Effects of 6-hydroxydopamine on putative transmitter substances in the central nervous system

Jacks, B.R.; Champlain, Jacques de; Cordeau, J. Pierre

doi:10.1016/0014-2999(72)90036-2

Cited by 98 publications

(14 citation statements)

References 22 publications

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“…Although destruction of the catecholaminergic nerve terminals occurs with high or repeated doses of 6-OHDA (Bloom, Algeri, Groppetti, Revuelta & Costa, 1969;Ungerstedt, 1971), the catecholamine content with low doses (200 µg) can be reduced without detectable ultrastructural changes (Bartholini, Thoenen & Pletscher, 1971). Brain concentrations of serotonin (5-HT) and y-aminobutyric acid (GABA) are not significantly altered by 6-OHDA treat¬ ment (Bloom et al, 1969;Uretsky & Iversen, 1970;Jacks et al, 1972). The specificity of 6-OHDA for catecholaminergic neurons appears to be due to differences in the ability of the neurons to take up and concentrate 6-OHDA (Ungerstedt, 1971) and degeneration presumably depends upon the attainment of a critical intraneuronal concentration of either 6-OHDA itself (Malmfors & Sachs, 1968) or its oxidation products and metabolites.…”

Section: Concentrations Of Lh and Fshmentioning

confidence: 99%

Effects of Intraventricular Injections of 6-Hydroxydopamine on Plasma Lh and FSH in Male Rats

Kitchen¹,

Ruf²,

Younglai³

1974

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Section: Concentrations Of Lh and Fshmentioning

confidence: 99%

Effects of Intraventricular Injections of 6-Hydroxydopamine on Plasma Lh and FSH in Male Rats

Kitchen¹,

Ruf²,

Younglai³

1974

Reproduction

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“…Subsequent studies demonstrated that injection of 6-OHDA intracisternally or into the lateral ventricle depletes central norepinephrine (NE) and dopamine (DA) Iversen, 1969, 1970), destroying noradrenergic (Bloom et al, 1969;Tranzer and Thoenen, 1968) and dopaminergic (Bartholini et al,'1970;Hedreen and Chalmers, 1972) nerve terminals. Whole brain levels of serotonin (5-HT), acetylcholine and gamma-aminobutyric acid, on the other hand, are generally reported to be unaffected by 6-OHDA (Uretsky and Iversen, 1970;Breese and Traylor, 1970;Jacks et al, 1972). On the basis of these observations, as well as a number of anatomical investigations (Bloom et al, 1969;Bartholini et al, 1970;Lungdahl et al, 1971;Tranzer and Thoenen, 1968;Constantinidis et al, 1971;Ungerstedt, 1971;Kostrzewa and Jacobowitz, 1974), it is widely accepted that 6-OHDA is selectively toxic to catecholamine-containing neurons.…”

Section: Introductionmentioning

confidence: 99%

Variability among brain regions in the specificity of 6-hydroxydopamine (6-OHDA)-induced lesions

Commins

Shaughnessy

Axt

et al. 1989

J. Neural Transmission

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6-Hydroxydopamine (6-OHDA; 200 micrograms, 150 micrograms or 110 micrograms) or vehicle was infused stereotaxically into the lateral ventricles of rats, usually following pretreatment with desmethylimipramine (DMI). Various brain regions were then assayed for dopamine (DA), serotonin (5-HT) and norepinephrine (NE). As expected, 6-OHDA depleted DA in all brain regions examined. Unexpectedly, however, the two highest doses of 6-OHDA significantly decreased 5-HT levels in the hippocampus and increased 5-HT levels in the striatum. In addition, despite pretreatment with doses of DMI commonly considered adequate to block 6-OHDA-induced depletion of NE, all doses of 6-OHDA tested significantly reduced NE levels in the hippocampus, hypothalamus and septum. We interpret our data as suggesting that some brain regions are susceptible to nonspecific toxic effects of 6-OHDA at doses commonly employed. Furthermore, these nonspecific effects may or may not occur, depending on seemingly minor variations in experimental technique.

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“…Although dopamine concentrations are also found to be de pleted after treatment with the drug [37], the tubero-infundibular system innervating the hypothalamus is found to be unaffected [12]. Treatment with 6-OHDA does not alter the brain concentration of 5-hydroxytryptamine [2,3] or y-amino butyric acid [16], As it has been suggested that the fast feedback action of corticosterone on CRF secretion may be mediated via inhibitory noradrenergic neurones [20], the ef fect of pretreatment with 6-OHDA on the corticosteroid feedback mechanisms was also investigated. …”

mentioning

confidence: 99%

Effects of 6-Hydroxydopamine on the Hypothalamo-Pituitary-Adrenocortical Axis

Nicholson¹,

Holmes²,

Sutanto³

et al. 1986

Neuroendocrinology

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Female rats were treated with two intraventricular injections each of 350 µg 6-hydroxydopamine (6-OHDA) and used for experiment 4 or 14 days later. The response to laparotomy, as assessed by subsequent in vitro corticosterone release, was unaffected by the drug, but that to the smaller stress of a skin cut was significantly reduced. Both fast and delayed feedback responses to corticosterone administration were still evident in 6-OHDA-treated animals. When determined 14 days after treatment, hypothalamic concentrations of epinephrine (E) and norepinephrine (NE) were reduced by 46 and 84%, respectively. There was no significant change in content of immunoreactive corticotropin-releasing factor (CRF-41). The acetylcholine-stimulated release of CRF bioactivity from control hypothalami incubated in vitro was significantly inhibited by E or NE, with E being at least 10 times more potent on a molar basis. This effect of NE was enhanced in hypothalami removed from 6-OHDA-treated rats, complete inhibition of acetylcholine-stimulated release of CRF being produced by 0.6 nMNE, as opposed to 6.0 nM for untreated controls. At the level of the anterior pituitary gland, tissue content of adrenocorticotropin (ACTH) was unaffected by treatment, but that of luteinizing hormone (LH) in the same tissues was significantly increased. The corticotrophic response of fragments of the gland incubated or perifused in vitro to hypothalamic extract, CRF-41, arginine vasopressin or E was reduced. In contrast, the response of the tissue to gonadotro-pin-releasing hormone (GnRH) added in vitro was not significantly affected. There was no difference in release of corticosterone from adrenals glands removed from control and 6-OHDA-treated rats and incubated in vitro, either basally or in response to synthetic ACTH 1–24. Treatment with 6-OHDA had no significant effect on adrenal gland weight or the compensatory adrenal hypertrophy seen 4 days after unilateral adrenalectomy.

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Effects of 6-hydroxydopamine on putative transmitter substances in the central nervous system

Cited by 98 publications

References 22 publications

Effects of Intraventricular Injections of 6-Hydroxydopamine on Plasma Lh and FSH in Male Rats

Effects of Intraventricular Injections of 6-Hydroxydopamine on Plasma Lh and FSH in Male Rats

Variability among brain regions in the specificity of 6-hydroxydopamine (6-OHDA)-induced lesions

Effects of 6-Hydroxydopamine on the Hypothalamo-Pituitary-Adrenocortical Axis

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