Ontogeny of brain catecholamine turnover and susceptibility to audiogenic seizures in DBA/2J mice

Shaywitz, Bennett A.; Yager, Robert D.; Gordon, Judith W.

doi:10.1002/dev.420110308

Cited by 13 publications

(2 citation statements)

References 15 publications

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“…Derangements in brain dopamine have also been documented for epilepsy-sensitive mice (Table 11). An elevated synthesis and turnover of dopamine was detected in audiogenic DBM2 mice (Kellogg, 1976;Shaywitz et al, 1978), although dopamine uptake was normal (Bondy et al, 1979). By contrast, mice of the E l strain were found to be dopamine-deficient by Sutoo et al (1987) and by Suzuki and Mori (1992) but not by Hiramatsu et al (1976;cited in Jobe and Laird, 1981) in a comparative study with ten other mouse strains.…”

Section: Nonseizing Animalsmentioning

confidence: 95%

The role of dopamine in epilepsy

Starr

1996

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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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Section: Nonseizing Animalsmentioning

confidence: 95%

The role of dopamine in epilepsy

Starr

1996

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“…Experiments have shown that DBA/2 mice, which are genetically predisposed to seizures, and C57B1 mice, which are resistant, also differ in the activity of the serotoninergic, noradrenergic, gamma-aminobutyric acid, and several other brain systems [3,4,13,14]. The DBA/2 brain has been found to have much lower levels of serotonin (5-HT) and norepinephrine (NE), fewer binding sites for 3H-prazosin (a ligand of c~l-adrenergic receptors) [2], and a lower affinity of these receptors [5] than the C57B1 brain.…”

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confidence: 99%

Role of the interaction between different types of serotonin and α2-adrenergic receptors in the regulation of audiogenic seizures in DBA/2 micereceptors in the regulation of audiogenic seizures in DBA/2 mice

Семенова

Ticku

1995

Bull Exp Biol Med

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It is shown that the serotonin receptors 5-HTlc , 5-HT3, and 5-HT 4 and ~2-adrenergic receptors are involved in the regulation of audiogenic seizures in DBA/2 mice, and that the effects of these serotonin receptors on the duration and magnitude of convulsive activity are the opposite of those produced by ct2-adrenergic receptors.Key Words: audiogenic seizures; cyproheptadine; ketanserin; mianserin; yohimbine; zakopride Knowledge of how the susceptibility to audiogenic seizures correlates with the activity of neurotransmitter systems is essential for understanding the mechanisms by which these seizures are regulated [1]. Experiments have shown that DBA/2 mice, which are genetically predisposed to seizures, and C57B1 mice, which are resistant, also differ in the activity of the serotoninergic, noradrenergic, gamma-aminobutyric acid, and several other brain systems [3,4,13,14]. The DBA/2 brain has been found to have much lower levels of serotonin (5-HT) and norepinephrine (NE), fewer binding sites for 3H-prazosin (a ligand of c~l-adrenergic receptors) [2], and a lower affinity of these receptors [5] than the C57B1 brain. Moreover, the temporal cortex of DBA/2 mice is reported to have far fewer monoamine-containing synapses than that of mice not susceptible to audiogenic seizures [8].Our previous studies demonstrated the importance of a balance between the activities of the brain serotoninergie and noradrenergic systems for the regulation of behavior; in particular, the two systems were shown to interact in a reciprocal

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Summation of the workshops and discussion: The new wave of research in the epilepsies

Delgado‐Escueta

1984

Ann Neurol.

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In addition to yielding new routes of navigation, the workshops from which the material in this supplement comes developed a conceptual blueprint for priority challenges in epilepsy research. All participants called attention to the ultimate goal, namely, understanding the mechanisms of human epilepsies. And, foremost to achieving this goal is the search for polymorphisms of restriction endonuclease patterns in monogenic forms of epilepsies in an attempt to localize the abnormal gene, or genes, to a specific chromosome. In human temporal lobe epilepsy, a priority challenge is to record paroxysmal depolarization shifts in hippocampal slices in vitro, slices excised from the known site of epileptogenicity. Parallel experiments exploring biochemical membrane abnormalities in neuronal and glial membranes isolated from the hippocampal seizure focus are especially valuable. Together with genetic studies using restriction-fragment-length polymorphisms, these experiments should distinguish between the respective contributions of genetic and environmental factors in multifactorial forms of partial epilepsies, such as temporal lobe epilepsy. In the genesis and spread of human temporal lobe epilepsy, the role of kindling and the mirror focus must be resolved. Recent successful applications of positron emission tomography, single-photon-emission computed tomography, and nuclear magnetic resonance computed tomography show promise in finally constructing the ion transport pathways, neurotransmitter systems, and metabolic processes within the functioning brains of epileptic patients.

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Ontogeny of brain catecholamine turnover and susceptibility to audiogenic seizures in DBA/2J mice

Cited by 13 publications

References 15 publications

The role of dopamine in epilepsy

The role of dopamine in epilepsy

Role of the interaction between different types of serotonin and α2-adrenergic receptors in the regulation of audiogenic seizures in DBA/2 micereceptors in the regulation of audiogenic seizures in DBA/2 mice

Summation of the workshops and discussion: The new wave of research in the epilepsies

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