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

In rabbits, generalized seizures were induced by methoxypyridoxine, and changes in amino acid concentrations of 15 brain regions were investigated before seizure onset and during the course of sustained epileptiform activity. As previously reported, gamma-aminobutyric acid (GABA) concentration decreased preictally in most regions. At the same time, taurine level was elevated in the hypothalamus, thalamus, hippocampus, caudatum, and frontal cortex. After 90 min of seizures, it was significantly decreased in the hypothalamus, periaqueductal grey, substantia nigra, frontal cortex, and cerebellum. Glycine content was reduced preictally only in the substantia nigra; after seizure onset its concentration rose in all brain areas. Glutamate content in the frontal cortex decreased before seizure onset; after 1.5 h of seizures, its concentration in cerebellum, caudatum, and hippocampus was reduced. Aspartate level was decreased in most areas after sustained seizures; in putamen, however, it was elevated. In contrast, glutamine content increased preictally in the superior colliculus and in all brain areas by approximately 200% after 90 min of seizures. Alanine and valine content also rose markedly in most brain areas after prolonged seizures, and threonine showed the same tendency. The single brain regions were observed to respond to methoxypyridoxine in highly individualistic ways. For example, the glycine content of the substantia nigra, which is believed to utilize this amino acid as a neurotransmitter, decreased preictally. The potential importance of the superior colliculus in seizure induction is considered in view of the early rise in glutamine level. The antagonistic preictal behavior of taurine and GABA is discussed with respect to synthesis, uptake from the blood, and antiepileptic properties.
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PMID:Alterations in the content of amino acid neurotransmitters before the onset and during the course of methoxypyridoxine-induced seizures in individual rabbit brain regions. 613 13

The respiratory depression induced by two mu-opiate agonists morphine and Tyr-D-Ala-Gly-N-Me-Phe-Met(O)-ol (FK-33824), and two delta-agonists Tyr-D-Ala-Gly-Phe-D-Leu (DADLE) and Tyr-D-Ser-Gly-Phe-Leu-Thr (D-Ser2-Thr6) was studied in rats by using the intracerebroventricular route. The four opioids caused a dose-dependent depression of respiratory frequency down to apnea but high doses of morphine elicited motor activation and seizure activity. FK-33824 was the most potent, followed by DADLE, D-Ser2-Thr6 and morphine. The in vivo apparent pA2 values were determined for naloxone against FK-33824, DADLE and D-Ser2-Thr6. The pA2 value of naloxone interacting with the mu-agonist FK-33824 was significantly lower than those obtained against the two delta-agonists. It is proposed that different types of opiate receptors are involved in the opiate-induced respiratory depression.
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PMID:Interaction of naloxone with mu- and delta-opioid agonists on the respiration of rats. 630 57

The anticonvulsant effect of either phenobarbital or dilantin was potentiated by exogenous glycine in DBA/2 audiogenic seizure mice and in 3-mercaptopropionic acid-induced seizures. In seizures caused by pentylenetetrazol, glycine potentiated the anticonvulsant effect of phenobarbital only slightly; in combination with dilantin, which was ineffective by itself, it did not have an effect. Valproic acid, in large doses, prevented 3-mercaptopropionic acid-induced seizures; glycine did not potentiate its effect. Glycine thus potentiates anticonvulsant effects, but only of some drugs and only in some of the seizure models. This suggests that the mechanism of the anticonvulsant effect of glycine is similar to that of some of the anticonvulsant drugs such as dilantin and different from others, and that this mechanism is not effective in all seizure models.
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PMID:Glycine potentiates the action of some anticonvulsant drugs in some seizure models. 644 97

Administration of muscimol to mice in subcutaneous doses between 0.34 and 1.25 mg/kg produced partial protection against 3-mercaptopropionic acid (MPA)-induced seizures. Glycine at a dose of 750 mg/kg (10 mmol/kg) protected 20% of the animals 45 min after its administration. Combined treatment with the two compounds gave a near to complete protection against MPA-induced seizures. These observations suggest that the concomitant enhancement of glycinergic and GABAergic activities amplify the anticonvulsant effect of these neuronal systems against seizures induced by impairment of GABA-mediated transmission.
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PMID:Synergistic anticonvulsant effects of a GABA agonist and glycine. 648 32

FK-33,824 (Tyr-D-Ala-Gly-MePhe-Met(O)-ol) and metkephamid (Tyr-D-Ala-Gly-Phe-N(Me)Met-CONH2; LY 127623) are two parenterally active synthetic analogues of the endogenous morphinomimetic pentapeptide, [Met5]-enkephalin. Acute s.c. administration of each analogue raised the seizure threshold in a dose-related manner in rats challenged with flurothyl, a volatile convulsant. The anticonvulsant action was antagonized by a low dose of naloxone (0.10 mg/kg s.c.). FK-33,824 and metkephamid can therefore be classified with typical mu-receptor agonists such as morphine and etorphine in this procedure.
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PMID:A comparison of the anticonvulsant effects of two systemically active enkephalin analogues in rats. 723 80

