Corticotropin-releasing hormone microinfusion in the central amygdala diminishes a cardiac parasympathetic outflow under stress-free conditions

Wiersma, A.; Bohus, B.; Koolhaas, J.M.

doi:10.1016/0006-8993(93)91062-w

Cited by 59 publications

(42 citation statements)

References 55 publications

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“…The systemic administration of ACTH decreases the expression of CRH, which stimulates sympathetic outflow and inhibits parasympathetic outflow (Brown et al 1982;Fisher et al 1983;Wiersma et al 1993;Brunson et al 2001;Wang et al 2004). These facts suggest that ACTH enhances vagal activity in patients with WS at least partly through CRH suppression.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Vagal Activation by Adrenocorticotropic Hormone Treatment in Infants with West Syndrome

Hattori

Hayano

Fujimoto

et al. 2007

Tohoku J. Exp. Med.

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West syndrome (WS) is a generalized epileptic syndrome of infancy and early childhood with various etiologies, and consists of a triad of infantile spasm, arrest or regress of psychomotor development and specific electroencephalogram (EEG) pattern of hypsarrhythmia. WS had been believed to be refractory, but recent evidence supports effectiveness of adrenocorticotropic hormone (ACTH) treatment. The ACTH treatment, however, has a problem that it is often accompanied by adverse autonomic symptoms. We therefore examined heart rate variability (HRV) for assessing cardiac autonomic functions in WS and prospectively observed the changes during ACTH treatment. We studied 15 patients with WS and 9 age-matched controls during sleep (EEG stage 2). Compared with controls, the patients with WS were greater in the low-frequency component (LF) of HRV, an index reflecting sympatho-vagal interaction ( p = 0.02), but were comparable for high-frequency component (HF) and LF-to-HF ratio (LF/HF), indices reflecting cardiac vagal activity and sympathetic predominance, respectively. During ACTH treatment, heart rate decreased ( p < 0.01), LF and HF increased ( p < 0.01), and LF/HF did not differ significantly. These results indicate that West syndrome might be accompanied by autonomic changes and that ACTH treatment enhances parasympathetic function and causes bradycardia. West syndrome; ACTH; heart rate variability; bradycardia; autonomic function

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Section: Discussionmentioning

confidence: 99%

Cardiac Vagal Activation by Adrenocorticotropic Hormone Treatment in Infants with West Syndrome

Hattori

Hayano

Fujimoto

et al. 2007

Tohoku J. Exp. Med.

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“…In brain slice preparations CRF produces postsynaptic depolarization in most of amygdala cells (Eberly et al, 1983;Rainnie et al, 1992) but presynaptic inhibitory effects on CRF-IR neurons have also been proposed (Wiersma et al, 1993). CRF binding sites are located on the perikarya, dendrites, and terminals of peptide-containing medium spiny neurons of the Ce, including CRF-IR neurons.…”

Section: Discussionmentioning

confidence: 99%

“…CRF binding sites are located on the perikarya, dendrites, and terminals of peptide-containing medium spiny neurons of the Ce, including CRF-IR neurons. Incidentally, receptors on CRF-IR neurons may represent autoreceptors that regulate CRF-IR release, locally (Wiersma et al, 1993) or in their projection fields in hypothalamic and brainstem nuclei. Thus, a rise in extracellular CRF-IR levels in the Ce may contribute to activate peptidecontaining medium spiny neurons of the amygdala, activation recently demonstrated using Fos immunostaining technique in rats exposed to restraint stress (Honkaniemi, 1992).…”

Section: Discussionmentioning

confidence: 99%

Increase of extracellular corticotropin-releasing factor-like immunoreactivity levels in the amygdala of awake rats during restraint stress and ethanol withdrawal as measured by microdialysis

et al. 1995

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Previous research has suggested a role for corticotropin-releasing factor (CRF) in the anxiogenic effects of stressful stimuli and ethanol withdrawal. This hypothesis was explored in a series of experiments using intracranial microdialysis to monitor CRF-like immunoreactivity (CRF-IR) in the extracellular compartment of the rat amygdala. The synaptic origin of CRF-IR release in the amygdala was determined in vitro by assessing the Ca2+ dependency of 4-aminopyridine stimulated CRF-IR release from tissue preparations of rat amygdala. In vivo experiments were performed in awake rats after the placement of microdialysis probes in the amygdala. In the first experiment, transient restraint stress (20 min) produced an increase of CRF-IR release (basal levels, 1.19 +/- 0.15 fmol/50 microliters; stress levels, 4.54 +/- 1.33 fmol/50 microliters; p < 0.05) that returned to basal values within 1 hr. When 4-aminopyridine (5 mM) was added to the perfusion medium, it consistently increased CRF-IR release (4.83 +/- 0.92 fmol/50 microliters, p < 0.05). In the second experiment, CRF-IR release was measured during ethanol withdrawal in rats previously maintained for 2–3 weeks on a liquid diet containing ethanol (8.5%). Basal CRF-IR levels were 2.10 +/- 0.43 fmol/50 microliters in ethanol exposed rats and 1.30 +/- 0.19 fmol/50 microliters in control rats. During withdrawal, a progressive increase of CRF-IR levels over time was observed, reaching peak values at 10–12 hr after the onset of withdrawal (10.65 +/- 0.49 fmol/50 microliters vs 1.15 +/- 0.30 fmol/50 microliters of control rats, p < 0.01).

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“…CRF further acts in several areas of the brain as a transmitter enhancing sympathetic nervous and adrenomedullary activity 298 B. Buwalda et al (Fisher, 1989). By a concurrent inhibition of vagal nerve activity (Fisher, 1989;Wiersma et al, 1993) CRF causes a shift in balance towards the sympathetic division of the autonomic nervous system.…”

Section: Introductionmentioning

confidence: 99%

Physiological and behavioral effects of chronic intracerebroventricular infusion of corticotropin-releasing factor in the rat

Buwalda

Boer

Kalkeren

et al. 1997

Psychoneuroendocrinology

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Corticotropin-releasing hormone microinfusion in the central amygdala diminishes a cardiac parasympathetic outflow under stress-free conditions

Cited by 59 publications

References 55 publications

Cardiac Vagal Activation by Adrenocorticotropic Hormone Treatment in Infants with West Syndrome

Cardiac Vagal Activation by Adrenocorticotropic Hormone Treatment in Infants with West Syndrome

Increase of extracellular corticotropin-releasing factor-like immunoreactivity levels in the amygdala of awake rats during restraint stress and ethanol withdrawal as measured by microdialysis

Physiological and behavioral effects of chronic intracerebroventricular infusion of corticotropin-releasing factor in the rat

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