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Coffee and nicotine consumption are frequently combined, indicating possible intensifying effect of caffeine on smoking behavior, although neurobiological background of this phenomenon remains unknown. We aimed at determining the effect of caffeine and nicotine, applied separately or simultaneously, on activation of six structures of the brain reward system: nucleus accumbens (NAc), ventral tegmental area (VTA), amygdala (Amg), hippocampus (Hip), medial prefrontal cortex (mPfr) and dorsal striatum (CdP) in the adult male Wistar rats. Activation of two transcription factors, the phosphorylated form of cyclic AMP-response element binding protein (pCREB) and DeltaFosB (ΔFosB) was assessed by immunohistochemistry after multiple-dose five-days psychostimulants administration followed by 20min and 24h survival, respectively. Nicotine evoked the highest increase of pCREB-immunoreactivity (-ir) in NAc, while caffeine exerted the weakest effect in mPfr and CdP. Nicotine/caffeine co-administration resulted in decrease of pCREB-ir in NAc and increase in Amg, compared with the effect of each psychostimulant used separately. Nicotine was the strongest psychostimulant activating ΔFosB-ir in Amg, whereas caffeine - in Hip. Nicotine/caffeine-exerted effect upon ΔFosB-ir in Amg was weaker, whereas in mPfr stronger, than nicotine-evoked effect in these structures. In summary, pCREB and ΔFosB activation is dependent on the type of stimulus, brain structure and functional context. Activation of both transcription factors is responsible for caffeine's modifying effect upon nicotine-related behaviors and must be taken into account while quitting cigarette smoking., (Copyright © 2017 Elsevier B.V. All rights reserved.)

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.

It seems that age-dependent changes in stress response may be correlated with alterations in the hypothalamic brain derived neurotrophin factor (BDNF). Two hypothalamic nuclei, ie. paraventricular (PVN) and supraoptic (SON) are closely related to the stress response. Therefore, the aim of our study was to explore the influence of acute and chronic high-light open field (HL-OF) or forced swim (FS) stimulation on the density of BDNF immunoreactive (ir) neurons in the PVN and SON in adult (postnatal day 90; P90) and aged (P720) Wistar Han rats. Our data demonstrated that in comparison with non-stressed rats, neither acute nor chronic FS caused significant changes in the density of BDNF-ir neurons of PVN and SON in P90 or P720 rats. However, a significant increase in the density of BDNF-ir neurons in the SON of P90 and a decrease in the PVN of the P720 rats were noted after acute HL-OF. Despite the lack of change in the density of BDNF-ir neurons between P90 and P720 non-stressed and FS stressed rats, there was an age-dependent decrease in the BDNF-ir cells of HL-OF stressed rats, especially in the PVN. We may conclude that in terms of its influence on the BDNF-ir neurons in PVN and SON, acute HL-OF was the factor inducing changes in the density of BDNF-ir neurons in the hypothalamic nuclei of adult or aged rats. Furthermore, ageing involutional processes, which can impair hypothalamic-pituitary-adrenal axis functioning, may have been able to cause an age-related decrease in the BDNF-ir PVN and/or SON neurons in HL-OF stressed rats., (Copyright © 2016 Elsevier B.V. All rights reserved.)

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., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

The ontogenetic period of life and stress can have different effects on the nerve growth factor (NGF) in the hypothalamus. The aim of our study was to investigate the influence of two mild stressors, acute and chronic exposure to forced swim (FS) or high-light open field (HL-OF), on neurons containing NGF. Immunofluorescence staining was used to reveal the density of NGF-immunoreactive (ir) cells in the hypothalamic supraoptic nucleus (SON) in adult (postnatal day 90; P90) and aged (P720) rats. The P90 and P720 rats that were subjected to acute and chronic FS showed no differences in the density of NGF-ir neurons in the SON compared with nonstressed rats. However, a significant increase in NGF-ir cells was noted after acute but not after chronic HL-OF only in P90 rats. What is more, there were no age-related (P90 vs. P720) changes in the density of NGF-ir neurons in non-stressed and FS- or HL-OF-stressed rats. Our results indicate that acute HL-OF was the only factor inducing changes in the density of NGF-ir neurons in the SON of adult rats. This could be related to the neuroprotective role of NGF-ir cells in response to acute HL-OF. The absence of age-dependent changes in the density of NGF-ir neurons may indicate that the ageing processes in SON do not generate changes in the NGF immunoreactivity of its neurons.

