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Corticotropin‐Releasing Factor in Brain: Executive Gating of Neuroendocrine and Functional Outflow

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Abstract

The sections in this article are:

1 Neurobiological Reactivity of Corticotropin‐Releasing Factor Systems to Environmental Challenge
1.1 Ligand and Receptor Distribution
1.2 Coordination of Neurobehavioral Outflow
1.3 Corticotropin‐Releasing Factor as an Integrative Peptide Neurotransmitter
2 Adaptive Role of Corticotropin‐Releasing Factor System Activation in Active Coping Responses
2.1 Restoration of Homeostasis
2.2 “Eustress” Revisited
3 Significance of Brain Corticotropin‐Releasing Factor in Maladaptive Distress
3.1 Depression and Anxiety
3.2 Substance Abuse
3.3 A Phenotype Resulting from Corticotropin‐Releasing Factor Excess
4 Conclusion
Figure 1. Figure 1.

CRF receptor subtype, R1 and R2, and CRF binding‐protein, BP, distribution illustrated schematically in a sagittal view of the rat brain.

Figure 2. Figure 2.

Mean ± SEM percent time spent on open arms of the elevated plus‐maze in saline‐treated, nonstressed rats (control) or rats administered saline, an antibody buffer control (artificial cerebrospinal fluid) or a CRF polyclonal antibody (150 nmol) by an intracerebroventricular (ICV) route 5 minutes prior to swim stress exposure and a 5 minute plus‐maze test (n = 4/group).

Figure 3. Figure 3.

Promotion of negative energy balance by CRF system activation is exerted in a multifaceted manner by suppression of appetite, stimulation of autonomic nervous system and thermogenesis within innervated fat depots.

Figure 4. Figure 4.

Mean ± SEM latency to reach a submerged platform in the Morris water maze over untreated baseline (days 1–3), noninjected retest (days 10‐11) and chlordiazepoxide‐injection (days 18–20) testing phases. Thirty minutes prior to testing on each of days 18–20, chlordiazepoxide (10 mg/kg) was administered by an intraperitoneal route to both littermate control (n = 16) and CRF transgenic (CRF Tg; n = 10) mice.



Figure 1.

CRF receptor subtype, R1 and R2, and CRF binding‐protein, BP, distribution illustrated schematically in a sagittal view of the rat brain.



Figure 2.

Mean ± SEM percent time spent on open arms of the elevated plus‐maze in saline‐treated, nonstressed rats (control) or rats administered saline, an antibody buffer control (artificial cerebrospinal fluid) or a CRF polyclonal antibody (150 nmol) by an intracerebroventricular (ICV) route 5 minutes prior to swim stress exposure and a 5 minute plus‐maze test (n = 4/group).



Figure 3.

Promotion of negative energy balance by CRF system activation is exerted in a multifaceted manner by suppression of appetite, stimulation of autonomic nervous system and thermogenesis within innervated fat depots.



Figure 4.

Mean ± SEM latency to reach a submerged platform in the Morris water maze over untreated baseline (days 1–3), noninjected retest (days 10‐11) and chlordiazepoxide‐injection (days 18–20) testing phases. Thirty minutes prior to testing on each of days 18–20, chlordiazepoxide (10 mg/kg) was administered by an intraperitoneal route to both littermate control (n = 16) and CRF transgenic (CRF Tg; n = 10) mice.

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How to Cite

Stephen C. Heinrichs, Errol B. De Souza. Corticotropin‐Releasing Factor in Brain: Executive Gating of Neuroendocrine and Functional Outflow. Compr Physiol 2011, Supplement 23: Handbook of Physiology, The Endocrine System, Coping with the Environment: Neural and Endocrine Mechanisms: 125-137. First published in print 2001. doi: 10.1002/cphy.cp070407