Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study the relationship between seizures and the thyrotropin-releasing hormone (TRH) neural system, immunoreactive TRH (IR-TRH) and TRH receptor binding activity were determined by pentylenetetrazol (PTZ)-induced seizures and amygdaloid (AM) kindling. IR-TRH markedly increased in the septum 40 and 150 seconds after the PTZ injection. A significant increase in the IR-TRH concentrations was also noted in the hippocampus and thalamus/midbrain 40 and 150 seconds after the PTZ injection, respectively. However, no significant changes were observed in the TRH receptor binding before, during or after the PTZ-induced seizures. In addition, a lasting change in the striatal TRH receptors after AM kindling as well as a transient IR-TRH increase in the limbic structures were seen 48 hours after Am-kindled convulsions. TRH and its analog (DN-1417) inhibited PTZ-induced generalized seizures dose-dependently. These findings indicate the involvement of the TRH neural system in seizure mechanisms, and suggest that endogenous TRH may be an antiepileptic substance in the brain.
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PMID:Seizures and thyrotropin-releasing hormone (TRH) neural system in the rat brain. 393 40

The diverse behavioral and biochemical effects induced by ethanol suggest that ethanol exerts differential effects on the CNS. When the neuroactive amino acids, glycine, glutamate, aspartate, GABA and taurine, were measured in the cortex, striatum, hippocampus, midbrain, and brain stem of acute or chronic ethanol-treated rats, site specific changes were observed for glutamate, glycine, and aspartate. No changes were found for GABA or taurine. Upon in vivo application, it was found that the microinjection of thyrotropin-releasing hormone (TRH, 500 ng) into the medial septum significantly shortened ethanol's impairment of the righting reflex, while microinjection of muscimol (30 ng) markedly potentiated ethanol's impairment of the righting reflex. When these studies are combined with previous work showing that microinjection of muscimol (30 ng) into the inferior colliculus blocks audiogenically induced seizures in ethanol-withdrawn rats, the convergence implies that specific sites in the CNS may modulate certain actions of ethanol. Therefore, we propose that the medial septum and inferior colliculus can be used as in vivo models to study the acute and chronic actions of ethanol, respectively.
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PMID:Evidence for site specific ethanol actions in the CNS. 393 88

Plasma prolactin, growth hormone, cortisol, luteinising-hormone-releasing hormone (LHRH), thyrotropin-releasing hormone (TRH), and nicotine and oestrogen stimulated neurophysin (NSN and ESN) were measured before and for 6 min after electroconvulsive therapy (ECT) in eight women with severe electroconvulsive therapy (ECT) in eight women with severe depression. Plasma concentrations of NSN and ESN had increased significantly (as much as 10-fold for NSN) within 1 min of the seizure, and concentrations of prolactin had increased within 2-4 min after the seizure. Whereas plasma prolactin and ESN either continued to increase or remained raised throughout the 6 min after seizure, the concentrations of NSN fell to reach a value at 6 min that was approximately 50% of the maximum. There were no increases in any of the other hormones or peptides within the 6 min period under study. Thus ECT has selective effects on hormone release which cannot be attributed simply to a generalised release of pituitary or hypothalamic hormones in response to brain stimulation and/or stress.
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PMID:Immediate increases in plasma prolactin and neurophysin but not other hormones after electroconvulsive therapy. 612 44

