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Cystathionine beta synthase (CBS) is the main contributor to the production of hydrogen sulfide (H2S) in the brain. Exogenously administered H2S has been reported to protect neurons against hypoxic injury, ischemia and LPS-induced neuro-inflammation and in the facilitating of long term potentiation (LTP). Dysregulation of CBS leads to different diseases, which all have mental retardation in common. Although multiple studies have implicated a link between the CBS/H2S pathway and neurodegeneration, no studies have been performed examining the pathway in healthy aging animals. We hypothesize that CBS/H2S pathway plays an important role in the protection of learning and memory functions in the brain at the level of the hippocampus. Thus, we studied a set of 8 young (4 months) and 14 aged (24 months (n=6) and 28 months (n=8)) C57Bl6 mice. The 24-month-old mice displayed a significant decrease of CBS immunoreactivity in the MoDG only, compared to 4-month-old mice. In 28-month-old mice, we observed a significant increase of CBS immunoreactivity in the MoDG, compared to 4-month-old mice. When comparing 28-month-old mice to 24-month-old mice, all areas showed a significant increase of CBS immunoreactivity. Thus, throughout aging, CBS expression is maintained in the hippocampus, and many other forebrain regions as well. Mice at the unusual age of 28 months even have a higher hippocampal CBS expression than young mice. Maintenance (and increase) of CBS levels may sustain memory and learning by precluding neuronal loss in areas of the hippocampus., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)

Natural hypothermia during hibernation results in physiological and behavioral deficits. These changes may be traced at the level of hippocampal signal transduction. We investigated synaptophysin immunoreactivity (SYN-ir) in the hippocampus after short and long periods of hypothermia and short and long periods of euthermy in hibernating ground squirrels. SYN-ir in the stratum lucidum of the hippocampus was transiently reduced during natural hypothermia. Natural hypothermia thus reduces synaptic efficacy. This may play a role in the reduced neuronal connectivity of CA3 pyramidal cell dendrites observed in hibernating ground squirrels.

In the present study we report the effect of corticosterone in the regulation of hippocampal muscarinic acetylcholine receptor immunoreactivity (mAChR-ir) expression in rats. Adrenalectomy (ADX) or a single injection of a mineralocorticoid antagonist RU-28318 (1.0 mg/100 g body weight (b.w.)) in adrenally intact rats 24 h prior to sacrifice revealed an increased mAChR-ir in hippocampal CA1 and CA3 areas. Corticosterone replacement (100 microg/100 g b.w.) prevented the increase in mAChR-ir of ADX animals. However, glucocorticoid receptor antagonist (RU38486) treatment in adrenally intact rats failed to affect the mAChR immunolabeling. These results point to a modulation of muscarinic receptors by corticosterone that is predominantly mediated by the mineralocorticoid receptor.

Vasopressin (AVP) is a major neuropeptide in the suprachiasmatic nucleus, the mammalian hypothalamic circadian pacemaker. Protein kinase Calpha is a putatively coupled intracellular messenger. Mean numbers of AVP- and protein kinase Calpha-immunoreactive neurons were determined in the suprachiasmatic nucleus of common voles, entrained to a 12:12 h light-dark (LD) cycle, at the beginning of the light period (zeitgeber time zero) and 6 h later (zeitgeber time six). At zeitgeber time zero, mean numbers of AVP- and protein kinase Calpha- immunoreactive neurons were 2194 and 9897, respectively. Both numbers decreased significantly with about 40% at zeitgeber time six. This concurrent decrease was most pronounced in the dorsomedial aspect of the suprachiasmatic nucleus. These findings are consistent with the findings of a peak of AVP release in rats during the early light phase.

The suprachiasmatic nuclei (SCN) have been identified as a pacemaker for many circadian rhythms in mammals. Photic entrainment of this pacemaker can be accomplished via the direct retino-hypothalamic tract (RHT). Glutamate is a putative transmitter of the RHT. In the present study it is demonstrated that glutamate injections in the SCN cause phase shifts of the circadian activity rhythm of the hamster. In contrast, glutamate injections outside the SCN or vehicle injections inside the SCN did not affect the circadian phase. These data suggest that glutamate could be involved in photic entrainment of the circadian pacemaker.