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We observed immunostaining for vitamin D binding protein (DBP) in rat hypothalamus. Part of the supraoptic and of the paraventricular neurons showed DBP immunoreactivity, in part colocalized with Arg-vasopressin. DBP was also observed in widespread axonal projections throughout the lateral hypothalamus, the median eminence and the posterior pituitary lobe. A portion of ependymal cells, the choroids plexus epithelium and some of the endocrine cells in the anterior pituitary lobe contained DBP immunoreactivity. In situ hybridization of semithin sections with a synthetic oligonucleotide probe to DBP mRNA resulted in staining of magnocellular hypothalamic neurons, but not of ependymal cells or anterior lobe cells. Our observations indicate an intrinsic expression of DBP in the rat hypothalamus. DBP may be synthesized and transported along with the classical neurohypophyseal hormones. The multiple locations of DBP-expressing neurons indicate multiple functional properties: DBP may be released from in the posterior lobe, it may act as a hypophyseotropic factor and as a central neuroactive substance.

Summary Chronic stress affects brain areas involved in learning and emotional responses through modulation of neurotropic factors or neurotransmitters. Therefore, we investigated the role of exercise and thiamine supplementation on spatial memory and on brain-derived neurotrophic factor (BDNF) and acetylcholine (Ach) content in the hippocampus of the stressed animals. Male Wistar rats were randomly assigned to 4 groups (8 rats/group): control group; stress group; swimming and stress group; and thiamine and stress group. All animals were assessed by a T maze for spatial memory or open fi eld test for locomotion and anxiety. BDNF and Ach were estimated in the hippocampus. Chronic immobilization stress resulted in a signifi cant decrease in BDNF and Ach levels in the hippocampus and impairment in spatial memory functions and decreased basal activity. However, either swimming training or thiamine intake for 30 d was proved to induce a signifi cant increase both in BDNF and Ach in conjunction with improved performance in the T maze, marked anxiolytic effect and enhanced ambulation in the open fi eld test, as compared to the stress group. Interestingly, swimming-exercised rats showed signifi cantly higher levels of BDNF versus thiaminereceiving rats, while thiamine-receiving rats showed higher locomotor activity and less freezing behavior in the open fi eld test compared to the swimming group. It was concluded that decreased BDNF and Ach after stress exposure could be a mechanism for the deleterious actions of stress on memory function; swimming exercise or vitamin B 1 supplementation for 30 d was a protective tool to improve coping with chronic stress by modulating BDNF and Ach content along with enhancement of memory functions and motor activities.

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With combined immunoperoxidase and immunofluorescence, we observed colocalization of cytochrome P450 aromatase with the posterior lobe peptide oxytocin and its associated neurophysin 1 in adult male rats. P450 was most abundant in the anterior hypothalamus. Colocalization of OT with P450 was observed in the preoptic region, the periventricular nucleus of the hypothalamus, the lateral subcommissural nucleus, and in the zona incerta. Magnocellular perikarya in the supraoptic and in the paraventricular nuclei contained only occasionally both antigens. P450 immunostaining overlapped to a great extent with known estrogen target regions. Oxytocinergic functions are controlled by estradiol while androgen receptors are mostly absent in neuroendocrine hypothalamic nuclei. Our findings suggest that systemic androgens may be aromatized to estrogens in male oxytocinergic neurons linked to the limbic system.

Although monosodium glutamate (MSG)-induced neurotoxicity has been recognized for decades, the potential similarities of the MSG model to Alzheimer’s disease (AD)-type neuropathology have only recently been investigated. MSG-treated mice were examined behaviourally and histologically in relation to some features of AD. Four-week old mice received 5 subcutaneous MSG (2 g/kg) injections on alternate days, or saline. At age 10–12 weeks, they were given a battery of behavioural tests for species-typical behaviours and working memory. The mice were killed at 12 weeks and the brains excised. Accumulation of hyperphosphorylated tau protein was assessed in cortical and hippocampal neurons by immunohistochemistry, and in cerebral cortical homogenates. A 78% increase in cortical concentrations of phosphorylated tau protein was observed in the MSG mice. Intracellular hyperphosphorylated tau immunostaining was observed diffusely in the cortex and hippocampus, together with cortical atrophic neurons, extensive vacuolation and dysmorphic neuropil suggestive of spongiform neurodegeneration. Nest-building was significantly impaired, and spontaneous T-maze alternation was reduced, suggesting defective short-term working memory. Subcutaneous MSG treatment also induced a 56% reduction in exploratory head dips in a holeboard (P = 0.009), and a non-significant tendency for decreased burrowing behaviour (P = 0.085). These effects occurred in the absence of MSG-induced obesity or gross locomotor deficits. The findings point to subcutaneous MSG administration in early life as a cause of tau pathology and compromised species-typical behaviour in rodents. Determining whether MSG can be useful in modelling AD requires further studies of longer duration and full behavioural characterization.

In response to a stressful unexpected experience, the brain activates a complex stress system that involves the organism in an adaptive response to the threatening situation. This stress system acts on several peripheral tissues and feeds back to the brain. One of its key players is oxytocin hormone. The neuropeptide, oxytocin (OT), has well-established roles during parturition and lactation. In addition to its peripheral actions, OT is released within multiple areas of the brain and influences behavioural and neuroendocrine responses to stress. Several studies suggest that oxytocin is implicated in the central control of responses to stress through modulation of corticotrophin releasing hormone (CRH). Intranasal OT application was associated with an inhibitory effect on adrenocorticotrophic hormone (ACTH) secretion and subsequent impairment of corticosterone secretion. This may be of importance for understanding and perhaps suggesting its utility to buffer stress. Synthesis and release of OT depend to a great extent on steroid hormones particularly on estradiol and corticosterone. Estrogens stimulate synthesis and release of OT and increase the number of OT receptors in some areas of the brain. However, the role of OT in mediating stress is variable and may also depend on gender and on external factors.