PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31260652-9 2019 The results showed that intra-CA1 injection of an ineffective dose of ghrelin (0.03 nmol/microl) potentiated the nicotine (0.2 mg/kg, s.c.) response on amnesia induced by morphine. Nicotine 113-121 carbonic anhydrase 1 Rattus norvegicus 30-33 2054621-0 1991 Nicotine exerts differential effects on different CA1 hippocampal cell types. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 50-53 8321394-1 1993 The effect of aging upon the responsiveness of hippocampal CA1 pyramidal neurons to nicotine was investigated using electrophysiological techniques in male Fischer 344 rats. Nicotine 84-92 carbonic anhydrase 1 Rattus norvegicus 59-62 8321394-6 1993 Nicotine was locally applied to electrophysiologically identified CA1 pyramidal neurons using pressure microejection from two-barreled glass microelectrodes. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 66-69 8321394-9 1993 An age-related increase in the responsiveness of CA1 pyramidal neurons to locally applied nicotine was observed. Nicotine 90-98 carbonic anhydrase 1 Rattus norvegicus 49-52 8321394-10 1993 The results of this study suggest that an increase in hippocampal CA1 pyramidal cell responsiveness to nicotine could be related to the impaired place learning ability seen with aging. Nicotine 103-111 carbonic anhydrase 1 Rattus norvegicus 66-69 31260652-12 2019 In conclusion, present study suggests the significant role of ghrelin in morphine-related memory and its interactive effect with nicotine in avoidance task via CA1 nicotinic receptors. Nicotine 129-137 carbonic anhydrase 1 Rattus norvegicus 160-163 28433649-7 2017 STZ did not precipitate neuronal death, while Nic alone was associated with higher neuronal density in CA1 when compared to vehicle-injected animals. Nicotine 46-49 carbonic anhydrase 1 Rattus norvegicus 103-106 28541827-8 2017 It seems that there is a different contribution of the basolateral amygdala, the medial prefrontal cortex or the CA1 nicotinic acetylcholine receptors in stress-induced potentiation of nicotine-induced conditioned place preference. Nicotine 185-193 carbonic anhydrase 1 Rattus norvegicus 113-116 29883681-3 2018 Previously, we have reported that the combination of stress and AD causes more severe inhibition of synaptic plasticity of hippocampal area CA1 than chronic stress or AD alone, and that chronic nicotine treatment prevents this impairment. Nicotine 194-202 carbonic anhydrase 1 Rattus norvegicus 140-143 26578264-4 2016 ZSET1446 significantly potentiated the facilitatory effect of nicotine and ACh on the frequency of spontaneous postsynaptic currents (sPSCs) recorded in CA1 pyramidal neurons with a maximum effect at 100 pM (tested range, 10 pM-1000 pM). Nicotine 62-70 carbonic anhydrase 1 Rattus norvegicus 153-156 28638710-10 2017 CONCLUSION: This study suggests that changes in DREAM protein expression in CA1, CA2, CA3, and DG regions of rat"s hippocampus and mean relative level of DREAM protein may involve in the mechanism of nicotine treatment-prevented REM sleep deprivation-induced learning and memory impairment in rats. Nicotine 200-208 carbonic anhydrase 1 Rattus norvegicus 76-79 26867505-3 2016 Here, we investigated how nicotine contributes to the disruption of stabilized LTP in the hippocampal CA1 region. Nicotine 26-34 carbonic anhydrase 1 Rattus norvegicus 102-105 27072849-5 2016 Pre-test intra-CA1 microinjection of nicotine (0.3-0.5mug/rat) reversed TAM-induced memory impairment. Nicotine 37-45 carbonic anhydrase 1 Rattus norvegicus 15-18 26386153-8 2016 However, these alpha2*-nAChR-mediated effects were profoundly reduced after early postnatal nicotine exposure, suggesting altered control of CA1 circuits by alpha2*-nAChR-expressing OLM cells. Nicotine 92-100 carbonic anhydrase 1 Rattus norvegicus 141-144 23352971-0 2013 Varenicline and nicotine enhance GABAergic synaptic transmission in rat CA1 hippocampal and medial septum/diagonal band neurons. Nicotine 16-24 carbonic