Reciprocal cross-desensitization of locus coeruleus electrophysiological responsivity to corticotropin-releasing factor and stress

Conti, Lisa H.; Foote, Stephen L.

doi:10.1016/0006-8993(96)00175-8

Cited by 37 publications

(17 citation statements)

References 74 publications

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“…One study demonstrated that repeated auditory stress desensitizes LC neurons to CRF and hypotensive stress (Conti and Foote, 1996), consistent with reported agonist-and stress-induced CRF type 1 receptor (CRF1) internalization (Reyes et al, 2006. A common stressor encountered by humans that has been implicated in psychiatric disease is social stress (Faravelli et al, 2012;Taylor et al, 2011).…”

Section: Introductionmentioning

confidence: 67%

Social Stress Engages Opioid Regulation of Locus Coeruleus Norepinephrine Neurons and Induces a State of Cellular and Physical Opiate Dependence

Chaijale

Curtis

Wood

et al. 2013

Neuropsychopharmacol

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Stress is implicated in diverse psychiatric disorders including substance abuse. The locus coeruleus-norepinephrine (LC-NE) system is a major stress response system that is also a point of intersection between stress neuromediators and endogenous opioids and so may be a site at which stress can influence drug-taking behaviors. As social stress is a common stressor for humans, this study characterized the enduring impact of repeated social stress on LC neuronal activity. Rats were exposed to five daily consecutive sessions of social stress using the resident-intruder model or control manipulation. LC discharge rate recorded 2 days after the last manipulation was decreased in stressed rats compared with controls. By 10 days after the last manipulation, LC rates were comparable between groups. Systemic administration of the opiate antagonist, naloxone, robustly increased LC discharge rate in a manner suggestive of opiate withdrawal, selectively in stressed rats when administered 2 or 10 days after the last manipulation. This was accompanied by behavioral signs of mild opiate withdrawal. Western blot and electron microscopic studies indicated that repeated social stress decreased corticotropin-releasing factor type 1 receptor and increased m-opioid receptor levels in the LC. Together, the results suggest that repeated social stress engages endogenous opioid modulation of LC activity and induces signs of cellular and physical opiate dependence that endure after the stress. These cellular effects may predispose individuals with a history of repeated social stress to substance abuse behaviors.

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Section: Introductionmentioning

confidence: 67%

Social Stress Engages Opioid Regulation of Locus Coeruleus Norepinephrine Neurons and Induces a State of Cellular and Physical Opiate Dependence

Chaijale

Curtis

Wood

et al. 2013

Neuropsychopharmacol

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“…This effect of CRF on LC neuronal firing rates is potentiated by two weeks of daily cold exposure (Jedema et al, 2001) or in animals subjected to a forced swim test (Curtis et al, 1999), indicating that chronic physiological stressors can modulate the effect of CRF on the LC. However, the effects of CRF on LC firing rates can be desensitized by 1 or 5 days of prior (30 min) footshock stress (Curtis et al, 1995) or intracerebral application of CRF (Conti and Foote, 1996), indicating different responses of LC firing rates to CRF depending upon the quantity and quality of stressor exposure. The ability of CRF to induce behavioral correlates of fear and anxiety (defensive withdrawal) after intraventricular delivery is potentiated by infusion into the LC region (Butler et al, 1990) and two weeks of chronic, unpredictable stress produces increased concentrations of CRF in the LC of laboratory rats (Chappell et al, 1986).…”

