Long term alterations in synaptic physiology, expression of β2 nicotinic receptors and ERK1/2 signaling in the hippocampus of rats with prenatal nicotine exposure

Kodeeswaran Parameshwaran, Manal A. Buabeid, Subhrajit Bhattacharya, Subramaniam Uthayathas, Thiruchelvam Kariharan, Muralikrishnan Dhanasekaran, Vishnu Suppiramaniam

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Abstract

Smoking during pregnancy is associated with long lasting, hippocampus dependent, cognitive deficits in children. The current study was performed to investigate the effect of prenatal nicotine exposure on excitatory synaptic physiology and cellular signaling in the hippocampus using a rodent model. Excitatory synaptic physiology was analyzed using electrophysiological methods to detect changes in synaptic plasticity, excitatory synaptic transmission and synaptic currents mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in the hippocampus. Additionally, western blot experiments were performed to quantify alterations in protein expression levels in the hippocampus. Prenatal nicotine exposure resulted in a decrease in long term potentiation (LTP) and an increase in long term depression (LTD). Basal synaptic transmission was also reduced with a concomitant decline in AMPAR mediated synaptic currents at the cellular and single channel levels. Presynaptic pool of vesicles docked close to release sites were also diminished in nicotine exposed rats. Moreover, reduced levels of β2 subunit containing nicotinic receptors and extracellular signal regulated kinase1/2 (ERK1/2) were observed in nicotine exposed rats. These results suggest that long lasting alterations in excitatory synaptic physiology, AMPAR synaptic currents and ERK1/2 signaling may serve as the molecular mechanisms for cognitive deficits associated with prenatal nicotine exposure.

Original languageEnglish
Pages (from-to)102-111
Number of pages10
JournalNeurobiology of Learning and Memory
Volume106
DOIs
Publication statusPublished - 1 Jan 2013

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Nicotinic Receptors
Nicotine
Hippocampus
Neurotransmitter Receptor
Synaptic Transmission
Acids
Neuronal Plasticity
Long-Term Potentiation
Rodentia
Western Blotting
Smoking
Depression
Pregnancy
Proteins

Keywords

  • AMPA receptors
  • Glutamate
  • Nicotinic receptors
  • Single channel
  • Synaptic plasticity

Cite this

Parameshwaran, Kodeeswaran ; Buabeid, Manal A. ; Bhattacharya, Subhrajit ; Uthayathas, Subramaniam ; Kariharan, Thiruchelvam ; Dhanasekaran, Muralikrishnan ; Suppiramaniam, Vishnu. / Long term alterations in synaptic physiology, expression of β2 nicotinic receptors and ERK1/2 signaling in the hippocampus of rats with prenatal nicotine exposure. In: Neurobiology of Learning and Memory. 2013 ; Vol. 106. pp. 102-111.
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abstract = "Smoking during pregnancy is associated with long lasting, hippocampus dependent, cognitive deficits in children. The current study was performed to investigate the effect of prenatal nicotine exposure on excitatory synaptic physiology and cellular signaling in the hippocampus using a rodent model. Excitatory synaptic physiology was analyzed using electrophysiological methods to detect changes in synaptic plasticity, excitatory synaptic transmission and synaptic currents mediated by α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) in the hippocampus. Additionally, western blot experiments were performed to quantify alterations in protein expression levels in the hippocampus. Prenatal nicotine exposure resulted in a decrease in long term potentiation (LTP) and an increase in long term depression (LTD). Basal synaptic transmission was also reduced with a concomitant decline in AMPAR mediated synaptic currents at the cellular and single channel levels. Presynaptic pool of vesicles docked close to release sites were also diminished in nicotine exposed rats. Moreover, reduced levels of β2 subunit containing nicotinic receptors and extracellular signal regulated kinase1/2 (ERK1/2) were observed in nicotine exposed rats. These results suggest that long lasting alterations in excitatory synaptic physiology, AMPAR synaptic currents and ERK1/2 signaling may serve as the molecular mechanisms for cognitive deficits associated with prenatal nicotine exposure.",
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Long term alterations in synaptic physiology, expression of β2 nicotinic receptors and ERK1/2 signaling in the hippocampus of rats with prenatal nicotine exposure. / Parameshwaran, Kodeeswaran; Buabeid, Manal A.; Bhattacharya, Subhrajit; Uthayathas, Subramaniam; Kariharan, Thiruchelvam; Dhanasekaran, Muralikrishnan; Suppiramaniam, Vishnu.

In: Neurobiology of Learning and Memory, Vol. 106, 01.01.2013, p. 102-111.

Research output: Contribution to journalArticleResearchpeer-review

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