anhydrase 1 Rattus norvegicus 72-75 26164716-11 2015 Conversely, nicotine attenuated methamphetamine-induced deficits in alpha4beta2 nicotinic acetylcholine receptor density in the hippocampal CA1 region. Nicotine 12-20 carbonic anhydrase 1 Rattus norvegicus 140-143 25095782-3 2015 In the present study, we found treatment with nicotine 2, 6, and 12 h after ischemia for 7 days significantly increased the survival of CA1 pyramidal neurons in ischemia/reperfusion rats. Nicotine 46-54 carbonic anhydrase 1 Rattus norvegicus 136-139 23352971-5 2013 KEY FINDINGS: Both varenicline (10 muM) and nicotine (10 muM) applications alone resulted in small but significant increases in amplitude, as well as robustly enhanced frequency of mIPSCs in hippocampal CA1 pyramidal neurons and medial septum/diagonal band (MS/DB) neurons. Nicotine 44-52 carbonic anhydrase 1 Rattus norvegicus 203-206 20865738-8 2011 However, concurrent, acute treatment of rats with nicotine significantly attenuated SD-induced impairment of learning and STM and prevented SD-induced impairment of LTP in the CA1 and DG regions. Nicotine 50-58 carbonic anhydrase 1 Rattus norvegicus 176-179 22119395-12 2012 These data indicate that neonatal nicotine exposure has long lasting effects and results in increased excitation within the CA1 hippocampus in adulthood, with males showing increased sensitivity to nicotine"s effects. Nicotine 34-42 carbonic anhydrase 1 Rattus norvegicus 124-127 21596105-11 2011 The effects of nicotine persisted in P63 young adult brains which exhibited significantly downregulated GluR2, NR1, and NR2c expression levels in hippocampal homogenates and a considerably muted overall distribution of [3H]AMPA binding in areas CA1, CA2 and CA3, and the dentate gyrus. Nicotine 15-23 carbonic anhydrase 1 Rattus norvegicus 245-248 18316071-4 2008 Post-training intra-CA1 microinjection of nicotine (0.5-1 microg/rat) decreased significantly the amnesia induced by post-training morphine (7.5 mg/kg). Nicotine 42-50 carbonic anhydrase 1 Rattus norvegicus 20-23 21334425-7 2011 These results showed for the first time that nicotine with oral contraceptives did indeed exacerbate post-ischemic CA1 damage as compared to nicotine alone in naive female rats. Nicotine 45-53 carbonic anhydrase 1 Rattus norvegicus 115-118 19464074-7 2011 The results indicate that 6 weeks of nicotine treatment reduced the levels of Abeta(1-40) and BACE1 peptides in hippocampal area CA1 and prevented Abeta-induced impairment of learning and short-term memory. Nicotine 37-45 carbonic anhydrase 1 Rattus norvegicus 129-132 19464074-8 2011 Chronic nicotine also prevented the Abeta-induced inhibition of basal synaptic transmission and LTP in hippocampal area CA1. Nicotine 8-16 carbonic anhydrase 1 Rattus norvegicus 120-123 21325526-2 2011 In hippocampal slices from rats treated with nicotine for 1 week, withdrawal from nicotine in vivo produces an increase in CA1 pyramidal cell excitability that persists up to 9 months. Nicotine 45-53 carbonic anhydrase 1 Rattus norvegicus 123-126 21325526-2 2011 In hippocampal slices from rats treated with nicotine for 1 week, withdrawal from nicotine in vivo produces an increase in CA1 pyramidal cell excitability that persists up to 9 months. Nicotine 82-90 carbonic anhydrase 1 Rattus norvegicus 123-126 19442878-0 2009 Chronic nicotine exposure inhibits 17beta-estradiol-mediated protection of the hippocampal CA1 region against cerebral ischemia in female rats. Nicotine 8-16 carbonic anhydrase 1 Rattus norvegicus 91-94 19371581-0 2009 Effects of nicotine on K+ currents and nicotinic receptors in astrocytes of the hippocampal CA1 region. Nicotine 11-19 carbonic anhydrase 1 Rattus norvegicus 92-95 19371581-2 2009 We studied electrical effects elicited by nicotine in cultured astrocytes from the CA1 area of the rat hippocampus. Nicotine 42-50 carbonic anhydrase 1 Rattus norvegicus 83-86 19371581-7 2009 Thus, these results indicate that nicotine activates nAChRs and directly inhibits K+ currents in cultured