Catecholamines in Individual Hypothalamic Nuclei of Acutely and Repeatedly Stressed Rats

Květňanský, Richard; Palkovits, M; Mitro, A; Torda, T; Mikulaj, L

doi:10.1159/000122673

Cited by 132 publications

(60 citation statements)

References 10 publications

(17 reference statements)

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“…These results support many earlier studies of an involvement of catecholamines in stress reactions as measured with biochemical and histochemical (formaldehyde fluorescence) methods. Thus acute and/or chronic stress has been shown to affect norepinephrine (36)(37)(38)(39)(40)(41)(42)(43)(44)(45), epinephrine (46)(47)(48), and catecholamine-synthesizing enzymes (45)(46)(47)(48)(49)(50)(51). In agreement, both norepinephrine and epinephrine medullary neurons have been shown to contain the glucocorticoid receptor (52).…”

Section: Discussionmentioning

confidence: 81%

Expression of c-Fos immunoreactivity in transmitter-characterized neurons after stress.

Ceccatelli

Villar

Goldstein

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

396

167

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The effect of intracerebroventricular injection of the mitosis inhibitor colchicine and of immobilization stress, subcutaneous injection of capsaicin, and intraperitoneal injection of hypertonic salt solution on expression of c-Fos-like immunoreactivity was studied in the rat brain with immunohistochemistry. All the procedures induced c-Fos immunoreactivity in parvocellular neurons of the paraventricular nucleus, and many of these neurons also contained corticotropinreleasing factor immunoreactivity. c-Fos immunoreactivity was also observed, for example, in subpopulations of neurons in the locus coeruleus, the ventrolateral medulla oblongata, and the nucleus tractus solitarii. Many of these cells also expressed catecholamine-synthesizing enzymes. The results suggest that intraventricular injection of colchicine is a stressful stimulus and support the view that several catecholamine cell groups in the lower brainstem are part of the brain circuitry mediating stress reactions, as are the hypothalamic neurons that contain corticotropin-releasing factor.The c-fos gene (1, 2) is expressed in many tissues in response to growth factor stimulation (3-9). It has been suggested that induction of protooncogenes such as c-fos may be important in the establishment of prolonged functional changes in neurons (10). It has been demonstrated by immunohistochemical methods that various types of stimulation induce a c-Fos protein-like immunoreactivity in specific neuron populations in various brain regions (11)(12)(13). Thus, immunohistochemical analysis of expression of c-Fos protein in nervous tissue may represent a new tool in neurobiology for metabolic mapping at the cellular level (14). In fact, numerous papers based on this methodology have appeared during the last 2 years.In the present study we have used immunohistochemistry to analyze to what extent various stressors may induce expression of c-Fos-like immunoreactivity in certain brain regions. In addition, antisera to neuropeptides and transmitter-synthesizing enzymes were used to further characterize c-Fos-activated neurons. Of particular interest to us has been the question whether or not intracerebroventricular (i.c.v.) injections of the mitosis inhibitor colchicine (15) may affect stress-related systems. Ever since colchicine was shown to inhibit axonal transport (16,17) and to cause marked accumulation of amine storage granules in cell bodies (18), this drug has been used to improve histochemical visualization of transmitters, peptides, and related substances in neuronal cell bodies (19,20). Our results demonstrate that several stress-inducing procedures as well as i.c.v. colchicine treatment, including the i.c.v. injection procedure per se, cause expression of c-Fos protein in restricted neuronal cell populations both in the hypothalamus, including the corticotropin-releasing factor (CRF)-positive neurons in the paraventricular nucleus (PVN), and in the lower brainstem, particularly in catecholamine neurons. MATERIALS AND METHODSMale Sprague-Dawley rats (250...

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Section: Discussionmentioning

confidence: 81%

Expression of c-Fos immunoreactivity in transmitter-characterized neurons after stress.

