95 research outputs found
Mineralocorticoid receptors are indispensable for nongenomic modulation of hippocampal glutamate transmission by corticosterone
The adrenal hormone corticosterone transcriptionally regulates responsive genes in the rodent hippocampus through nuclear mineralocorticoid and glucocorticoid receptors. Via this genomic pathway the hormone alters properties of hippocampal cells slowly and for a prolonged period. Here we report that corticosterone also rapidly and reversibly changes hippocampal signaling. Stress levels of the hormone enhance the frequency of miniature excitatory postsynaptic potentials in CA1 pyramidal neurons and reduce paired-pulse facilitation, pointing to a hormone-dependent enhancement of glutamate-release probability. The rapid effect by corticosterone is accomplished through a nongenomic pathway involving membrane-located receptors. Unexpectedly, the rapid effect critically depends on the classical mineralocorticoid receptor, as evidenced by the effectiveness of agonists, antagonists, and brain-specific inactivation of the mineralocorticoid but not the glucocorticoid receptor gene. Rapid actions by corticosterone would allow the brain to change its function within minutes after stress-induced elevations of corticosteroid levels, in addition to responding later through gene-mediated signaling pathways
The Origin of Glucocorticoid Hormone Oscillations
Characterization of a peripheral hormonal system identifies the origin and mechanisms of regulation of glucocorticoid hormone oscillations in rats
Reduced parahippocampal and lateral temporal GABA(A)-[C-11]flumazenil binding in major depression: preliminary results
Purpose: Major depressive disorder (MDD) has been related to both a dysfunctional γ-amino butyric acid (GABA) system and to hyperactivity of the hypothalamic-pituitary-adrenal axis (HPA). Although GABA has been suggested to inhibit HPA axis activity, their relationship has never been studied at the level of the central GAB
Effects of transportation, transport medium and re-housing on Xenopus laevis (Daudin)
Understanding the immediate and longer-term effects of transportation and re-housing in a laboratory species is crucial in order to refine the transfer process, enable the optimal introduction of new animals to a novel environment and to provide a sufficient acclimatisation period before usage. Whilst consideration of animal welfare in most model vertebrate species has received attention, little quantitative evidence exists for the optimal care of the common laboratory amphibian Xenopus laevis. Techniques for the non-invasive welfare assessment of amphibians are also limited and here a non-invasive physiological assay was developed to investigate the impacts of transportation, transport medium and re-housing on X. laevis. First the impacts of transportation and transport medium (water, damp sponge or damp sphagnum moss) were investigated. Transportation caused an increase in waterborne corticosterone regardless of transport medium. Frogs transported in damp sphagnum moss also had a greater decrease in body mass in comparison to frogs not transported, suggesting that this is the least suitable transport medium for X. laevis. Next the prolonged impacts of transportation and re-housing were investigated. Frogs were transported between research facilities with different housing protocols. Samples were collected prior to and immediately following transportation, as well as 1 day, 7 days and 35 days after re-housing. Water-borne corticosterone increased following transportation and remained high for at least 7 days, decreasing to baseline levels by 35 days. Body mass decreased following transportation and remained lower than baseline levels across the entire 35 day observation period. These findings suggest the process of transportation and re-housing is stressful in this species. Together these findings have important relevance for both improving animal welfare and ensuring optimal and efficient scientific research
Corticosterone-sensitive monoamine transport in the rat dorsomedial hypothalamus: potential role for organic cation transporter 3 in stress-induced modulation of monoaminergic neurotransmission
Rapid changes in monoamine levels following administration of corticotropin-releasing factor or corticosterone are localized in the dorsomedial hypothalamus
Local inhibition of organic cation transporters increases extracellular serotonin in the medial hypothalamus
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