Section: Discussionmentioning

confidence: 99%

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Bissette

Klimek

Pan

et al. 2003

Neuropsychopharmacol

130

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Research evidence that corticotropin-releasing factor (CRF) plays a role in the pathophysiology of major depressive disorder (MDD) has accumulated over the past 20 years. The elevation of lumbar cerebrospinal fluid (CSF) concentrations of CRF decreased responsiveness of pituitary CRF receptors to challenge with synthetic CRF, and increased levels of serum cortisol in MDD subjects support the hypothesis that CRF is chronically hypersecreted in at least the endocrine circuits of the hypothalamic-pituitary-adrenal (HPA) axis and may also involve other CRF brain circuits mediating emotional responses and/or arousal. One such circuit includes the excitatory CRF input to the locus coeruleus (LC), the major source of norepinephrine in the brain. Furthermore, there are now reports of decreased levels of CRF in lumbar CSF from MDD patients after symptom relief from chronic treatment with antidepressant drugs or electroconvulsive therapy. Whether this normalization reflects therapeutic effects on both endocrine-and limbic-associated CRF circuits has not yet been effectively addressed. In this brief report, we describe increased concentrations of CRF-like immunoreactivity in micropunches of post-mortem LC from subjects with MDD symptoms as established by retrospective psychiatric diagnosis compared to nondepressed subjects matched for age and sex.

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“…Chronic stress increases NE neuron responsivity (Simson and Weiss, 1988;Pavcovich and Ramirez, 1991;Conti and Foote, 1996;Mana and Grace, 1997;Jedema et al, 2001) and the levels and activity of TH in the locus ceruleus (LC) (Mamalaki et al, 1992;Watanabe et al, 1995;Rusnak et al, 1998), the source of PFC NE (Loughlin et al, 1982). If NET and TH localization are linked to activity states, then chronic stress should increase plasmalemmal NET and TH expression, thus altering the dynamics of NE transmission and impacting cognition and affect.…”

Section: Introductionmentioning

confidence: 99%

Chronic Stress Increases the Plasmalemmal Distribution of the Norepinephrine Transporter and the Coexpression of Tyrosine Hydroxylase in Norepinephrine Axons in the Prefrontal Cortex

et al. 2006

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Norepinephrine (NE) potently modulates the cognitive and affective functions of the prefrontal cortex (PFC). Deficits in NE transmissionare implicated in psychiatric disorders, and antidepressant drugs that block the NE transporter (NET) effectively treat these conditions. Our initial ultrastructural studies of the rat PFC revealed that most NE axons (85-90%) express NET primarily within the cytoplasm and lack detectable levels of the synthetic enzyme tyrosine hydroxylase (TH). In contrast, the remaining 10 -15% of PFC NE axons exhibit predominantly plasmalemmal NET and evident TH immunoreactivity. These unusual characteristics suggest that most PFC NE axons have an unrecognized, latent capacity to enhance the synthesis and recovery of transmitter. In the present study, we used dual-labeling immunocytochemistry and electron microscopy to examine whether chronic cold stress, a paradigm that persistently increases NE activity, would trigger cellular changes consistent with this hypothesis. After chronic stress, neither the number of profiles exhibiting NET labeling nor their size was changed. However, the proportion of plasmalemmal NET nearly doubled from 29% in control animals to 51% in stressed rats. Moreover, the expression of detectable TH in NET-labeled axons increased from only 13% of profiles in control rats to 32% of profiles in stressed animals. Despite the consistency of these findings, the magnitude of the changes varied across individual rats. These data represent the first demonstration of activity-dependent trafficking of NET and expression of TH under physiological conditions and have important implications for understanding the pathophysiology and treatment of stress-related affective disorders.

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Reciprocal cross-desensitization of locus coeruleus electrophysiological responsivity to corticotropin-releasing factor and stress

Cited by 37 publications

References 74 publications

Social Stress Engages Opioid Regulation of Locus Coeruleus Norepinephrine Neurons and Induces a State of Cellular and Physical Opiate Dependence

Social Stress Engages Opioid Regulation of Locus Coeruleus Norepinephrine Neurons and Induces a State of Cellular and Physical Opiate Dependence

Elevated Concentrations of CRF in the Locus Coeruleus of Depressed Subjects

Chronic Stress Increases the Plasmalemmal Distribution of the Norepinephrine Transporter and the Coexpression of Tyrosine Hydroxylase in Norepinephrine Axons in the Prefrontal Cortex

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