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At least 37 records · Page 2Linked to original sources
PubMed1979

Influences of adrenocortical hormones on pituitary and brain function.

Adrenocortical secretions influence neuroendocrine function and behavior, and it is possible to recognize separate physiologic actions of gluco- and mineralocorticoids. The search for neuroanatomical sites and cellular modes of adrenocorticoid action has revealed a system of putative glucocorticoid receptors in neurons of the hippocampus, septum, amygdala, and entorhinal cortex, and in the pituitary. No part of the brain is totally devoid of receptor activity, however, and glial cells may also contain glucocorticoid receptors. Mineralocorticoid receptors are less well characterized neuroanatomically or biochemically. One reason for this is the considerable degree to which both gluco- and mineralocorticoids bind to both classes of receptors in vitro. Another reason may be the overwhelming quantitative predominance of glucocorticoid over mineralocorticoid receptors in neural tissue. Glucocorticoid receptors of the pituitary, which have a high avidity for dexamethasone, appear to participate in the delayed negative feedback effects of glucocoticoids. Functional correlates of neural glucocorticoid receptors remain to be clearly established. Among the possibilities are several reported effects on hippocampal neural activity that have an onset latency of 20--30 min and a duration of several hours. The relative rapidity of such effects does not preclude genomic mediation, as genomic effects of glucocorticoids on thymus lymphocytes have been detected within as little as 15 min of steroid application [117]. What are not so far explained by the intracellular receptor mechanism are the extremely rapid effects of glucocorticoids such as the rate-sensitive negative feedback on CRF and ACTH secretion. These may involve a direct action of the steroid on cell membranes in the pituitary and hypothalamus.

Adrenal Cortex↗
PubMed2026

The interplay between circadian misalignment or sleep disturbances and cognition and brain function in individuals with different degrees of insulin resistance - a systematic review.

Disruption of sleep increases the risk of type 2 diabetes and worsens cognitive outcomes, yet few studies have evaluated the interaction between insulin resistance and sleep parameters in relation to cognitive outcomes or the risk of dementia. This systematic review examines how circadian misalignment and sleep disturbances affect cognition and neuroimaging findings in individuals with varying degrees of insulin resistance. Across 27 studies, disrupted circadian rhythmicity and sleep disturbances were negatively associated with brain health, possibly through its effects on insulin sensitivity, whereas the impact of sleep duration and quality were inconclusive. Methodological heterogeneity, reliance on cross-sectional designs, and limited control for confounders restricted definitive conclusions and highlighted the need for longitudinal and interventional studies with objective measurements. Nonetheless, the findings support circadian rhythmicity as a potentially modifiable risk factor for preserving cognition in insulin-resistant populations. Future research should prioritise prospective and interventional studies and focus on biological markers rather than self-reported outcomes.

Humans↗
PubMed1978

Influence of the cerebrovascular sympathetic innervation on regional flow, autoregulation, and blood-brain barrier function.

Experiments have been done on rats, rabbits and baboons to elucidate the role of the cranial sympathetic nerves originating in the superior cervical ganglia in the regulation of local cerebral blood flow, including its autoregulation, and in blood-brain barrier functions. Flow was measured by the [14C] ethanol technique, thermoclearance, and xenon-133 clearance. Blood-brain barrier functions were studied by the extravasation of an Evan's blue-albumin complex and by calculation of brain uptake index for two compounds (noradrenaline and inulin). Electrical stimulation of the sympathetic nerves reduces regional flow to a degree that is related to the amount of local perivascular innervation. The breakthrough of autoregulation during induced systemic hypertension is prevented by bilateral stimulation of the superior cervical ganglia. Acute sympathectomy markedly enhances the vascular penetration both at normotension (tested by brain uptake index for noradrenaline and inulin) and rapidly induced hypertension (evidenced by extravasation of Evans' blue). This extravasation of Evans' blud during acute hypertension can be counteracted by sympathetic nerve stimulation. The results give further support for the view that the cranial sympathetic nerves afford an efficient control of the cerebrovascular bed.

Animals↗