The way hippocampal neurons function during stress in old age (critical times of life) is dependent on brain derived neurotrophin factor (BDNF). This study examined the influence of acute and chronic forced swim (FS) or high-light open field (HL-OF) stimulation on the density of BDNF immunoreactive (ir) neurons in the hippocampal pyramidal layers of CA1, CA2, CA3 regions and the granular layer of dentate gyrus (DG) in old (postnatal day 720; P720) Wistar Han rats. Our data showed that in comparison with non-stressed rats, acute FS caused a significant increase in the density of BDNF-ir neurons in CA2 and CA3, while acute HL-OF led to an increase in this factor in all hippocampal subfields with the exception of DG. However, the density of BDNF-ir cells remained unchanged after exposure to chronic FS or HL-OF in the hippocampal regions in relation to the control rats. These results indicate that acute FS or HL-OF proved to be a stressor that induces an increase in the density of BDNF-ir pyramidal neurons, which was probably connected with up-regulation of HPA axis activity and short-time memory processing of the stressful situation. Moreover, as far as the influence on BDNF-ir cells in hippocampus is concerned, chronic FS or HL-OF was not an aggravating factor for rats in the ontogenetic periods studied.

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The type and duration of stress stimulation are postulated to affect the expression of the brain derived neurotrophic factor (BDNF) differentially during ontogenetic life. The aim of our study was to investigate the influence of two different stressors, i.e. chronic (15 min daily for 21 days) exposure to the forced swim (FS) test or the high light open field (HL-OF) test, on the BDNF contained in magnocellular (PVm) and parvocellular (PVp) neurons of the hypothalamic paraventricular (PV) and the supraoptic (SO) nuclei. The immunofluorescence (-ir) method was used to detect BDNF-ir cells. The research showed that only the PVp part of the PV in juvenile (P28; P-postnatal day) control rats had a significantly lower density of BDNF-ir neurons than that in middle-aged (P360) control subjects. After chronic FS, a significant decrease in BDNF-ir cells was observed in the studied hypothalamic nuclei of the juvenile rats, but no changes were noted in the middle-aged individuals. The PV (PVm, PVp) and the SO nuclei in juvenile rats showed a significantly lower density of BDNF-ir neurons than the corresponding area of the hypothalamus in middle-aged rats. However, following the HL-OF test, the density of BDNF-ir neurons remained unaltered both in the P28 and the P360 groups. The data suggest that the type of the stressor applied was the factor that differentiated the number of BDNF-ir cells in the PVm and the SO only in juvenile rats: chronic HL-OF was more severe than FS. The age of the animals was the main factor that conditioned the BDNF hypothalamic PV (PVm, PVp) and the SO response to FS stimulation. The different density of BDNF-ir containing cells in the PVp of juvenile versus middle-aged rats can be explained by a functional, age-related change in the demand of PVp neurons for BDNF.

Nerve growth factor (NGF) seems to play an important role in the ageing limbic system in response to stress. This study aimed to explore the influence of acute and chronic exposure to high-light open field (HL-OF) or forced swim (FS) stressors on the density of NGF immunoreactive (ir) neurons in the amygdala central (CeA), medial (MeA), lateral (LA) and basolateral (BLA) nuclei in adult (postnatal day 90; P90) and aged (P720) rats. In comparison with non-stressed rats, neither acute nor chronic HL-OF produced significant changes in the density of NGF-ir neurons of studied nuclei in P90 and P720 rats. However, not acute but chronic FS was the factor inducing an increase in the density of NGF-ir neurons in the CeA of both age groups and in the LA of P720 rats. Despite the lack of change in the density of NGF-ir neurons between P90 and P720 non-stressed rats, there were significant age-related changes in NGF-ir cells in FS and/or HL-OF stressed rats in all the tested nuclei, with the exception of the LA. It may be concluded that as far as the influence on NGF-ir cells in amygdaloid nuclei is concerned, HL-OF did not constitute an aggravating factor for rats in the ontogenetic periods studied. Moreover, upregulation of NGF-ir neurons predominantly in CeA after chronic FS seems to be neuroprotective. Age-dependent changes in the density of NGF-ir neurons in stressed rats are probably caused by ageing processes and they may point to dysregulation of excitatory control exerted by the amygdala.