Excitatory synapses on dendritic shafts of the caudal basal amygdala exhibit elevated levels of GABAA receptor α4 subunits following the induction of activity-based anorexia

Gauri S. Wable, Nicole C. Barbarich-Marsteller, Tara G. Chowdhury, Nicole A. Sabaliauskas, Claudia R. Farb, Chiye Aoki

Research output: Contribution to journalArticle

Abstract

Anorexia nervosa (AN) is an eating disorder characterized by self-imposed severe starvation, excessive exercise, and anxiety. The onset of AN is most often at puberty, suggesting that gonadal hormonal fluctuations may contribute to AN vulnerability. Activity-based anorexia (ABA) is an animal model that reproduces some of the behavioral phenotypes of AN, including the paradoxical increase in voluntary exercise following food restriction. The basal amygdala as well as the GABAergic system regulate trait anxiety. We therefore examined the subcellular distribution of GABA receptors (GABARs) in the basal amygdala of female pubertal rats and specifically of their α4 subunits, because expression of α4-containing GABARs is regulated by gonadal hormone fluctuations. Moreover, because these GABARs reduce neuronal excitability through shunting of EPSPs, we quantified the frequency of occurrence of these GABARs adjacent to excitatory synapses. Electron microscopic immunoctychemistry revealed no change in the frequency of association of α4 subunits with excitatory synapses on dendritic spines, whether in the anterior (Bregma -2.8 mm) or caudal (Bregma -3.8 mm) portion of the basal amygdala. Sholl analysis of golgi-stained neurons also revealed no change in the extent of dendritic branching by these densely spiny, pyramidal-like neurons. However, there was an increase of membranous α4 subunits near excitatory synapses on dendritic shafts, specifically in the caudal basal amygdala, and this was accompanied by a rise of α4 subunits intracellularly. Because most dendritic shafts exhibiting excitatory synapses are GABAergic interneurons, the results predict disinhibition, which would increase excitability of the amygdaloid network, in turn augmenting ABA animals' anxiety. Synapse, 68:1-15, 2014.

Original languageEnglish (US)
Pages (from-to)1-15
Number of pages15
JournalSynapse
Volume68
Issue number1
DOIs
StatePublished - Jan 2014

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Anorexia
GABA-A Receptors
Amygdala
GABA Receptors
Synapses
Anorexia Nervosa
Anxiety
Gonadal Hormones
Dendritic Spines
Pyramidal Cells
Excitatory Postsynaptic Potentials
Interneurons
Puberty
Starvation
Animal Models
Electrons
Phenotype
Neurons
Food

Keywords

  • Anorexia nervosa
  • Anxiety
  • Disinhibition
  • Exercise
  • Food restriction
  • Hyperactivity

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience

Cite this

Excitatory synapses on dendritic shafts of the caudal basal amygdala exhibit elevated levels of GABAA receptor α4 subunits following the induction of activity-based anorexia. / Wable, Gauri S.; Barbarich-Marsteller, Nicole C.; Chowdhury, Tara G.; Sabaliauskas, Nicole A.; Farb, Claudia R.; Aoki, Chiye.

In: Synapse, Vol. 68, No. 1, 01.2014, p. 1-15.

Research output: Contribution to journalArticle

Wable, Gauri S. ; Barbarich-Marsteller, Nicole C. ; Chowdhury, Tara G. ; Sabaliauskas, Nicole A. ; Farb, Claudia R. ; Aoki, Chiye. / Excitatory synapses on dendritic shafts of the caudal basal amygdala exhibit elevated levels of GABAA receptor α4 subunits following the induction of activity-based anorexia. In: Synapse. 2014 ; Vol. 68, No. 1. pp. 1-15.
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AB - Anorexia nervosa (AN) is an eating disorder characterized by self-imposed severe starvation, excessive exercise, and anxiety. The onset of AN is most often at puberty, suggesting that gonadal hormonal fluctuations may contribute to AN vulnerability. Activity-based anorexia (ABA) is an animal model that reproduces some of the behavioral phenotypes of AN, including the paradoxical increase in voluntary exercise following food restriction. The basal amygdala as well as the GABAergic system regulate trait anxiety. We therefore examined the subcellular distribution of GABA receptors (GABARs) in the basal amygdala of female pubertal rats and specifically of their α4 subunits, because expression of α4-containing GABARs is regulated by gonadal hormone fluctuations. Moreover, because these GABARs reduce neuronal excitability through shunting of EPSPs, we quantified the frequency of occurrence of these GABARs adjacent to excitatory synapses. Electron microscopic immunoctychemistry revealed no change in the frequency of association of α4 subunits with excitatory synapses on dendritic spines, whether in the anterior (Bregma -2.8 mm) or caudal (Bregma -3.8 mm) portion of the basal amygdala. Sholl analysis of golgi-stained neurons also revealed no change in the extent of dendritic branching by these densely spiny, pyramidal-like neurons. However, there was an increase of membranous α4 subunits near excitatory synapses on dendritic shafts, specifically in the caudal basal amygdala, and this was accompanied by a rise of α4 subunits intracellularly. Because most dendritic shafts exhibiting excitatory synapses are GABAergic interneurons, the results predict disinhibition, which would increase excitability of the amygdaloid network, in turn augmenting ABA animals' anxiety. Synapse, 68:1-15, 2014.

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