The immunoreactivity of c-Fos, NGF and its receptor TrkA after open-field exposure in the central and medial nuclei of the rat amygdala.
The amygdala is a critical component of the neuroanatomical stress circuit. It plays a role in the generation of responses to emotional stimuli. The central (CeA) and medial (MeA) amygdaloid nuclei are implicated in activation of the hypothalamic-pituitary-adrenocortical (HPA) axis. The immunoreactivity (-ir) of c-Fos, NGF and its receptor, TrkA, following acute and chronic open-field stress were studied in the CeA and MeA nuclei of the amygdala. The material consisted of 21 male adult rats divided into three groups: non-stressed (control) animals, rats exposed to acute (once only lasting 15 min) and chronic (15 min daily over 21 days) aversive stimulation (open-field exposure). The brains were stained with the use of immunohistochemical methods for c-Fos, NGF or TrkA. In the control rats c-Fos-, TrkA- and NGF-ir cells were observed in the nuclei studied, but the quantity varied, being moderate or high (immunoreactive to TrkA and NGF) or low (immunoreactive to c-Fos). In the animals exposed to acute open-field stress the number of c-Fos-ir, NGF-ir and TrkA-ir cells in the nuclei under examination was differentiated but higher than that in the control animals. In the animals exposed to chronic open-field stress the number of c-Fos-ir cells in the nuclei studied was similar and was smaller than those in animals exposed to acute stress. The number of TrkA-ir neurons was also lower in comparison to that in animals exposed to acute stress. However, no significant differences in the number of NGF-ir cells were observed between the groups exposed to acute and chronic stress. Diverse expression of c-Fos protein following both acute and chronic stress stimulation may prove the functional heterogeneity of the amygdaloid nuclei investigated. The decrease observed in both c-Fos- and TrkA-ir in MeA (only TrkA in CeA) of animals exposed to chronic stress may indicate the phenomenon of habituation.
Badowska-Szalewska
E
E
Department of Anatomy and Neurobiology, Medical University of Gdańsk, Gdańsk, Poland. ewabadowska@amg.gda.pl
Ludkiewicz
B
B
Domaradzka-Pytel
B
B
Dziewiatkowski
J
J
Spodnik
J H
JH
Moryś
J
J
D000679:Amygdala / Q000166:cytology / Q000378:metabolism*; D000818:Animals; D001522:Behavior, Animal; D005106:Exploratory Behavior / Q000502:physiology*; D008297:Male; D020932:Nerve Growth Factor / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D020917:Receptor, trkA / Q000378:metabolism*; D013315:Stress, Psychological / Q000378:metabolism
D016760:Proto-Oncogene Proteins c-fos; D020932:Nerve Growth Factor; D020917:Receptor, trkA