Enhancement of audiogenic seizure by 6-hydroxydopamine

Bourn, W.M.; Chin, Lincoln; Picchioni, Albert L.

doi:10.1111/j.2042-7158.1972.tb08916.x

Cited by 57 publications

(9 citation statements)

References 2 publications

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“…Heightened startle responses to auditory stimulation in rats treated with 6-OHDA were observed in this study, as well as by Sorenson and Davis (1975). In addition, it has been reported that 6-OHDA augmented audiogenic seizures in rats (Bourn et al, 1972). Our previous study also indicates that during alcohol withdrawal there was an increased sensitivity to auditory stimulation, and the majority of the seizures were audiogenic (Chu et al, 1978).…”

Section: Nai-shin Chvsupporting

confidence: 81%

Enhancement of Alcohol Withdrawal Seizures with 6‐Hydroxy dopamine

Chu

1978

Epilepsia

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The relationship between central catecholamine neurons and alcohol withdrawal seizures was studied in rats pretreated with 6-hydroxydopamine to selectively destroy the central catecholamine nerve terminals. The alteration of alcohol withdrawal seizures was manifested by (1) a higher percentage of the rats developing the seizures, (2) an earlier onset of seizures, and (3) a greater severity of seizure activity. Seizure status was exhibited in 25% of the 6-hydroxydopamine-treated rats.

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Section: Nai-shin Chvsupporting

confidence: 81%

Enhancement of Alcohol Withdrawal Seizures with 6‐Hydroxy dopamine

Chu

1978

Epilepsia

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“…7 However, when a bilateral 6-OHDA lesion is severe, animals often die primarily due to the occurrence of marked aphagia, adipsia, and seizures. 23,24 Accordingly, a much more popular and practical model of 6-OHDA is the unilateral intracerebral injection. The latter can be successfully used to target a particular catecholaminergic pathway of the brain.…”

Section: -Ohda or The Prototypic Oxidative Stress Neurotoxinmentioning

confidence: 99%

Toxin-induced models of Parkinson’s disease

et al. 2005

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Summary:Parkinson's disease (PD) is a common neurodegenerative disease that appears essentially as a sporadic condition. It results mainly from the death of dopaminergic neurons in the substantia nigra. PD etiology remains mysterious, whereas its pathogenesis begins to be understood as a multifactorial cascade of deleterious factors. Most insights into PD pathogenesis come from investigations performed in experimental models of PD, especially those produced by neurotoxins. Although a host of natural and synthetic molecules do exert deleterious effects on dopaminergic neurons, only a handful are used in living laboratory animals to recapitulate some of the hallmarks of PD. In this review, we discuss what we believe are the four most popular parkinsonian neurotoxins, namely 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat. The main goal is to provide an updated summary of the main characteristics of each of these four neurotoxins. However, we also try to provide the reader with an idea about the various strengths and the weaknesses of these neurotoxic models.

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“…Reserpine abolished the flexion and hastened the extension of supramaximal electroshock in rats (Koslow and Roth, 1971). Also, Alexander et al (1980Alexander et al ( , 1985 found that 6-OHDA, unusually administered by the intraperitoneal route, suppressed the tonicclonic phase of PTZ seizures and prevented generalisa- Alexander and Kopeloff, 1978Boggan and Seiden, 1971Bourn et al, 1972Jobe et al, 1973bAlexander et al, 1985Lannes et al, 1991Lehmann, 1977Albala et al, 1986Corcoran et al, 1974McIntyre et al, 1979Michelson and Buterbaugh, 1985Wilkison and Halpern, 1979Arnold et al, 1973Corcoran and Mason, 1980NGouemo et al, 1990Browning and Maynert, 1978Browning and Simonton, 1978Mason and Corcoran, 1979Oishi et al, 1979Quattrone et al, 1978Stull et al, 1973Waller and Buterbaugh, 1985Corcoran et al, 1973Gross and Ferrendelli, 1979Tabakoff et al, 1978Alexander et al, 1980 Veliskova et al, 1991Morgan, 1976Chu, 1978Snead, 1987Lapin and Ryzov, 1990Lapin and Ryzov, 1990Farjo and McQueen, 1979Browning and Maynert, 1978Stockmaier et al, 1985Wurpel et al, 1985Bonuccelli et al, 1991…”

Section: Dopamine Antagonists In Manmentioning

confidence: 99%

The role of dopamine in epilepsy

Starr

1996

Synapse

239

157

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The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine‐epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism). © 1996 Wiley‐Liss, Inc.

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Enhancement of audiogenic seizure by 6-hydroxydopamine

Cited by 57 publications

References 2 publications

Enhancement of Alcohol Withdrawal Seizures with 6‐Hydroxy dopamine

Enhancement of Alcohol Withdrawal Seizures with 6‐Hydroxy dopamine

Toxin-induced models of Parkinson’s disease

The role of dopamine in epilepsy

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