L-glycine (1-12.5 micrograms, intracerebroventricularly, i.c.v.) completely prevented seizures induced by i.c.v. administration of L-kynurenine, and practically did not modify those induced by another convulsant quinolinic acid, a metabolite of tryptophan, and by strychnine. L-Glycine administered intraperitoneally (i.p.) (1000 mg/kg) decreased lethality after K-kynurenine and quinolinic acid; at doses of 3000 and 4000 mg/kg which are sedative and hypothermic it prolonged the latency of strychnine and L-kynurenine seizures. The convulsant action of pentylenetetrazol was not modified. Kynurenine seizures are suggested to be related to the action of kynurenine on glycine receptors in the central nervous system.
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PMID:Antagonism of L-glycine to seizures induced by L-kynurenine, quinolinic acid and strychnine in mice. 725 Feb 1

With GABA, glycine and beta-alanine are inhibitory amino acids. They act mainly in the spinal cord and in the brain stem via the strychnine sensitive glycine receptor. Glycine exhibits also a key rule in the excitatory neurotransmission in the N-methyl-D-aspartate receptor complex. These two hydrophilic molecules suffer from the lack of small neutral amino acid carriers at the luminal side of the blood-brain barrier. The purpose of this study is to design molecular entities able, by an enhanced lipophilicity, to increase the pharmacological properties of these amino acids. From the synthesis and from the anticonvulsant evaluation in the maximal electroshock seizure test, we can underline: 1) In the case of a monosubstitution, a N-substitution is more important than amidation or esterification of the carboxylate. 2) Specially in the case of N-substitution, carbamates derivatives are the most active compounds compared to the correspondent amides. N-benzyloxycarbonylglycine is really attractive. The pharmacological properties, the tentative schedule of the mode of action are presented too.
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PMID:[Simple derivatives of amino acid neurotransmitters. Anticonvulsant evaluation of derived amides, carbamates and esters of glycine and beta-alanine]. 767 19

Three cases of ketotic hyperglycinemia are described. Spongy encephalopathy was present in white as well as gray matter. The cell type that predominantly exhibited swelling was the astrocyte. Glycine binding is required for activation of the NMDA receptor. By constant excitation a surplus of glycine could disturb the ion balance. This might provide the pathogenetic principle of seizures and cytotoxic edema in hyperglycinemia.
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PMID:Spongy encephalopathy in ketotic hyperglycinemia. 769 92

1. After a series of electroconvulsive seizures, levels of TRH-Gly (the immediate precursor of TRH) in four limbic regions correlate significantly and highly with increased swimming in the forced-swim test model of antidepressant efficacy. Only in hippocampus did TRH itself correlate with swimming. 2. After ECS, limbic forebrain regions differ in the relationship of TRH to its precursor peptides. This probably results from differences in the coordination of induction of TRH-processing enzymes, as well as differences in the level of prepro-TRH following seizures. 3. Sprague-Dawley rats that are partially kindled with corneal stimulation swim less in the forced-swim test, opposite to the effect seen with antidepressant agents. 4. Pyriform cortex is unique among the four limbic regions examined in showing decreased amounts of the TRH precursor following swim/stress. 5. Combining ECS with the forced-swim test of antidepressant effects creates a useful model for studying the involvement of TRH and its precursor peptides in both the antidepressant and anticonvulsant effects of controlled therapeutic seizures in the treatment of major depressive disorders. Regional differences between the effects of pinnate and corneal ECS on peptides and behavior support the idea that corneal ECS is a better model than pinnate ECS for human bitemporal ECT. 6. Together with recent results in other laboratories, our results suggest that a series of generalized seizures results in prolonged and increased release and action of TRH in limbic forebrain.
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PMID:TRH gene products are implicated in the antidepressant mechanisms of seizures. 783 67

Glycine blocked the anticonvulsant effects of felbamate on electroshock- and NMDA-induced seizures in mice. In contrast to its effects on felbamate, glycine either potentiated or had no effect on the anticonvulsant actions of phenytoin, valproate, carbamazepine and phenobarbital on electroshock seizures in mice. The data support that the glycine-felbamate blockade is a specific interaction. Felbamate is likely to be the first clinically available anticonvulsant drug that acts through this unique mechanism.
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PMID:Selective antagonism of the anticonvulsant effects of felbamate by glycine. 805 Apr 61


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