astrocytes from the CA1 region of the rat hippocampus. Nicotine 34-42 carbonic anhydrase 1 Rattus norvegicus 126-129 20381593-6 2010 Furthermore, microinjection of nicotine (0.5-1 microg/rat) into both CA1 regions (intra-CA1) and the BLA (intra-BLA) did not produce a significant CPP. Nicotine 31-39 carbonic anhydrase 1 Rattus norvegicus 69-72 20381593-7 2010 Interestingly, intra-CA1 or -BLA administration of nicotine plus ethanol (0.5 g/kg) during conditioning phase significantly induced a strong CPP. Nicotine 51-59 carbonic anhydrase 1 Rattus norvegicus 21-24 20381593-9 2010 However, intra-CA1 or -BLA microinjection of mecamylamine (1-4 microg/rat) reversed the response induced by the microinjection of nicotine (1 microg/rat, intra-CA1 or -BLA) plus ethanol (0.5 g/kg i.p.) Nicotine 130-138 carbonic anhydrase 1 Rattus norvegicus 15-18 20381593-12 2010 Moreover, intra-CA1 administration of nicotine plus ethanol increased the locomotor activity on the test day which was reversed by pretreatment with mecamylamine, while other treatments had no effect on locomotor activity. Nicotine 38-46 carbonic anhydrase 1 Rattus norvegicus 16-19 18638553-9 2008 Our results indicate that changes in the levels of calcineurin and P-CaMKII during expression of LTD in the CA1 region may explain the enhanced magnitude of LTD in hypothyroid rats, and its reversal by chronic nicotine treatment. Nicotine 210-218 carbonic anhydrase 1 Rattus norvegicus 108-111 18070822-5 2008 In contrast, P0 AMCs from pups born to nicotine-treated dams showed a marked suppression or loss of hypoxic sensitivity, although hypercapnic sensitivity and the expression of CO(2) markers (i.e., carbonic anhydrase I and II) appeared normal. Nicotine 39-47 carbonic anhydrase 1 Rattus norvegicus 197-224 18316071-7 2008 Interestingly, pre-test intra-CA1 microinjection of nicotine (0.25 and 0.5 microg/rat) improved post-training morphine (7.5 mg/kg)-induced retrieval impairment. Nicotine 52-60 carbonic anhydrase 1 Rattus norvegicus 30-33 17330864-12 2007 These results indicate that at immature Schaffer collateral-CA1 synapses, activation of presynaptic calcium stores is not necessary for but contributes to nicotine-elicited increase of neurotransmitter release. Nicotine 155-163 carbonic anhydrase 1 Rattus norvegicus 60-63 18189313-0 2008 The effect of nicotine on spiking activity and Ca2+ dynamics of dendritic spines in rat CA1 pyramidal neurons. Nicotine 14-22 carbonic anhydrase 1 Rattus norvegicus 88-91 17174071-3 2007 failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 microg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration. Nicotine 55-63 carbonic anhydrase 1 Rattus norvegicus 181-184 17301675-6 2007 In-vivo acute nicotine (0.4 mg/kg) activated Elk-1 in the CA1 area but not in the dentate gyrus. Nicotine 14-22 carbonic anhydrase 1 Rattus norvegicus 58-61 17523180-1 2007 We have shown previously that chronic nicotine treatment reverses adult-onset hypothyroidism-induced impairment of late-phase long-term potentiation (L-LTP) in area CA1 of the hippocampus. Nicotine 38-46 carbonic anhydrase 1 Rattus norvegicus 165-168 17331737-6 2007 Chronic nicotine treatment (1 mg/kg, 2x day) of hypothyroid rats reversed hypothyroidism-induced enhancement and facilitation of LTD. Western blot analysis of the NMDA receptor subunits in the membranous fractions of hippocampal area CA1 neurons revealed that hypothyroidism reduced NR1 and increased NR2B without affecting NR2A protein levels. Nicotine 8-16 carbonic anhydrase 1 Rattus norvegicus 234-237 17156213-0 2006 Nicotine withdrawal suppresses nicotinic modulation of long-term potentiation induction in the hippocampal CA1 region. