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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

When studying the role of the locus coeruleus (LC) in the regulation of seizure susceptibility in rats, we found that bilateral LC lesion significantly lowered the electroshock seizure threshold for the tonic extension of forelegs. The pattern of maximal electroshock seizure was not affected by LC lesion, although the recovery time was slightly prolonged. In the pentylenetetrazol (PTZ) seizure threshold test, LC lesion significantly elevated the twitch threshold, but did not affect the threshold for the generalized clonic seizure or clonic convulsion. Incidence of the tonic extension in the PTZ seizure test tended toward an increase with LC lesion. Biochemical determinations revealed that LC lesion significantly decreased the norepinephrine contents in various brain regions as well as the 5-hydroxytryptamine contents of some brain regions, but not the 5-hydroxyindoleacetic acid contents. These results suggest that while the LC is involved in the regulation of seizure susceptibility, the involvement differs with various types of seizures.
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PMID:The role of the locus coeruleus in regulation of seizure susceptibility in rats. 618 32

Hindlimb extension (HLE) induced by maximal electroshock seizures (MES) can be markedly affected by drugs which affect CNS 5-hydroxytryptamine (5-HT). Consequently, it has been proposed that the natural resistance of certain rats (flexor rats) to HLE is due to elevated levels of 5-HT. We have tested the hypothesis that the increased resistance of flexor rats to MES-induced HLE is due to elevated serotonergic levels in some region(s) of the CNS by examining 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels in 8 regions of the CNS in rats classified by MES as either flexors or extensors. Furthermore, we compared the in vivo synthesis rate of 5-HT between flexor and extensor rats in 6 regions of the brain by measuring the accumulation of 5-HTP following aromatic amino acid decarboxylase inhibition with NSD-1015. All neurochemical analyses were carried out on rats sacrificed one week after their last seizure test. No differences in 5-HT, 5-HIAA or 5-HTP synthesis rate were detected between flexor and extensor rats for any of the regions examined, suggesting that enhanced serotonergic levels are not responsible for the unusual resistance of flexor rats to HLE.
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PMID:Comparison of regional brain 5-HT and 5-HIAA content in flexor and extensor rats. 619 44

Norepinephrine, dopamine, and 5-hydroxytryptamine concentrations were determined in the central nervous systems of genetically epilepsy-prone rats (GEPR) and in control rats. Norepinephrine concentrations were abnormal in all major areas of the central nervous system of the GEPR, with decrements existing in the telencephalon, hypothalamus-thalamus, midbrain, pons-medulla and spinal cord. An increment in the concentration of this neurotransmitter existed in the cerebellum. Dopamine concentrations were normal in all areas of the GEPR brain. Abnormalities in 5-hydroxytryptamine concentrations were also present in the GEPR. They were exclusively decrements and occurred in the telencephalon, hypothalamus-thalamus, midbrain, and pons medulla. Concentrations of this neurotransmitter were normal in the cerebellum and spinal cord. Coupled with our earlier pharmacologic data, these observations support our concept that noradrenergic and/or 5-hydroxytryptaminergic decrements are etiologically important in seizure susceptibility in the GEPR. The lack of abnormalities in brain dopamine concentrations strengthens our hypothesis that dopaminergic transmission does not regulate seizure susceptibility in this model.
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PMID:Abnormalities in monoamine levels in the central nervous system of the genetically epilepsy-prone rat. 628 98

Inbred E1 mice are highly susceptible to convulsive seizures upon "throwing" stimulation. The strain is known to have an abnormal 5-hydroxytryptamine (5-HT) metabolism. In the study here 5-HT level, [14C]5-hydroxytryptophan (5-HTP) metabolism, MAO activity and [3H]5-HT receptor binding were examined in the cortex, brainstem and cerebellum. In the interictal period cortical and brainstem 5-HT level and [3H]5-HT receptor binding were significantly lower. In the same period cortical biosynthesized [14C]5-HT from [14C]5-HTP taken up was higher, and MAO activity was not changed. L-DOPA with MK486 induced a low threshold of seizures and decreased cortical 5-HT level. Abnormally functioning 5-HT neurones may exist in the E1 mouse cortex.
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PMID:Brain 5-hydroxytryptamine level, metabolism, and binding in E1 mice. 641 6

d-Amphetamine protected young chicks against electroconvulsive seizure (ECS) in a dose-dependent manner in the dose range of 1-10 mg/kg. Reserpine pretreatment reduced ECS threshold and decreased the anticonvulsant effect of d-amphetamine in chicks. FLA-63 protected chicks against ECS and potentiated the anticonvulsant effect of d-amphetamine, whereas the dopamine antagonist pimozide antagonised the protective effect of d-amphetamine against ECS. Both the alpha-adrenoceptor antagonist phentolamine, and the serotonin antagonist cyproheptadine, had no significant influence on the anticonvulsant effect of d-amphetamine. d-Amphetamine significantly increased the levels of 5-hydroxytryptamine, noradrenaline and dopamine in the hyperstriatum, brain stem and optic tectum of the chick respectively. The present data suggests that brain dopamine may be the principal monoamine involved in the protective influence of d-amphetamine against ECS in young chicks.
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PMID:Studies on the pharmacology of d-amphetamine on maximal electroconvulsive seizure in young chicks. 641 41

