Catecholamine release in the rat hypothalamic paraventricular nucleus in response to haemorrhage, desipramine and potassium

Morris, Margaret J.; Hastings, Jacqueline; Pavia, Jillian M.

doi:10.1016/0006-8993(94)91145-2

Cited by 22 publications

(13 citation statements)

References 35 publications

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“…Changes in concentrations of the catecholaminergic precursor, DOPA, are thought to reflect changes in the rate of tyrosine hydroxylation and, therefore, of catecholamine biosynthesis [32]. In our study, the lack of a significant change in DOPA concentrations in either sex in response to stress is consistent with studies in rats that measured concentrations of DOPA in extracellular fluid by microdialysis [11, 32]. This lack of change in DOPA concentrations in response to stress is thought to be due to efficient decarboxylation of DOPA to dopamine [32].…”

Section: Discussionsupporting

confidence: 81%

“…Our finding that adrenaline was not detected in CSF collected from the third ventricle following stress is consistent with a microdialysis study in rats that found no adrenaline in microdialysates from the PVN following stress [11]. In sheep, adrenaline-producing neurones are found only in the C 2 cell group of the brain stem [31].…”

Section: Discussionsupporting

confidence: 77%

“…Thus, it appears that the sex differences in the stress-induced activity of the hypothalamo-pituitary-adrenal axis in sheep are not likely to be due to stress-induced stimulation of noradrenaline and/or NPY neurones that project directly, or via interneurones, to the PVN. While an increase in noradrenaline in the PVN following stress has previously been reported in male rats [9, 10, 11], this may not be the case in male and female sheep.…”

Section: Discussionmentioning

confidence: 59%

“…While these direct inputs to the PVN have not been demonstrated in sheep, the distribution of noradrenergic neurones in the A1, A2 and A6 cell groups in sheep [8]is similar to that of rats [7]. Microdialysis studies in male rats have shown that concentrations of noradrenaline increase in the PVN in response to a number of different stressors [9, 10, 11]. Furthermore, lesions in the brain stem cell groups that contain noradrenergic neurones blocked or reduced the hypothalamo-pituitary-adrenal axis response to ‘systemic’ stressors (i.e.…”

Section: Introductionmentioning

confidence: 99%

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Noradrenaline, but Not Neuropeptide Y, Is Elevated in Cerebrospinal Fluid from the Third Cerebral Ventricle following Audiovisual Stress in Gonadectomised Rams and Ewes

Turner

Rivalland²,

Clarke³

et al. 2002

Neuroendocrinology

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There are sex differences in the activation of the hypothalamo-pituitary-adrenal axis in response to stress, but the source of these differences is unknown. The hypothalamo-pituitary-adrenal axis is regulated by corticotropin-releasing hormone and arginine-vasopressin neurones located in the paraventricular nucleus and these, in turn, are regulated by neural systems that include afferent noradrenergic and neuropeptide Y (NPY)-producing neural pathways. We tested the hypothesis that concentrations of noradrenaline and NPY will be elevated in cerebrospinal fluid (CSF) sampled from the third cerebral ventricle in response to stress, and these responses will differ in males and females. We collected concurrent samples of CSF (1 ml) from the third ventricle and blood (5 ml) from the jugular vein from gonadectomised rams (n = 7) and ewes (n = 5) at 10-min intervals for 3 h. This procedure was conducted on a day when no stress was imposed and on a day when audiovisual stress was imposed for 5 min after 1 h of sampling. Following the audiovisual stress, plasma concentrations of cortisol and CSF concentrations of noradrenaline were elevated (p < 0.05), but CSF concentrations of NPY did not change. Adrenaline was not detected in samples of CSF. The rise in plasma cortisol following the stress was greater (p < 0.05) in ewes than in rams, but there were no sex differences in the rise in noradrenaline. Basal concentrations of NPY in the CSF were higher (p < 0.05) in rams than in ewes. We conclude that the sex differences in the stress-induced activity of the hypothalamo-pituitary-adrenal axis in sheep are not likely to be due to differences in the level of noradrenergic and/or NPY input to the hypothalamus.

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Section: Discussionsupporting

confidence: 81%

Section: Discussionsupporting

confidence: 77%

Section: Discussionmentioning

confidence: 59%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Noradrenaline, but Not Neuropeptide Y, Is Elevated in Cerebrospinal Fluid from the Third Cerebral Ventricle following Audiovisual Stress in Gonadectomised Rams and Ewes

Turner

Rivalland²,

Clarke³

et al. 2002

Neuroendocrinology

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“…The use of desipramine, a specific NE reuptake blocker, in the perfusion medium significantly increased basal extracellular levels of NE, as reported in other brain areas (Itoh et al, 1990;Li et al, 1996;Morris et al, 1994). The weak effect of desipramine upon basal NE levels observed in the present experimental conditions suggests that NE uptake plays a minor role in the maintenance of NE extracellular levels in the BNST.…”