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 107-110 17156213-1 2006 We have previously reported that acute and chronic nicotine exposure lower the threshold for long-term potentiation (LTP) induction in the rat hippocampal CA1 region, and acute application of nicotine in the chronic-nicotine-treated hippocampus further reduces the threshold. Nicotine 51-59 carbonic anhydrase 1 Rattus norvegicus 155-158 16530419-1 2006 Electrophysiological recording reveals that chronic nicotine treatment prevents stress-induced impairment of long-term potentiation (LTP) in the CA1 region of the hippocampus of anesthetized rats. Nicotine 52-60 carbonic anhydrase 1 Rattus norvegicus 145-148 16725127-4 2006 Herein, we investigated the effects of acute and chronic nicotine treatments on the chronic-stress-induced impairment of LTP in area CA1 of the hippocampus of urethane-anesthetized rats. Nicotine 57-65 carbonic anhydrase 1 Rattus norvegicus 133-136 16725127-5 2006 Extracellular in vivo recording from the hippocampal area CA1 showed that pre-treatment with nicotine (1 mg/kg; sc twice/day for 2 weeks prior to stress) protected LTP from the inhibitory effect of subsequent chronic psychosocial stress (4 additional weeks concurrently with nicotine). Nicotine 93-101 carbonic anhydrase 1 Rattus norvegicus 58-61 16316479-0 2006 Nicotine blocks stress-induced impairment of spatial memory and long-term potentiation of the hippocampal CA1 region. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 106-109 16316479-7 2006 Extracellular recordings from the CA1 region of anaesthetized rats showed severe reduction of LTP magnitude in stressed rats, which was normalized in nicotine-treated stressed rats. Nicotine 150-158 carbonic anhydrase 1 Rattus norvegicus 34-37 16530419-2 2006 We investigated the molecular mechanism of this action of nicotine in the CA1 region. Nicotine 58-66 carbonic anhydrase 1 Rattus norvegicus 74-77 16307449-0 2006 Nicotine prevents stress-induced enhancement of long-term depression in hippocampal area CA1: electrophysiological and molecular studies. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 89-92 16191443-8 2006 Moreover mecamylamine (8 microg/rat, intra-CA1) decreased the effect of nicotine-induced potentiation of the morphine response. Nicotine 72-80 carbonic anhydrase 1 Rattus norvegicus 43-46 16553775-0 2006 Reparatory effects of nicotine on NMDA receptor-mediated synaptic plasticity in the hippocampal CA1 region of chronically lead-exposed rats. Nicotine 22-30 carbonic anhydrase 1 Rattus norvegicus 96-99 16553775-4 2006 (1) Nicotine (1 microm) facilitated the induction of LTP in CA1 by a weak tetanic stimulation (100 Hz, 20 pulses), which does not by itself produce LTP in lead-exposed rats. Nicotine 4-12 carbonic anhydrase 1 Rattus norvegicus 60-63 16553775-9 2006 (3) Nicotine enhanced PPF in the hippocampal CA1 region, and the nicotine-facilitated LTP in lead-exposed rats was blocked by either d-(-)-2-amino-5-phosphonopentanoic acid, the N-methyl-d-aspartate (NMDA) receptor antagonist, or picrotoxin, an antagonist of gamma-aminobutyric acid(A) receptors. Nicotine 4-12 carbonic anhydrase 1 Rattus norvegicus 45-48 16191443-6 2006 Furthermore, intra-CA1 administration of nicotine (0.5, 0.75 and 1 microg/rat) with an ineffective dose of morphine (0.5 mg/kg) elicited a significant CPP. Nicotine 41-49 carbonic anhydrase 1 Rattus norvegicus 19-22 16248884-7 2005 In addition, DCP-LA (100 nM) increased the rate of nicotine-triggered GABA(A) receptor-mediated miniature inhibitory post-synaptic currents, monitored from CA1 pyramidal neurons of rat hippocampal slices, and the effect was also inhibited by GF109203X or alpha-bungarotoxin but not by mecamylamine. Nicotine 51-59 carbonic anhydrase 1 Rattus norvegicus 156-159 15795061-0 2005 Maternal exposure of rats to nicotine via infusion during gestation produces neurobehavioral deficits and elevated expression of glial fibrillary acidic protein in the cerebellum and CA1 subfield in the offspring at puberty. Nicotine 29-37 carbonic anhydrase 1 Rattus norvegicus 183-186 15795061-12 2005 These results indicate that maternal exposure to nicotine produces significant neurobehavioral deficits, a decrease in the surviving neurons and an increased expression of GFAP in cerebellum and CA1 subfield of hippocampus of the offspring on PND 