Presynaptic receptor systems on the noradrenergic neurones of rat brain

Taube, H. D.; Starke, Klaus; Borowski, Evelyn

doi:10.1007/bf00498554

Cited by 329 publications

(78 citation statements)

References 52 publications

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“…Since presynaptic 5-HT receptors have been shown to be present on the 5-hydroxytryptaminergic nerve terminals in the frontal cortex of the rat (Mounsey et al, 1982) and on noradrenergic nerve terminals in the cortex (Taube et al, 1977) the effect of the 5-HT antagonist, methiothepin, was investigated. Methiothepin has been shown to be active at either postsynaptic (Si) or autoreceptors (S2) in rat brain (Ennis & Cox, 1982).…”

Section: Discussionmentioning

confidence: 99%

“…The terms 'pre and post-synaptic' are even less relevant in the central nervous system but by the use of specific agonists and antagonists, a2-adrenoceptors have been shown to be present on noradrenergic nerve terminals in the rat cortex and hippocampus (Taube, Starke & Borowski, 1977;Frankhuyzen & Mulder, 1982). These a2-adrenoceptors appear to resemble closely the a2-adrenoceptors that have been characterized in the periphery.…”

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confidence: 99%

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Different α‐adrenoceptors modulate the release of 5‐hydroxytryptamine and noradrenaline in rat cortex

Ennis

1983

British J Pharmacology

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1The potassium-evoked release of [3H]-noradrenaline from slices of rat occipital cortex and the potassium-evoked release of [3H]-5-hydroxytryptamine from slices of rat frontal cortex were measured using a superfusion system. 2 The rank order of potency for a number of a-adrenoceptor agonists was different for the two neuronal systems, clonidine and azepexole being the most potent inhibitors of noradrenaline release and methoxamine and phenylephrine being the most potent against 5-hydroxytryptamine release. 3 The rank order of potency for a series of a-adrenoceptor antagonists in reversing the inhibition of noradrenaline release produced by clonidine was: phentolamine > rauwolscine = yohimbine = corynanthine >> WB4101, whereas against methoxamine-inhibition of 5-hydroxytryptamine release the rank order of potency was: WB4101 > phentolamine > corynanthine > yohimbine > rauwolscine. 4 The results suggest that the a-adrenoceptors which modulate potassium-evoked 5-hydroxytryptamine release are not identical with the a2-adrenoceptors located on noradrenergic nerve terminals and may more closely resemble a,-than a2-adrenoceptors.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Different α‐adrenoceptors modulate the release of 5‐hydroxytryptamine and noradrenaline in rat cortex

Ennis

1983

British J Pharmacology

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“…Basal tritium outflow rates were 2 to 3 orders of magnitude lower than after electrical stimulation. Basal outflow represents almost exclusively the release of tritiated NE metabolites (21), because axon terminals discontinued from their perikarya do not release significant amounts of NE. Both basal metabolite release and the maximal releasable NE fraction did not differ among the three experimental groups in both brain regions studied.…”

Section: Discussionmentioning

confidence: 99%

“…Unstimulated basal tritium outflow consists predominantly of tritiated NE metabolites (21). The overflow elicited by electrical stimulation was calculated as the difference of tritium outflow during the collection period in which stimulation was applied and the two collection periods thereafter minus estimated basal outflow; basal outflow was assumed to decline linearly from the collection period before to the collection period 10 to 15 min after onset of stimulation.…”

Section: Superfusion Experimentsmentioning

confidence: 99%

Impaired Autofeedback Regulation of Hypothalamic Norepinephrine Release in Experimental Uremia

