225-4 2011 In the hippocampal slices from the 6 months old Wt mice, the application of both nicotine (5muM) and SSR180711 (300nM) resulted in a significant enhancement of LTP expressed in area CA1. Nicotine 81-89 carbonic anhydrase 1 Mus musculus 182-185 21965190-7 2012 Moreover, pre-testing administration of nicotine (0.5 microg/mouse, intra-CA1) decreased memory retrieval, but induced anxiogenic-like behaviors. Nicotine 40-48 carbonic anhydrase 1 Mus musculus 74-77 22462479-0 2012 Endogenously released ACh and exogenous nicotine differentially facilitate long-term potentiation induction in the hippocampal CA1 region of mice. Nicotine 40-48 carbonic anhydrase 1 Mus musculus 127-130 22462479-12 2012 Thus, our study demonstrates that the activation of alpha7- and beta2-containing nAChRs differentially facilitates LTP induction via endogenously released ACh and exogenous nicotine, respectively, in the hippocampal CA1 region of mice. Nicotine 173-181 carbonic anhydrase 1 Mus musculus 216-219 17466021-0 2007 Nicotine gates long-term potentiation in the hippocampal CA1 region via the activation of alpha2* nicotinic ACh receptors. Nicotine 0-8 carbonic anhydrase 1 Mus musculus 57-60 20035769-10 2010 Moreover, intra-CA1 microinjection of MK-801 reversed the NMDA-induced potentiation of the nicotine response. Nicotine 91-99 carbonic anhydrase 1 Mus musculus 16-19 20035769-11 2010 SIGNIFICANCE: The results suggest the importance of NMDA glutamate system(s) in the CA1 regions of dorsal hippocampus for improving the effect of nicotine on the ethanol-induced amnesia. Nicotine 146-154 carbonic anhydrase 1 Mus musculus 84-87 17466021-5 2007 Optical imaging with a voltage-sensitive dye revealed significantly stronger membrane depolarization in the presence of nicotine in the SC path, facilitating spread of excitatory neural activity along both the somatodendritic and the CA1 proximodistal axes. Nicotine 120-128 carbonic anhydrase 1 Mus musculus 234-237 16873411-0 2006 Nicotine-induced enhancement of synaptic plasticity at CA3-CA1 synapses requires GABAergic interneurons in adult anti-NGF mice. Nicotine 0-8 carbonic anhydrase 1 Mus musculus 59-62 16873411-5 2006 Field excitatory postsynaptic potentials were recorded in order to examine whether nicotine was able to regulate induction of long-term potentiation at CA3-CA1 synapses in hippocampal slices from adult anti-NGF transgenic mice (AD 11), a comprehensive animal model of AD, in which cholinergic deficits due to nerve growth factor depletion are accompanied by progressive Alzheimer-like neurodegeneration. Nicotine 83-91 carbonic anhydrase 1 Mus musculus 156-159 35053378-9 2022 However, nicotine stimulation promoted CA3-CA1 synaptic potentiation in mature adult (not adolescent) wild-type and suppressed MPP-DG synaptic potentiation in miRNA-132/212-/- mice. Nicotine 9-17 carbonic anhydrase 1 Mus musculus 43-46 9634548-6 1998 However, the long-term delivery of nicotine (11 months) to 14-month-old animals corresponded with the highly specific preservation of nAChRalpha4 expression in some neurons of the dentate gyrus region and in neurite processes of remaining neurons of the hippocampal CA1 region. Nicotine 35-43 carbonic anhydrase 1 Mus musculus 266-269 2334841-1 1990 Previous data indicated that bath-application of nicotine to mouse hippocampal slices resulted in a concentration-dependent increase in the amplitude of the orthodromic population spike and the appearance of multiple population spikes in the CA1 pyramidal cell layer. Nicotine 49-57 carbonic anhydrase 1 Mus musculus 242-245