30 and 60. Nicotine 49-57 carbonic anhydrase 1 Rattus norvegicus 195-198 15272042-0 2004 Persistent decrease in synaptic efficacy induced by nicotine at Schaffer collateral-CA1 synapses in the immature rat hippocampus. Nicotine 52-60 carbonic anhydrase 1 Rattus norvegicus 84-87 15651137-3 2005 We have performed a dose-response study for intrahippocampal nicotine (CA1) on acquisition and extinction of the lever-press response and antagonization test by co-administration of mecamylamine. Nicotine 61-69 carbonic anhydrase 1 Rattus norvegicus 71-74 11173554-9 2000 The delayed death of the CA1 hippocampal neurons occurring after transient occlusion was attenuated by pretreatment with nicotine (30--100 microg/kg) to approximately 50% of the total neurons. Nicotine 121-129 carbonic anhydrase 1 Rattus norvegicus 25-28 15045467-1 2004 We previously showed that maternal exposure to nicotine, alone or in combination with chlorpyrifos, caused an increase in glial fibrillary acidic protein (GFAP) immunostaining in the CA1 subfield of hippocampus and cerebellum in postnatal day (PND) 30 offspring. Nicotine 47-55 carbonic anhydrase 1 Rattus norvegicus 183-186 12740173-0 2003 Different synaptic mechanisms of long-term potentiation induced by nicotine and tetanic stimulation in hippocampal CA1 region of rats. Nicotine 67-75 carbonic anhydrase 1 Rattus norvegicus 115-118 12740173-1 2003 AIM: To investigate whether long-term potentiation (LTP) induced by nicotine and tetanic stimulation in the hippocampal CA1 region shares different mechanisms. Nicotine 68-76 carbonic anhydrase 1 Rattus norvegicus 120-123 11285026-6 2001 Similarly, acute nicotine significantly increased 5-HT(1A) receptor mRNA in the dentate gyrus (DG), CA3 and CA1 regions of the dorsal hippocampus 2 h and 24 h after injection. Nicotine 17-25 carbonic anhydrase 1 Rattus norvegicus 108-111 11146126-3 2000 However, with 7 days nicotine treatment, tolerance developed to the inhibitory effect of nicotine on BDNF mRNA expression and there was a significant increase in BDNF expression 2 h after the final injection in the CA1 region. Nicotine 21-29 carbonic anhydrase 1 Rattus norvegicus 215-218 11146126-3 2000 However, with 7 days nicotine treatment, tolerance developed to the inhibitory effect of nicotine on BDNF mRNA expression and there was a significant increase in BDNF expression 2 h after the final injection in the CA1 region. Nicotine 89-97 carbonic anhydrase 1 Rattus norvegicus 215-218 11044743-0 2000 Nicotine at concentrations found in cigarette smokers activates and desensitizes nicotinic acetylcholine receptors in CA1 interneurons of rat hippocampus. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 118-121 11044743-3 2000 Thus, the objective of this study was to determine the concentration- and time-dependent effects of nicotine on alpha7 and alpha4beta2 nAChRs, the two major brain subtypes, natively expressed in CA1 interneurons of rat hippocampal slices. Nicotine 100-108 carbonic anhydrase 1 Rattus norvegicus 195-198 14555401-9 2003 A rise in glial fibrillary acidic protein (GFAP) immunostaining was observed in the CA1 subfield of hippocampus and cerebellum on PND 30 in female and male offspring of mothers treated with either nicotine or nicotine in combination with chlorpyrifos, but to a lesser extent in males. Nicotine 197-205 carbonic anhydrase 1 Rattus norvegicus 84-87 14555401-9 2003 A rise in glial fibrillary acidic protein (GFAP) immunostaining was observed in the CA1 subfield of hippocampus and cerebellum on PND 30 in female and male offspring of mothers treated with either nicotine or nicotine in combination with chlorpyrifos, but to a lesser extent in males. Nicotine 209-217 carbonic anhydrase 1 Rattus norvegicus 84-87 12582205-2 2003 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. Nicotine 62-70 carbonic anhydrase 1 Rattus norvegicus 103-106 11749838-0 2001 Activation of p42/44 mitogen-activated protein kinase pathway in long-term potentiation induced by nicotine in hippocampal CA1 