Proinflammatory cytokine - interleukin 1β (IL-1β) plays an important role in stress reactions in the structures of limbic system. The impact of stress on IL-1β may depend on the ontogenetic age. The study examined the influence of acute and chronic exposure to forced swim (FS) or high-light open-field (HL-OF) stressors on neurons containing IL-1β. Double immunofluorescence staining was used to reveal the density of IL-1β/NeuN (NeuN - a neuronal nuclear marker) - immunoreactive (ir) cells in the amygdaloid central (CeA) and medial (MeA) nuclei, which are closely involved in the regulation of emotional stressors and hypothalamic-pituitary-adrenal axis (HPA) activation. Adult (P90; P - postnatal day), middle-aged (P360), and aged (P720) male Wistar Han rats were used in these experiments. We observed an age-dependent increase in the basal density of IL-1β/NeuN-ir cells in CeA and MeA in P90 vs. P360 and P360 vs. P720 rats. Neither acute nor chronic FS caused significant changes in the density of IL-1β-ir neurons in any of the investigated nuclei in P90, P360, and P720 rats as compared with the non-stressed groups. However, chronic but not acute HL-OF caused a marked increase in the density of IL-1β/NeuN-ir cells in the CeA and MeA of P360 rats and in MeA of the P720 animals. Moreover, chronic HL-OF led to an increase in the density of IL-1β-ir neurons in relation to acute HL-OF in the CeA and MeA of both P360 and P720 rats. Our results may indicate the involvement of IL-1β neurons in the development of ageing processes in CeA and MeA. Furthermore, our results point out that chronic HL-OF is an aggravating factor that induces an increase in the density of IL-1β/NeuN-ir cells in the MeA and/or CeA of middle-aged and aged rats. The increase is possibly due to insufficient control of the HPA axis associated with involutional ageing processes and seems to be a common denominator of the ageing process and stress.

It is believed that the impact of stress on interleukin-1β (IL-1β) depends on the ontogenetic age. This study examines the influence of acute or chronic exposure to forced-swim (FS) stress or high-light open-field (HL-OF) stimulation on the expression of IL-1β. Double immunofluorescence staining was used to reveal the density of IL-1β/NeuN (NeuN is a neuronal nuclear marker)-immunoreactive (-ir) cells in the hippocampal subfields CA1 and CA3, dentate gyrus (DG), and paraventricular nucleus (PVN) of the hypothalamus. Adult postnatal day 90 (P90) and aged (P720) rats were used in this experiment. The data showed a significant increase in the density of IL-1β/NeuN-ir cells in the CA1, CA3, DG, and PVN in P720 nonstressed rats in relation to P90 control animals. Neither FS nor HL-OF acute stimulation caused alteration in the density of IL-1β-ir neurons in any of the investigated structures in P90 and P720 rats in comparison with control groups. However, chronic FS caused a significant increase in CA3 and DG of P720 rats, and chronic HL-OF led to a significant increase in the density of IL-1β-ir neurons in the PVN of P90 rats and in all hippocampal subfields of P720 animals. These results indicate that chronic HL-OF stimulation is a factor that induces changes in the number of IL-1β-ir neurons in the PVN of adult rats, whereas both chronic FS and HL-OF are aggravating factors for the hippocampus of aged (P720) animals., (Copyright © 2014 Wiley Periodicals, Inc.)