Klein

Daschner

Vogel

et al. 2005

Journal of the American Society of Nephrology

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Chronic renal failure (CRF) is associated with multiple hypothalamic dysfunctions, including reduced secretion of gonadotropin-releasing hormone (GnRH). Because GnRH release is tightly controlled by sympathetic neuronal input, a possible alteration of local noradrenergic neurotransmission in experimental CRF was evaluated. Basal, stimulated, and autoinhibited norepinephrine (NE) release was assessed in hypothalamic and hippocampal tissue slices obtained from 5/6-nephrectomized and control rats. Autoinhibition-free NE release from brain slices, prelabeled with [ 3 H]NE and superfused with physiologic buffer, was stimulated by six electrical pulses, 100 Hz (pseudo-one-pulse stimulation). Autoinhibited NE release was induced by 90 pulses at 3 Hz. The release of tritiated NE was measured upon addition of increasing concentrations of unlabeled NE to exogenously activate the inhibitory ␣ 2 -autoreceptor. Although neither basal nor stimulated NE release differed between the groups, significantly lower pIC 50 and I max estimates of the concentration-response curves of exogenous NE on [ 3 H]NE release were observed in CRF rats, suggesting a diminished autoinhibition of hypothalamic noradrenergic terminals in CRF. Western blotting of tissue homogenates disclosed a significantly reduced abundance of ␣ 2 -autoreceptor protein in hypothalamic tissue from CRF rats. These abnormalities were selectively observed in the hypothalamus, whereas noradrenergic autoinhibition seemed unaltered in the hippocampus. The results suggest a diminished autoinhibition of hypothalamic NE release in CRF. Although impaired hypothalamic NE autoinhibition does not explain reduced GnRH secretion in CRF, it may be involved in the pathogenesis of sympathetic hyperactivity associated with this condition. D isorders of the reproductive system, clinically manifesting by impaired libido and fertility in adults and delayed or arrested puberty in adolescents, are common in chronic renal failure (CRF) (1). We and others previously demonstrated defective neuroendocrine activation of the gonadotropic hormone axis both in patients with CRF and in experimental uremia, with evidence for reduced pulsatile release of gonadotropin releasing hormone (GnRH) from the mediobasal hypothalamus (2-5). Experimental findings suggest that uremia may influence the function of hypothalamic neurons by various mechanisms. We observed abnormal extracellular amino acid neurotransmitter concentrations in the mediobasal hypothalamus of uremic rats, compatible with disturbed regulation of hypothalamic neurons by higher neuronal centers (6). The function of brain synaptosomes is altered in experimental uremia (7-10). However, we also demonstrated direct inhibition of GnRH secretion from cultured hypothalamic neurons by a factor circulating in uremic serum (11).Norepinephrinergic axon terminals are located in proximity of GnRH cells in the anterior hypothalamus (12). Norepinephrine (NE) is able to stimulate GnRH release from the hypothalamus in a concentration-dependent manner in vitro ...

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“…In addition to the effects observed for opiate agonists in peripheral tissues, morphine-like drugs and [Met5]-enkephalin have been shown to reduce the electrically and potassium-evoked [3H]-noradrenaline overflow from slices of different regions of the rat brain: occipital cortex, hypothalamus and cerebellar cortex (Montel et al, 1974a, b;1975a, b;Taube, Borowski, Endo & Starke, 1976;Taube, Starke & Borowski, 1977;Arbilla & Langer, 1978). Naloxone blocked the inhibition of 3H-transmitter overflow obtained in the presence of morphine or [Met5]-enkephalin, but did not antagonize the inhibitory effect of the a-agonist, tramazoline (Taube et al, 1977).…”

Section: Methodsmentioning

confidence: 99%

Pharmacological Differentiation of Presynaptic Inhibitory Α‐adrenoceptors and Opiate Receptors in the Cat Nictitating Membrane

Dubocovich

Langer

1980

British J Pharmacology

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3 The synthetic opiate pentapeptides: BW 180 C (Tyr-D-Ala-Gly-Phe-E>-Leu), and BW834 C (Tyr-DAla-Gly-pClPhe-DLeu), which are resistant to enzymatic degradation were more potent than the enkephalins in reducing the stimulation-evoked transmitter overflow from the cat nictitating membrane. On the other hand, the tetrapeptide BW832 C, which lacks the D-leucine terminal of BW180 C was less potent than the enkephalins in inhibiting neurotransmission. 4 In the presence of phenoxybenzamine 1 gIM, 3H-transmitter overflow was increased 8 fold and the inhibition of neurotransmission by methionine-enkephalin was not affected. Exposure to phenoxybenzamine 10 gM increased [3H]-noradrenaline overflow 15 fold and antagonized the effects of methionine enkephalin on transmitter release. 5 In the cat nictitating membrane the inhibitory presynaptic opiate receptors are different from the presynaptic a-autoreceptors which regulate the release of noradrenaline elicited by nerve depolarization through a negative feed-back mechanism.

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Presynaptic receptor systems on the noradrenergic neurones of rat brain

Cited by 329 publications

References 52 publications

Different α‐adrenoceptors modulate the release of 5‐hydroxytryptamine and noradrenaline in rat cortex

Different α‐adrenoceptors modulate the release of 5‐hydroxytryptamine and noradrenaline in rat cortex

Impaired Autofeedback Regulation of Hypothalamic Norepinephrine Release in Experimental Uremia

Pharmacological Differentiation of Presynaptic Inhibitory Α‐adrenoceptors and Opiate Receptors in the Cat Nictitating Membrane

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