title: Activation of phenotypically distinct neuronal subpopulations in the anterior subdivision of the rat basolateral amygdala following acute and repeated stress.
abstract: The effects of acute and repeated stress on expression of the early immediate gene c-fos in the basolateral amygdala have previously been reported; however, characterization of which neuronal subpopulations are activated by these stimuli has not been investigated. This question is of considerable relevance, insofar as the basolateral amygdala houses a heterogeneous population of neurons, including those of gamma-aminobutyric acid (GABA)-ergic and glutamatergic phenotypes that may be subcategorized based on their expression of various calcium-binding proteins, including parvalbumin, calbindin, calretinin, and the calcium-sensitive enzyme calcium/calmodulin-dependent kinase II. Characterization of these subpopulations has revealed unique differences in their physiology, synaptology, and morphology, suggesting that each distinct phenotype may have profound effects on the local circuitry of the amygdala. Therefore, we examined the effects of acute and repeated restraint stress on expression of the immediate early gene c-fos in neurons containing parvalbumin, calbindin, calretinin, or calcium/calmodulin-dependent kinase II in the basolateral amygdala. Double-label immunohistochemistry revealed that acute restraint stress activated a proportion of parvalbumin-, calbindin-, or calcium/calmodulin-dependent kinase II-positive neurons. Prior exposure to repeated restraint stress markedly attenuated acute-stress mediated activation of these neuronal populations, although not equally. Expression of c-Fos protein was not detected in calretinin-positive neurons in any experimental group. These results demonstrate that distinct neuronal phenotypes in the basolateral amygdala are activated by acute restraint stress and that prior repeated restraint stress differentially affects this response.
authors.affiliation: Department of Pharmacology, Physiology and Neuroscience, School of Medicine, University of South Carolina, Columbia, South Carolina 29208, USA.
authors.forename: Leah R
authors.initials: LR
authors.lastname: Reznikov
authors.forename: Lawrence P
authors.initials: LP
authors.lastname: Reagan
authors.forename: Jim R
authors.initials: JR
authors.lastname: Fadel
mesh_terms: D000679:Amygdala / Q000473:pathology*; D000704:Analysis of Variance; D000818:Animals; D002452:Cell Count / Q000379:methods; D005452:Fluoresceins; D005786:Gene Expression Regulation / Q000502:physiology; D008297:Male; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009474:Neurons / Q000145:classification* / Q000473:pathology*; D009930:Organic Chemicals / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical / Q000379:methods; D013312:Stress, Physiological / Q000209:etiology / Q000473:pathology*; D013997:Time Factors
chemical_list: D005452:Fluoresceins; D009419:Nerve Tissue Proteins; D009930:Organic Chemicals; D016760:Proto-Oncogene Proteins c-fos; C435731:fluoro jade