Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory

Munir Gunes Kutlu, Thomas J. Gould

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

The hippocampus is a key brain structure involved in synaptic plasticity associated with long-term declarative memory formation. Importantly, nicotine and activation of nicotinic acetylcholine receptors (nAChRs) can alter hippocampal plasticity and these changes may occur through modulation of hippocampal kinases and transcription factors. Hippocampal kinases such as cAMP-dependent protein kinase (PKA), calcium/calmodulin-dependent protein kinases (CAMKs), extracellular signal-regulated kinases 1 and 2 (ERK1/2), and c-jun N-terminal kinase 1 (JNK1), and the transcription factor cAMP-response element-binding protein (CREB) that are activated either directly or indirectly by nicotine may modulate hippocampal plasticity and in parallel hippocampus-dependent learning and memory. Evidence suggests that nicotine may alter hippocampus-dependent learning by changing the time and magnitude of activation of kinases and transcription factors normally involved in learning and by recruiting additional cell signaling molecules. Understanding how nicotine alters learning and memory will advance basic understanding of the neural substrates of learning and aid in understanding mental disorders that involve cognitive and learning deficits.

Original languageEnglish (US)
Pages (from-to)162-171
Number of pages10
JournalPhysiology and Behavior
Volume155
DOIs
StatePublished - Mar 1 2016

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Learning
Nicotine
Hippocampus
Transcription Factors
Phosphotransferases
Calcium-Calmodulin-Dependent Protein Kinase Kinase
Mitogen-Activated Protein Kinase 8
Cyclic AMP Response Element-Binding Protein
Neuronal Plasticity
Mitogen-Activated Protein Kinase 3
Long-Term Memory
Mitogen-Activated Protein Kinase 1
Nicotinic Receptors
Cyclic AMP-Dependent Protein Kinases
Mental Disorders
Brain

All Science Journal Classification (ASJC) codes

  • Experimental and Cognitive Psychology
  • Behavioral Neuroscience

Cite this

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Nicotinic modulation of hippocampal cell signaling and associated effects on learning and memory. / Kutlu, Munir Gunes; Gould, Thomas J.

In: Physiology and Behavior, Vol. 155, 01.03.2016, p. 162-171.

Research output: Contribution to journalReview article

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AB - The hippocampus is a key brain structure involved in synaptic plasticity associated with long-term declarative memory formation. Importantly, nicotine and activation of nicotinic acetylcholine receptors (nAChRs) can alter hippocampal plasticity and these changes may occur through modulation of hippocampal kinases and transcription factors. Hippocampal kinases such as cAMP-dependent protein kinase (PKA), calcium/calmodulin-dependent protein kinases (CAMKs), extracellular signal-regulated kinases 1 and 2 (ERK1/2), and c-jun N-terminal kinase 1 (JNK1), and the transcription factor cAMP-response element-binding protein (CREB) that are activated either directly or indirectly by nicotine may modulate hippocampal plasticity and in parallel hippocampus-dependent learning and memory. Evidence suggests that nicotine may alter hippocampus-dependent learning by changing the time and magnitude of activation of kinases and transcription factors normally involved in learning and by recruiting additional cell signaling molecules. Understanding how nicotine alters learning and memory will advance basic understanding of the neural substrates of learning and aid in understanding mental disorders that involve cognitive and learning deficits.

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