GluR5-mediated glutamate signaling regulates hypothalamo–pituitary–adrenocortical stress responses at the paraventricular nucleus and median eminence

Evanson, Nathan K.; Hooren, Daniella C. Van; Herman, James P.

doi:10.1016/j.psyneuen.2009.04.011

Cited by 29 publications

(24 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Histological studies have shown that the par vocellular subdivision of the PVN expresses high levels of mRNAs for the kainatepreferring receptor subunits glutamate receptor ionotropic, kainate 1 (GLUK1; also known as GRIK1 and GLUR5) and GLUK5 (also known as GRIK5 and KA2) 49 , which are upregulated following stress 66 . Although the synaptic transmission to PNCs that is mediated by these kainate receptors remains to be characterized, GLUK1 expression is highly enriched in CRHreleasing axon terminals at the median eminence, and has been implicated in the release of the hormone during stress 67 . Histological studies have also reported low to moderate expression of group I mGluRs (mGluR1 and mGluR5) in PNCs 68,69 .…”

Section: Glutamatergic Synapsesmentioning

confidence: 99%

Stress-related synaptic plasticity in the hypothalamus

2015

View full text Add to dashboard Cite

Stress necessitates an immediate engagement of multiple neural and endocrine systems. However, exposure to a single stressor causes adaptive changes that modify responses to subsequent stressors. Recent studies examining synapses onto neuroendocrine cells in the paraventricular nucleus of the hypothalamus demonstrate that stressful experiences leave indelible marks that alter the ability of these synapses to undergo plasticity. These adaptations include a unique form of metaplasticity at glutamatergic synapses, bidirectional changes in endocannabinoid signalling and bidirectional changes in strength at GABAergic synapses that rely on distinct temporal windows following stress. This rich repertoire of plasticity is likely to represent an important building block for dynamic, experience-dependent modulation of neuroendocrine stress adaptation.

show abstract

Section: Glutamatergic Synapsesmentioning

confidence: 99%

Stress-related synaptic plasticity in the hypothalamus

2015

View full text Add to dashboard Cite

show abstract

“…Sections were placed in cryoprotectant [30% sucrose, wt/vol; 1% polyvinylpyrrolidone (PVP-40), wt/vol; 30% ethylene glycol, vol/vol; in 50 mM sodium phosphate buffer (pH 7.4)] and stored at Ϫ20 C until staining. Immunohistochemistry for c-Fos protein expression and for BSA was performed as previously described (29). Primary antibodies were rabbit anti-c-Fos used at 1:20,000 dilution (Calbiochem, La Jolla, CA), and rabbit anti-BSA (Rockland Immunochemicals, Gil- bertsville, PA), used at 1:1000 dilution.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Fast Feedback Inhibition of the HPA Axis by Glucocorticoids Is Mediated by Endocannabinoid Signaling

et al. 2010

Self Cite

View full text Add to dashboard Cite

Glucocorticoid hormones are secreted in response to stimuli that activate the hypothalamo-pituitary-adrenocortical (HPA) axis and self-regulate through negative feedback. Negative feedback that occurs on a rapid time scale is thought to act through nongenomic mechanisms. In these studies, we investigated fast feedback inhibition of HPA axis stress responses by direct glucocorticoid action at the paraventricular nucleus of the hypothalamus (PVN). Local infusion of dexamethasone or a membrane-impermeant dexamethasone-BSA conjugate into the PVN rapidly inhibits restraint-induced ACTH and corticosterone release in a manner consistent with feedback actions at the cell membrane. The dexamethasone fast feedback response is blocked by the cannabinoid CB1 receptor antagonist AM-251, suggesting that fast feedback requires local release of endocannabinoids. Hypothalamic tissue content of the endocannabinoid 2-arachidonoyl glycerol is elevated by restraint stress, consistent with endocannabinoid action on feedback processes. These data support the hypothesis that glucocorticoid-induced fast feedback inhibition of the HPA axis is mediated by a nongenomic signaling mechanism that involves endocannabinoid signaling at the level of the PVN.

show abstract

“…However, the glutamate receptor family has numerous members that may mitigate effects of glutamate at the cellular level. The ionotropic glutamate receptor GluR5, for example, appears to inhibit the HPA axis response to restraint when signaling at the PVN [5], while other ionotropic glutamate receptors typically play an excitatory role in HPA axis regulation [2]. In addition to the ionotropic glutamate receptors, metabotropic glutamate receptors are also involved in regulating the HPA axis.…”

Section: Introductionmentioning

confidence: 99%

Metabotropic glutamate receptor-mediated signaling dampens the HPA axis response to restraint stress

Evanson

Herman

2015

Physiology & Behavior

Self Cite

View full text Add to dashboard Cite

Glutamate is an important neurotransmitter in regulation of the neural portion of hypothalamus-pituitary-adrenal (HPA) axis activity, and signals through ionotropic and metabotropic receptors. In the current studies we investigated the role of hypothalamic paraventricular group I metabotropic glutamate receptors in regulation of the HPA axis response to restraint stress in rats. Direct injection of the group I metabotropic glutamate receptor agonist 3,5-dihydroxyphenylglycine (DHPG) into the PVN prior to restraint leads to blunting of the HPA axis response in awake animals. Consistent with this result, infusion of the group I receptor antagonist hexyl-homoibotenic acid (HIBO) potentiates the HPA axis response to restraint. The excitatory effect of blocking paraventricular group I metabotropic glutamate signaling is blocked by co-administration of dexamethasone into the PVN. However, the inhibitory effect of DHPG is not affected by co-administration of the cannabinoid CB1 receptor antagonist AM-251 into the PVN. Together, these results suggest that paraventricular group I metabotropic glutamate receptor signaling acts to dampen HPA axis reactivity. This effect appears to be similar to the rapid inhibitory effect of glucocorticoids at the PVN, but is not mediated by endocannabinoid signaling.

show abstract

GluR5-mediated glutamate signaling regulates hypothalamo–pituitary–adrenocortical stress responses at the paraventricular nucleus and median eminence

Cited by 29 publications

References 41 publications

Stress-related synaptic plasticity in the hypothalamus

Stress-related synaptic plasticity in the hypothalamus

Fast Feedback Inhibition of the HPA Axis by Glucocorticoids Is Mediated by Endocannabinoid Signaling

Metabotropic glutamate receptor-mediated signaling dampens the HPA axis response to restraint stress

Contact Info

Product

Resources

About