The effect of chronic para-chlorphenylalanine (PCPA) treatment was investigated in two different seizure models: the pentylenetetrazole (PTX) seizure model in rats and the kindled seizures from rabbit amygdala. Chronic PCPA treatment (21 days) in male albino rats caused a progressive decrease in the 5-hydroxytryptamine (5-HT) brain level between the 1st and the 7th day of PCPA administration. Then the 5-HT level remained low until the end of the experiment. On the background of the low 5-HT level there occurred changes in PTZ convulsive reactions: after the 3rd day of PCPA treatment the convulsive-seizure reactivity was significantly increased and after the 7th, 14th and 21st day the increased seizure reactivity performed only as a tendency, though the 5-HT level was still low. Chronic PCPA treatment (16 days) of rabbits delayed the development of the behavioural kindled seizures. This treatment also reduced the duration of bioelectrical seizures until the 8th day of treatment, especially in the motor cortex. The observed different effect of the chronic PCPA treatment in both seizure models: pentylenetetrazole in rats and kindling in rabbits might be explained by essential differences in the origin and mechanisms of development of the two seizure models.
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PMID:Effect of chronic para-chlorophenylalanine treatment on convulsive-seizure reactions. 645 89

Nisoxetine and desipramine (inhibitors of norepinephrine reuptake) each exerted a suppressant effect on spinal cord seizures by decreasing the duration of tonic extension. In addition, desipramine increased the duration of tonic flexion and nisoxetine decreased the total duration of seizure. In contrast, citalopram (an inhibitor of 5-hydroxytryptamine reuptake) did not affect any of these seizure components. These observations support the concept that spinal cord noradrenergic, but not 5-hydroxytryptaminergic neurons act as attenuators of convulsive activity.
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PMID:Effects of norepinephrine and 5-hydroxytryptamine reuptake inhibitors on electrically-induced spinal cord seizures in rats. 696 62

A convulsant dose (100 mg/kg) of l-methionine-RS-sulphoximine (MSO) produced temporally correlated decreases in central 5-hydroxytryptamine (5-HT) and plasma and brain tryptophan (TRY) concentrations in C57BL/6J mice. In contrast, a subconvulsant dose of MSO (50 mg/kg) had no effect on central 5-HT levels and only decreased brain tryptophan at one time-point after its administration. The pattern of findings suggests that the decrease in central 5-HT levels resulting from a convulsant dose of MSO is related to an impairment in 5-HT synthesis resulting from a restriction of tryptophan availability. Administration of 25 mg/kg and 100 mg/kg doses of l-tryptophan with convulsant doses of MSO significantly increased seizure latency. It is suggested that the central 5-HT system modulates the expression of MSO-induced seizures.
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PMID:Tryptophan availability, central serotonergic function and methionine sulphoximine-induced convulsions. 706 6

Nine 5-(3,4,5-trimethoxyphenyl)-4-substituted aryl-3-hydrazinocarbonylmethylthio-4H-1,2,4-triazoles were investigated for their anticonvulsant and monoamine oxidase inhibitory properties. The protection afforded by these compounds at a dose of 100 mg/kg ranged from 20-90% against pentylenetetrazol-induced seizures and 20-40% against electric shock-induced convulsions. The degree of in vitro monoamine oxidase inhibition by substituted triazoles ranged from 41-80%, 18-36% and 20-40% using kynuramine, tyramine and 5-hydroxytryptamine as substrate, respectively. The approximate LD50 values of greater than 1000 mg/kg exhibited low toxicity of substituted triazoles.
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PMID:Anticonvulsant activity and monoamine oxidase inhibitory properties of substituted 1,2,4-triazoles. 717 60

The effects of intrahippocampally administered catechol- and indoleamines on the two types of hippocampal seizure discharges elicited by electrical and chemical stimulation were examined in unanesthetized rabbits. The catecholamines norepinephrine (NE) and dopamine (DA), injected into the hippocampus in doses of 100--200 micrograms, inhibited electrically induced hippocampal seizure discharges with a 50% increase in the stimulation threshold. However 5-hydroxytryptamine (5-HT) at doses of 50 micrograms to 100 micrograms caused no effect on electrically induced seizure discharges. On the contrary, 5-HT and 5-hydroxytryptophan (5-HTP) at a dose of 50 micrograms potentiated carbachol (5 micrograms)-induced hippocampal seizure discharges, prolonging the duration of seizure discharge three times the control. NE and DA had no effect on this chemically induced hippocampal discharges. It is therefore suggested that the effects of monoamines on hippocampal seizure discharges are very much dependent on the type of stimulation employed for the induction of this phenomenon.
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PMID:Effects of monoamines injected into the hippocampus on hippocampal seizure discharges in the rabbit. 727 94


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