Alterations in brain norepinephrine metabolism and behavior induced by environmental stimuli previously paired with inescapable shock

Cassens, Geraldine; Kuruc, Alvin; Roffman, Mark; Orsulak, Paul J.; Schildkraut, Joseph J.

doi:10.1016/0166-4328(81)90020-6

Cited by 42 publications

(23 citation statements)

References 36 publications

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“…1986 26], Electrophysiological studies have implicated this nu cleus in behavioral arousal [1,16] and in the mediation of stress responses [8,13]. This is supported by studies demon strating that norepinephrine turnover in LC terminal re gions is substantially and reliably increased by many stres sors [6,7,19, 30] and that CRF levels double in the LC region in acutely and chronically stressed rats [9], Thus, CRF effects on LC neuronal activity could consti tute a mechanism for amplifying and coordinating many of the brain-mediated autonomic and behavioral components of stress responses. We have previously reported [33, 34] that CRF, via intracerebroventricular (i.c.v.)…”

supporting

confidence: 50%

Corticotropin-Releasing Factor Disrupts Sensory Responses of Brain Noradrenergic Neurons

1987

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In order to elucidate the possible role of noradrenergic neurons of the nucleus locus coeruleus (LC) in stress responses, the effects of corticotropin-releasing factor (CRF) on LC neuronal activity were characterized. In halothane-anesthetized rats, intracerebroventricular administration of CRF was found to have two distinct actions: (1) A dose-dependent increase in spontaneous discharge activity was observed 3 min after peptide injection, with 1.0 and 3.0 µg CRF increasing activity by 7 ± 2 and 47 ± 12%, respectively; Ala¹⁴CRF (3.0 µg), an inactive analogue of CRF, had no effect on LC spontaneous discharge rates. These results confirm and extend previous studies of CRF activation of LC basal discharge activity; (2) additionally, CRF (1.0 and 3.0 µg) disrupted sensory responses of LC cells to sciatic nerve stimulation. As previously reported, responses of LC neurons to electrical stimulation of the sciatic nerve usually consisted of a brief activation beginning 20–40 ms after stimulus followed by a period of relatively suppressed activity lasting 100–200 ms. CRF attenuated both components. Responses plotted as normalized, cumulative histograms became more linear in the presence of CRF (1.0 and 3.0 µg), suggesting that discharge rates during phasic responses to sciatic stimulation were similar to spontaneous rates. Statistical comparison using the Kolmogorov-Smirnoff test or correlation coefficients demonstrated that both 1.0 and 3.0 µg CRF reduced response components, while 0.3 µg CRF and Ala¹⁴CRF (3.0 µg) had no effect. The degree of attenuation of LC sensory responses by CRF was not linearly related to the magnitude of CRF-in-duced increases in spontaneous discharge rate, suggesting that these are distinct effects of CRF. These actions of CRF on LC activity may represent an important mechanism in the central mediation of stress responses.

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supporting

confidence: 50%

Corticotropin-Releasing Factor Disrupts Sensory Responses of Brain Noradrenergic Neurons

1987

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“…These physiological attributes and its general activation by stressors (Thierry et al 1968;Korf et al 1973;Cassens et al 1980Cassens et al , 1981Abercrombie and Jacobs 1987) suggest that the LC-NE system may be an important component in a cognitive limb of the stress response.…”

Section: Lc Anatomical and Physiological Characteristicsmentioning

confidence: 97%

Opposing regulation of the locus coeruleus by corticotropin-releasing factor and opioids

Valentino

Bockstaele

2001

Psychopharmacology

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Co-regulation of the LC-NE system by CRF and opioids may be important in acute adaptation to stress. Potential clinical consequences of an imbalance in this regulation as a result of prior stress include increased risk of opiate self administration and decreased sensitivity to opiates used in clinical settings. Conversely, chronic exposure to opiates may predispose individuals to stress-related psychiatric disorders.

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“…Other measurements, such a those of the metabolites of NA and DA (Cassens et al 1981 ;Herman et al 1982;Tanaka et al 1982) or the rate of turnover (Lane et al 1982), may be more sensitive.…”

Section: Discussionmentioning

confidence: 99%

High sensitivity of brain octopamine levels to stress

Ennaceur

Coulon²,

Delacour

et al. 1986

Psychopharmacology

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(1986) High sensitivity of brain octopamine levels to stress. Psychopharmacology, 88 (3 Abstract. Rats were submitted to unsignalled and uncontrolled electrical shocks. When re-exposed to the same situation but not shocked, 24 h later, their locomotor activity was significantly reduced compared to that of controls. This conditioned suppression was associated with a significant decrease in p-octopamine (OA) in brain stem and hypothalamus. Shocks delivered just before brain fixation produced an even larger decrease in cerebral OA. Heart levels of OA were not affected. Cerebral and peripheral levels of dopamine and noradrenaline were not significantly or reliably affected. These results, as those of previous experiments, suggest that octopamine is involved in emotional, neurovegetative responses to stress.

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Alterations in brain norepinephrine metabolism and behavior induced by environmental stimuli previously paired with inescapable shock

Cited by 42 publications

References 36 publications

Corticotropin-Releasing Factor Disrupts Sensory Responses of Brain Noradrenergic Neurons

Corticotropin-Releasing Factor Disrupts Sensory Responses of Brain Noradrenergic Neurons

Opposing regulation of the locus coeruleus by corticotropin-releasing factor and opioids

High sensitivity of brain octopamine levels to stress

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