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Aging and cholinergic deafferentation alter GluR1 expression in rat frontal cortex.

Irene Kim1, Randall E Wilson, Cara L Wellman

  • 1Department of Psychology, Indiana University, Bloomington, IN 47405, USA.

Neurobiology of Aging
|March 8, 2005
PubMed
Summary

Aging alters frontal cortex plasticity. Lesions to the nucleus basalis magnocellularis (NBM) increased GluR1 expression in young rats but not aged rats, suggesting a mechanism for age-related plasticity differences.

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Area of Science:

  • Neuroscience
  • Aging Research
  • Neuroplasticity

Background:

  • Frontal cortex plasticity is altered in aging.
  • Nucleus basalis magnocellularis (NBM) lesions cause greater dendritic morphology decline in aged rats.
  • Cholinergic NBM afferents modulate neocortical glutamatergic transmission, a process involved in plasticity.

Purpose of the Study:

  • To investigate age-related differences in AMPA receptor subunit GluR1 expression following cholinergic deafferentation.
  • To identify potential mechanisms for age-related differences in frontal cortex plasticity after NBM lesions.

Main Methods:

  • Young adult, middle-aged, and aged rats underwent sham or 192 IgG-saporin lesions of the NBM.
  • Unbiased stereology quantified intensely GluR1-immunopositive neurons in frontal cortex layer II-III.

Main Results:

  • Lesions significantly increased intensely GluR1-immunopositive neurons in young adult rats.
  • Aged rats showed an increase in GluR1-positive neurons independent of lesion status.
  • Lesion-induced GluR1 expression differences were observed between young and aged rats.

Conclusions:

  • Age-related differences in lesion-induced AMPA receptor subunit GluR1 expression may underlie altered frontal cortex plasticity in aging.
  • Cholinergic deafferentation impacts GluR1 expression differently across the lifespan.