Nicotine Exposure During a Critical Period of Development Leads to Persistent Changes in Nicotinic Acetylcholine Receptors of Adult Rat Brain

Miao, Hui; Liu, C.; Bishop, KM; Gong, Ze‐Hui; Nordberg, Agneta; Zhang, X.

doi:10.1046/j.1471-4159.1998.70020752.x

Cited by 94 publications

(58 citation statements)

References 58 publications

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“…Similarly, the up-regulation of nAChRs is reported to be induced in the central nervous system of experimental animals chronically treated with nicotine (38,39,58) and neural cells exposed to nicotine (13,59) when examined by a receptor binding assay using [ 3 H]nicotine as a radiolabeled ligand.…”

Section: Camentioning

confidence: 94%

Up-regulation of L-type Voltage-dependent Calcium Channels after Long Term Exposure to Nicotine in Cerebral Cortical Neurons

Katsura¹,

Mohri²,

Shuto³

et al. 2002

Journal of Biological Chemistry

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Section: Camentioning

confidence: 94%

Up-regulation of L-type Voltage-dependent Calcium Channels after Long Term Exposure to Nicotine in Cerebral Cortical Neurons

Katsura¹,

Mohri²,

Shuto³

et al. 2002

Journal of Biological Chemistry

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“…Other studies focusing on receptor expression also showed upregulation of nAChR binding sites, mostly α4β2* nAChRs (Sugiyama et al, 1985;Cairns and Wonnacott, 1988;van de Kamp and Collins, 1994;Miao et al, 1998;Eriksson et al, 2000;Mugnaini et al, 2002a). Thus, morphological and molecular changes in hippocampus and cerebellum in response to developmental nicotine exposure could very well contribute to decreased cognitive performance in the off-spring, and could be even more robust after postnatal exposure when hippocampus and cerebellum are still forming.…”

Section: Introductionmentioning

confidence: 96%

Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

2007

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Nicotine, the major psychoactive ingredient in tobacco interacting with nicotinic acetylcholine receptors (nAChR), is believed to have neuroprotective and neurotoxic effects on the developing brain. Neurotoxicity has been attributed to activation of homomeric α7 nAChRs, neuroprotection to heteromeric α4β2 nAChRs. Thus, developmental nicotine could have opposite effects in different brain regions, depending on nAChR subtype expression. Here, we determined if chronic neonatal nicotine exposure (CNN), during a period of brain growth corresponding to the third human trimester, differentially regulates nAChR expression, cell death, and morphological properties in hippocampus and cerebellum, two structures maturing postnatally. Rat pups were orally treated with 6 mg/kg/day nicotine from postnatal day (P)1 to P7. On P8, expression for α4, α7 and β2 mRNA was determined by in situ hybridization; nAChR binding sites in by receptor autoradiography, dying neurons by TUNEL and Fluoro-Jade staining and morphological properties by analysis of Cresyl-Violet stained sections. In control cerebellum, strong expression of α4, β2 mRNA and heteromeric nAChRs labeled with [ 125 I]-Epibatidine were found in granule cells, and α7 mRNA and homomeric nAChRs labeled with [ 125 I]-αBungarotoxin in the external germinal layer. In control hippocampus, low expression of α4 mRNA and heteromeric nAChRs and high expression of α7 mRNA and homomeric nAChRs were detected. CNN increased heteromeric nAChR binding in hippocampus but not cerebellum and significantly decreased neuronal soma size and increased packing density in hippocampal principal cells but not in cerebellum. CNN did not increase the number of dying cells in any area, but significantly fewer TUNEL-labeled cells were found in CA3 strata oriens and radiatum and cerebellar granule layer. Thus, the hippocampus seems to be more sensitive than the cerebellum to CNN which could result from different nAChR subtype expression and might explain long-lasting altered cognitive functions correlated with gestational nicotine exposure due to changes in hippocampal cell morphology.

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“…Neuronal intrinsic membrane properties also change rapidly during this period (Metherate and Aramakis 1999). Thus, as in other sensory cortices, this is a time of rapid change during which the development of neural circuitry may be particularly sensitive to external in¯uences, i.e., a potential critical period (Miao et al 1998;Aramakis et al 2000).…”

Section: Introductionmentioning

confidence: 99%

Postnatal Development of NR2A and NR2B mRNA Expression in Rat Auditory Cortex and Thalamus

Hsieh

Leslie

Metherate

2002

JARO - Journal of the Association for Research in Otolaryngolog

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Sensory cortex in the rat undergoes rapid postnatal development, especially following the onset of sensory function during so-called``critical periods.'' To investigate potential mechanisms in the auditory forebrain involving different NMDA receptor subunits, we have used in situ hybridization to determine expression patterns of NR2A and NR2B mRNA at postnatal days 4, 10, 13, 18, 25, and adult. In auditory cortex, NR2A mRNA expression is initially weak but increases rapidly over 2 weeks. NR2B mRNA levels are initially high and remain high. For both subunits, expression tends to be highest in super®cial layers of the cortex (except layer 1). Expression is weaker in the auditory thalamus (medial geniculate). Initially, NR2A mRNA expression is very low, whereas NR2B mRNA expression is moderate; both levels increase over 2 weeks. Among medial geniculate subdivisions, NR2A mRNA expression occurs preferentially in the medial division, whereas NR2B mRNA expression is strongest in the ventral division. For auditory cortex and thalamus, NR2A and NR2B mRNA expression peaks about 1 week after the onset of hearing before declining slightly into adulthood. The heterogeneous distribution of NMDAR subunit mRNA throughout development may play a role in auditory forebrain development and function.

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Nicotine Exposure During a Critical Period of Development Leads to Persistent Changes in Nicotinic Acetylcholine Receptors of Adult Rat Brain

Cited by 94 publications

References 58 publications

Up-regulation of L-type Voltage-dependent Calcium Channels after Long Term Exposure to Nicotine in Cerebral Cortical Neurons

Up-regulation of L-type Voltage-dependent Calcium Channels after Long Term Exposure to Nicotine in Cerebral Cortical Neurons

Effects of chronic neonatal nicotine exposure on nicotinic acetylcholine receptor binding, cell death and morphology in hippocampus and cerebellum

Postnatal Development of NR2A and NR2B mRNA Expression in Rat Auditory Cortex and Thalamus

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