Activation of noradrenergic locus coeruleus neurons by hemodynamic stress is due to local release of corticotropin-releasing factor

Valentino, Rita J.; Page, Michelle E.; Curtis, Andre L.

doi:10.1016/0006-8993(91)90855-p

Cited by 229 publications

(159 citation statements)

References 41 publications

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“…Figure 1 shows the time-course of mean LC activity during and after hypotensive challenge. LC activity was significantly increased during nitroprusside infusion in all groups of rats (po0.05, paired Student's t-test), although the magnitude of LC activation in these MI rats obtained from Charles River was less than that previously reported in MI rats from Taconic Farms (Valentino et al, 1991;Curtis et al, 1994Curtis et al, , 1995Curtis et al, , 2001Curtis et al, , 2002. This stress produced a substantially greater activation of LC neurons of all female groups, irrespective of hormonal status, compared to either MI or MG rats (Group effect; F(5,68) ¼ 5.2, po0.001, two way ANOVA with repeated measures 0-12 min).…”

Section: Lc Spontaneous Discharge Ratementioning

confidence: 49%

“…Previous studies demonstrated that LC activation during hypotensive challenge is mediated by CRF release within the LC (Valentino et al, 1991;Curtis et al, 1994). Therefore, sex differences in this response could reflect differences in either CRF release (presynaptic effect) or in the postsynaptic response to CRF.…”

Section: Sex Differences In Lc Activation By Crfmentioning

confidence: 99%

“…As endogenous CRF mediates LC activation by hypotensive stress (Valentino et al, 1991;Curtis et al, 2001), the effects of CRF microinfusion into the LC on discharge rate were compared. Complete CRF dose-response curves were compared between MI and FO rats because there were no differences in LC responses to hypotensive challenge between FO, FE, and FEP.…”

Section: Sex Differences In Lc Responses To Exogenous Crfmentioning

confidence: 99%

“…The present study investigated sex differences in the acute stress responsivity of the rat LC-NE system by comparing LC neuronal activation induced by hypotensive stress or CRF, which mediates LC activation by hypotensive stress (Valentino et al, 1991;Curtis et al, 1994). As prior exposure to stress has been demonstrated to produce long-term changes in CRF-LC interactions (Curtis et al, 1995(Curtis et al, , 1999, LC responses to hypotension and CRF were also compared 24 h after exposure to swim stress.…”

Section: Introductionmentioning

confidence: 99%

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Sexually Dimorphic Responses of the Brain Norepinephrine System to Stress and Corticotropin-Releasing Factor

Curtis

Bethea

Valentino

2005

Neuropsychopharmacol

193

196

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Stress-related psychiatric disorders are more prevalent in females than males, and this has been attributed to differences in stress sensitivity. As activation of the locus coeruleus (LC)-norepinephrine (NE) system is an important component of the stress response, this study compared LC responses to stress in female and male rats under different hormonal conditions in the halothane-anesthetized state. The mean basal LC discharge rate was similar between groups. However, the magnitude of LC activation elicited by hypotensive stress was substantially greater in females, regardless of hormonal status. The difference in stress sensitivity could be attributed to the differential postsynaptic sensitivity of LC neurons to corticotropin-releasing factor (CRF), which mediates LC activation by hypotension. CRF was 10-30 times more potent in activating LC neurons in female vs male rats. Interestingly, previous exposure to swim stress differentially regulated LC responses to CRF by sensitizing LC neurons of male, but not female, rats to CRF. The net effect of this was to abolish sex differences in LC sensitivity. Finally, CRF receptor (CRF-R) protein levels in the LC were greater in ovarectomized female vs male rats. This is the first study to demonstrate sex differences in the stress responsiveness of the brain noradrenergic system. Substantial sex differences were apparent in postsynaptic sensitivity to CRF and stress-induced regulation of postsynaptic sensitivity to CRF. These sex differences in the CRF regulation of the LC-NE system translate to a differential response to stress and may play a role in the increased vulnerability of females to stress-related psychiatric disorders.