Section: Participation Of Ne Uptake In the Regulation Of Extracellulasupporting

confidence: 68%

Regulation of norepinephrine release from the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

1997

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The microdialysis technique was used to study the in vivo extracellular levels of norepinephrine in the bed nucleus of the stria terminalis. A basal level of 2.34 +/-0.25 fmol/microl of norepinephrine was observed. Desipramine (2 and 10 microM), a norepinephrine uptake blocker, significantly increased extracellular levels of norepinephrine. Reversed perfusion with high potassium in the presence of 2 microM desipramine induced the release of norepinephrine. Instead, in the presence of 10 microM desipramine, a significant decrease in the induced release of norepinephrine was observed. Clonidine, an alpha2-adrenergic agonist, significantly decreased basal extracellular levels of norepinephrine and the K+-induced release of norepinephrine. In contrast, yohimbine and RX821002, two alpha2-adrenergic antagonists, significantly increased basal extracellular levels of norepinephrine but not the release of norepinephrine induced by 70 mM K+. Perfusion of tetrodotoxin through the probe located in the bed nucleus of the stria terminalis significantly decreased both the basal extracellular level and the K+-induced release of norepinephrine. Furthermore, perfusion of tetrodotoxin through a microdialysis probe implanted in the medial forebrain bundle also decreased basal extracellular levels of norepinephrine in the bed nucleus of the stria terminalis. The results show that in vivo there is a significant noradrenergic tonic activity in the bed nucleus of the stria terminalis. This tonic activity depends on the impulse flow through medial forebrain bundle nerve fibers. Under these conditions, extracellular levels of norepinephrine in the bed nucleus of the stria terminalis are regulated by the magnitude of norepinephrine uptake and by presynaptic alpha2-adrenergic receptors.

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Noradrenaline inhibits glutamate release in the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

1999

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The microdialysis technique was used to simultaneously study the in vivo extracellular levels of noradrenaline, glutamate, and gamma aminobutyric acid (GABA) in the bed nucleus of the stria terminalis in order to assess the regulation that noradrenaline may exert upon the release of amino acid neurotransmitters. Perfusion through the probe with UK14304, a selective alpha2-adrenergic agonist, produced a significant decrease of noradrenaline and glutamate extracellular levels. Perfusion through the probe with RX821002, a selective alpha2-adrenergic antagonist, produced a significant increase of noradrenaline and glutamate basal extracellular levels. Perfusion with prazosine, a selective alpha1-adrenergic antagonist, produced a significant decrease of noradrenaline basal extracellular levels without affecting glutamate levels. Under the same conditions, GABA basal extracellular levels were not changed in the presence of any of the alpha-adrenergic ligands studied. The perfusion of high potassium through the probe induced a significant Ca++dependent release of the three neurotransmitters; however, extracellular noradrenaline returned to normal levels even though potassium was still present. In addition, it was observed that alpha-adrenergic receptor ligands exerted differential effects upon K+-induced release of noradrenaline and glutamate. Perfusion with the nonselective alpha-adrenergic antagonist, phenoxybenzamine, presented a biphasic effect upon K+-induced release of noradrenaline; a significant decrease during the first 5 min of stimulation followed by a significant increase in the next 5 min of stimulation. Perfusion with RX821002 produced a significant increase in K+-induced release of noradrenaline that returned to normal basal values before the end of the stimulation period. In contrast, local perfusion with prazosine caused a significant decrease of K+-induced noradrenaline release. In the case of glutamate, perfusion through the probe with phenoxybenzamine produced a significant increase in K+-induced release of glutamate. In addition, RX821002 and prazosine produced a significant increase in K+-induced release of glutamate. Perfusion through the probe with UK14304 produced a significant decrease of both noradrenaline and glutamate K+-induced release. The present results show that noradrenaline in the bed nucleus of stria terminalis exerts a significant inhibition over its own release through alpha2-adrenergic receptors and over glutamate release mainly through alpha2-adrenergic receptors. Thus, the results suggest that noradrenaline in the bed nucleus of the stria terminalis maintains an inhibitory tone over the information flow mediated by glutamate.

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Catecholamine release in the rat hypothalamic paraventricular nucleus in response to haemorrhage, desipramine and potassium

Cited by 22 publications

References 35 publications

Noradrenaline, but Not Neuropeptide Y, Is Elevated in Cerebrospinal Fluid from the Third Cerebral Ventricle following Audiovisual Stress in Gonadectomised Rams and Ewes

Noradrenaline, but Not Neuropeptide Y, Is Elevated in Cerebrospinal Fluid from the Third Cerebral Ventricle following Audiovisual Stress in Gonadectomised Rams and Ewes

Regulation of norepinephrine release from the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

Noradrenaline inhibits glutamate release in the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

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