Ceccatelli

Villar

Goldstein

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

396

167

View full text Add to dashboard Cite

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“…Within 20 -30 min of exposure to a stressor or injection of corticosterone, concentrations of 5-HT increase in the DMH (Kvetnansky et al, 1977;Losada, 1988;Lowry et al, 2001Lowry et al, , 2003. In the DMH of rats and salamanders, increases in 5-HT are positively correlated with increases in dopamine and norepinephrine (Lowry et al, 2001(Lowry et al, , 2003 suggesting that 5-HT, dopamine, and norepinephrine are coregulated in this region.…”

Section: Introductionmentioning

confidence: 98%

Corticosterone-Sensitive Monoamine Transport in the Rat Dorsomedial Hypothalamus: Potential Role for Organic Cation Transporter 3 in Stress-Induced Modulation of Monoaminergic Neurotransmission

Gasser¹,

Lowry²,

Orchinik³

2006

J. Neurosci.

127

104

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“…Chronic stress increases the firing rate of LC neurons (18) and increases levels of NE in this nucleus and its terminal fields (19)(20)(21)(22). Chronic stress also increases the expression of tyrosine hydroxylase (TH) mRNA and protein in the LC, an effect that presumably underlies these neuronal adaptations (23-25).…”

Section: Introductionmentioning

confidence: 99%

Involvement of corticotropin-releasing factor in chronic stress regulation of the brain noradrenergic system.

Melia

Duman

1991

Proc. Natl. Acad. Sci. U.S.A.

144

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Corticotropin-releasing factor (CRF) and norepinephrine (NE) mediate many hormonal, autonomic, and behavioral effects of acute stress, and it is possible that an interaction between these neurotransmitters could underlie neuronal adaptations in response to chronic stress. To test this hypothesis, the influence of chronically administered CRF and a specific CRF antagonist, a-helical CRF, on the induction of tyrosine hydroxylase, the rate-limiting enzyme in NE biosynthesis, was examined in the rat locus coeruleus (LC). We now report that adnitration of a-helical CRF specifically blocks the induction of tyrosine hydroxylase in response to a repeated intermittent stress paradigm involving foot shock and noise stress but has no effect on steady-state levels of the enzyme in nostressed animals or on the induction of the enzyme in response to reserpine treatment. In addition, repeated administration of CRF alone for 5 days, lke chronic stress, increases levels of tyrosine hydroxylase in LC. The results demonstrate that endogenous CRF is necessary for the induction of tyrosine hydroxylase in response to this stress pardigm and that exogenously administered CRF is sufficient for the regulation of this enzyme in nonstressed rats. These ings may prove important in elucidating mechanisms by which chronic stress triggers and sustains the biochemical alterations associated with some stress-related psychiatric disorders.The administration of corticotropin-releasing factor (CRF) initiates a constellation of changes typically seen in response to stress, including increased central and peripheral levels of catecholamine and catecholamine metabolites, increased plasma levels of adrenocorticotropin hormone (ACTH), and increased stress-related behaviors (1-5). Activation of the noradrenergic neurotransmitter system similarly increases stress-related behaviors, whereas inhibition of this system attenuates stress-induced changes in behavior (6-8). Recent studies suggest that some of the effects of acute stress may be mediated by CRF interactions with the locus coeruleus (LC), a near homogeneous nucleus containing approximately 50%o of brain norepinephrine (NE) neurons (9, 10). CRFimmunoreactive fibers (11,12) and receptors (13) have been localized in the LC, and acute and chronic stress increase immunoreactivity to CRF in this nucleus (14). Moreover, infusion of CRF directly into the LC increases catecholamine and catecholamine metabolite levels in the cerebral cortex, plasma corticosterone levels, and certain stress-related behaviors (15). Finally, CRF, like acute stress, increases the firing rate of LC neurons, whereas administration of a CRF antagonist blocks the activation of these neurons by acute stress (16,17).Given the above findings, it is possible that endogenous CRF may influence the biochemical adaptive responses of LC noradrenergic neurons to chronic stress. Chronic stress increases the firing rate of LC neurons (18) and increases levels of NE in this nucleus and its terminal fields (19)(20)(21)(22). Chronic stres...

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Catecholamines in Individual Hypothalamic Nuclei of Acutely and Repeatedly Stressed Rats

Cited by 132 publications

References 10 publications

Expression of c-Fos immunoreactivity in transmitter-characterized neurons after stress.

Expression of c-Fos immunoreactivity in transmitter-characterized neurons after stress.

Corticosterone-Sensitive Monoamine Transport in the Rat Dorsomedial Hypothalamus: Potential Role for Organic Cation Transporter 3 in Stress-Induced Modulation of Monoaminergic Neurotransmission

Involvement of corticotropin-releasing factor in chronic stress regulation of the brain noradrenergic system.

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