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Section: Lc Spontaneous Discharge Ratementioning

confidence: 49%

Section: Sex Differences In Lc Activation By Crfmentioning

confidence: 99%

Section: Sex Differences In Lc Responses To Exogenous Crfmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Sexually Dimorphic Responses of the Brain Norepinephrine System to Stress and Corticotropin-Releasing Factor

Curtis

Bethea

Valentino

2005

Neuropsychopharmacol

193

196

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“…However different stressors recruit different CRH pathways projecting to LC. For instance, during hypotensive stress CeA as a primary source of LC-activating CRH (Curtis et al 2002, Valentino et al 1991. Intra-BNST CRH system has also been implicated in coordination of stress-associated cardiovascular changes.…”

Section: Life Without Crh -From Paraventricular Lesions To Crh-ko Micmentioning

confidence: 99%

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Kovács

2013

Journal of Chemical Neuroanatomy

108

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Two major and mutually interconnected brain systems are recruited during stress reaction. One is the hypothalamic paraventricular nucleus (PVH) and the second is the extended amygdala. PVH governs the neuroendocrine stress response while CeA regulates most of the autonomic and behavioral stress reactions. The common neurohormonal mediator of these responses is the corticotropin-releasing hormone, CRH, which is expressed in both centers. CRH belongs to a larger family of neuropeptides that also includes urocortins 1, 2, and 3 all have different affinity towards the two types of CRHR receptors and have been implicated in regulation of stress and HPA axis activity. One functionally relevant aspect of CRH systems is their differential regulation by glucocorticoids. While corticosterone inhibits CRH transcription in the PVH, stress-induced glucocorticoids stimulate CRH expression in the extended amygdala. This review summarizes past and recent findings related to CRH gene regulation and its involvement in the neuroendocrine, autonomic and behavioral stress reaction.Key words: Corticotropin-releasing hormone, paraventricular nucleus, central amygdala, bed nucleus of stria terminalis, corticosterone, cAMP-response element.

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Corticotropin-releasing factor-containing axon terminals synapse onto catecholamine dendrites and may presynaptically modulate other afferents in the rostral pole of the nucleus locus coeruleus in the rat brain

1996

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Physiological and immunohistochemical studies have suggested that corticotropin-releasing factor (CRF), the hypophysiotropic peptide that initiates endocrine responses to stress, may serve as a neurotransmitter to activate noradrenergic neurons in the nucleus locus coeruleus (LC). We combined immunoperoxidase labeling for CRF and immunogold-silver localization of the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH) in single sections through the rat LC to determine potential substrates for interactions between these two transmitters. Light microscopic analysis indicated that CRF processes are dense and highly varicose in the rostral LC region in the vicinity of noradrenergic dendrites. Electron microscopy of this rostral region revealed that immunoperoxidase labeling for CRF was mainly restricted to axons and axon terminals and was rarely seen in somata or dendrites. Axon terminals containing CRF immunoreactivity varied in size, content of synaptic vesicles, and formation of synaptic specializations. The postsynaptic targets of the CRF-labeled axon terminals consisted of both TH-labeled dendrites and dendrites lacking detectable TH-immunoreactivity. Of 113 CRF-immunoreactive axon terminals, approximately 70% were in direct contact with TH-labeled and unlabeled dendrites. Of the CRF-labeled axon terminals forming synapses with TH-labeled and unlabeled dendrites, they were either of the asymmetric (excitatory type; 19%) or symmetric (inhibitory type; 11%) variety or did not form identifiable contacts in the plane of section analyzed. Unlabeled axon terminals and glial processes were also commonly located adjacent to the plasma membranes of CRF-labeled axon terminals. These results provide the first direct ultrastructural evidence that axon terminals containing CRF-immunoreactivity 1) directly contact catecholamine-containing dendrites within the rostral pole of the LC, 2) may presynaptically modulate other afferents, and 3) are often enveloped by astrocytic processes.

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Activation of noradrenergic locus coeruleus neurons by hemodynamic stress is due to local release of corticotropin-releasing factor

Cited by 229 publications

References 41 publications

Sexually Dimorphic Responses of the Brain Norepinephrine System to Stress and Corticotropin-Releasing Factor

Sexually Dimorphic Responses of the Brain Norepinephrine System to Stress and Corticotropin-Releasing Factor

CRH: The link between hormonal-, metabolic- and behavioral responses to stress

Corticotropin-releasing factor-containing axon terminals synapse onto catecholamine dendrites and may presynaptically modulate other afferents in the rostral pole of the nucleus locus coeruleus in the rat brain

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