region in rats. Nicotine 99-107 carbonic anhydrase 1 Rattus norvegicus 123-126 11749838-1 2001 AIM: To investigate the relationship between activation of p42/44 mitogen-activated protein kinase (MAPK) pathway and hippocampal long term potentiation (LTP) induced by nicotine in area CA 1. Nicotine 170-178 carbonic anhydrase 1 Rattus norvegicus 187-191 11749838-3 2001 RESULTS: PD98059 concentration-dependently (25 micromol/L, 50 micromol/L) attenuated the induction of LTP induced by nicotine 10 micromol/L; both p42 and p44 MAPK were activated with their total protein expression increasing in CA1 subregion in response to LTP induced by nicotine. Nicotine 117-125 carbonic anhydrase 1 Rattus norvegicus 228-231 11251213-0 2001 Nicotine accelerates reversal of long-term potentiation and enhances long-term depression in the rat hippocampal CA1 region. Nicotine 0-8 carbonic anhydrase 1 Rattus norvegicus 113-116 11251213-2 2001 Because nicotine enhances learning and memory, we examined if nicotine modulates DP and LTD in the hippocampal CA1 region. Nicotine 62-70 carbonic anhydrase 1 Rattus norvegicus 111-114 11251213-3 2001 Bath application of nicotine during LFS accelerated DP, that is, potentiated synaptic responses in hippocampal CA1 neurons returned to pre-tetanic control levels more rapidly in the presence of nicotine. Nicotine 20-28 carbonic anhydrase 1 Rattus norvegicus 111-114 11251213-3 2001 Bath application of nicotine during LFS accelerated DP, that is, potentiated synaptic responses in hippocampal CA1 neurons returned to pre-tetanic control levels more rapidly in the presence of nicotine. Nicotine 194-202 carbonic anhydrase 1 Rattus norvegicus 111-114 10825655-1 2000 Acute and chronic nicotine exposure differentially facilitate the induction of long-term potentiation (LTP), a synaptic model of learning and memory, in the hippocampal CA1 region. Nicotine 18-26 carbonic anhydrase 1 Rattus norvegicus 169-172 10556667-2 1999 Perfusion of nicotine (50 microM) reduced the amplitude of electrically evoked population spikes in the CA1 pyramidal cells of the vehicle control rats, but not in those of the beta-amyloid protein-infused rats, suggesting the impairment of nicotinic signaling in the beta-amyloid protein-infused rats. Nicotine 13-21 carbonic anhydrase 1 Rattus norvegicus 104-107 11324441-0 2000 Long-term potentiation induced by nicotine in CA1 region of hippocampal slice is Ca(2+)-dependent. Nicotine 34-42 carbonic anhydrase 1 Rattus norvegicus 46-49 11324441-1 2000 AIM: To observe the effects of Ca2+ on hippocampal long-term potentiation (LTP) induced by nicotine in CA1 region of rat hippocampal slice. Nicotine 91-99 carbonic anhydrase 1 Rattus norvegicus 103-106 11324441-3 2000 RESULTS: Nicotine 1 mumol.L-1 induced LTP in the hippocampal CA1 region. Nicotine 9-17 carbonic anhydrase 1 Rattus norvegicus 61-64 11324441-6 2000 CONCLUSION: LTP induced by nicotine in hippocampal CA1 region is Ca(2+)-dependent. Nicotine 27-35 carbonic anhydrase 1 Rattus norvegicus 51-54 8842401-1 1996 We tested whether cholinergic denervation of the hippocampus of young rats would result in an enhancement of CA1 pyramidal cell responsiveness to nicotine. Nicotine 146-154 carbonic anhydrase 1 Rattus norvegicus 109-112 8842401-3 1996 One month later the rats were anesthetized with pentobarbital and nicotine was locally applied to CA1 pyramidal neurons using pressure microejection. Nicotine 66-74 carbonic anhydrase 1 Rattus norvegicus 98-101 9832189-4 1998 Both Ach and nicotine produced NO signals ranging from 0.04 to 2.14 microM in the CA1, CA3, and dentate gyrus of the rat hippocampus that lasted for 2-5 min. Nicotine 13-21 carbonic anhydrase 1 Rattus norvegicus 82-85 9697973-8 1998 Ultrastructurally the granule cells and the pyramidal neurons of the CA3 and CA1 regions showed increase in free ribosomes and dilatation of rough endoplasmic reticulum (RER) and Golgi apparatus cisternae in the nicotine-treated group. Nicotine 212-220 carbonic anhydrase 1 Rattus norvegicus 77-80