Ethanol (2.0-5.0 g/kg, IP) caused a dose-related impairment of the aerial righting reflex of mice 60 min after injection. Ethanol (3.5 g/kg, IP) given simultaneously with neurotensin (30 micrograms, IC), bombesin (30 micrograms, IC) or beta-endorphin (20 micrograms, IC) caused a greater impairment of the reflex than ethanol alone. Simultaneous treatment with ethanol (4.0 g/kg, IP) and thyrotropin-releasing hormone (TRH, 3.0-30 micrograms, IC) caused less impairment of this measure than ethanol alone. None of the peptides altered the height of aerial righting when administered alone, or when administered with ethanol no peptide altered blood or brain ethanol content. Unexpectedly, TRH (20 and 40 mg/kg, IP) potentiated the action of ethanol by increasing punished licking in water-deprived rats, rather than antagonizing this acute action of ethanol. Like ethanol (1.0 and 2.0 g/kg, IP), beta-endorphin (100 micrograms, IC) suppressed ethanol-withdrawal tremor and audiogenic-seizure susceptibility in ethanol-dependent rats. beta-Endorphin (1 microgram) and bombesin (10 and 30 micrograms, IC) reduced only audiogenic-seizure susceptibility. TRH (10-100 micrograms, IC, or 1-40 mg/kg, IV) and neurotensin (10-100 micrograms, IC) had no effect on these ethanol-withdrawal signs. These findings suggest that centrally active peptides may play a role in certain acute and chronic actions of ethanol. Because TRH, neurotensin, bombesin and beta-endorphin do not alter all actions of ethanol in the same way, an interaction of ethanol with many functionally independent neuronal circuits is suggested.
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PMID:Modification of the actions of ethanol by centrally active peptides. 626 62

The comparative antiepileptic effects of the thyrotropin-releasing hormone and its new derivative, gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide citrate (DN-1417), were examined in feline amygdaloid kindling preparations. When tested in kindled animals, both agents showed a transient and non-dose-dependent anticonvulsant effect, in addition to raising the generalized convulsive seizure-triggering threshold for a prolonged period of time. Furthermore, DN-1417 exerted a significant effect on postictal events: shortening the electrographic silence, leaving the duration of slow activity intact, while prolonging the period of seizure refractoriness. When tested in kindling animals, DN-1417 showed a significant but non-dose-dependent prophylactic effect on both primary and secondary amygdaloid sites.
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PMID:Antiepileptic effects of thyrotropin-releasing hormone and its new derivative, DN-1417, examined in feline amygdaloid kindling preparation. 643 94

The efficacy of thyrotropin-releasing hormone in children with intractable epilepsy was investigated and changes in cerebrospinal fluid monoamine metabolites were analyzed. The 18 patients had either West syndrome (12 patients) or Lennox-Gastaut syndrome (6 patients), which was intractable to antiepileptic drug therapy and to adrenocorticotrophic hormone. Thyrotropin-releasing hormone-tartrate was administered for 4 weeks. Before and after the thyrotropin-releasing hormone administration, cerebrospinal fluid was collected and analyzed for 5-hydroxyindoleacetic acid, kynurenine, homovanillic acid, and 3-methoxy-4-hydroxyphenyl glycol. The patients were classified into 3 groups, based on seizure frequency and electroencephalographic effects: cessation of seizures and seizure discharges (very effective; group A), reduction of seizures and/or seizure discharges (effective; group B), and no changes in frequency of seizures or discharges (not effective; group C). There were 6 patients in group A, 3 in group B, and 9 in group C. There were no significant differences in monoamine metabolites before and after the thyrotropin-releasing hormone therapy. A trial of thyrotropin-releasing hormone for the treatment of intractable epilepsy is warranted and further study is required on the mechanism of the antiepileptic action of thyrotropin-releasing hormone.
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PMID:Thyrotropin-releasing hormone in treatment of intractable epilepsy: neurochemical analysis of CSF monoamine metabolites. 754 12

A male infant with early infantile epileptic encephalopathy (EIEE) was reported. Tonic spasms in series appeared since 1 month after birth and EEG showed a typical suppression-burst pattern. The patient was treated with a high-dose pyridoxal phosphate and thyrotropin-releasing hormone (TRH), but seizures were not controlled. ACTH was administered and the seizures disappeared transiently. The seizures reappeared during tapering ACTH and apparent cerebral shrinkage followed the ACTH therapy. Then, the patient who evolved into West syndrome was treated with ketogenic diet. The seizures disappeared immediately and EEG findings were improved. It is suggested that the ketogenic diet should be tried early for the treatment of EIEE.
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PMID:[Effect of the ketogenic diet for West syndrome into which early infantile epileptic encephalopathy with suppression-burst was evolved]. 757 84

Male epileptic patients frequently complain of sexual dysfunction, particularly impotence and loss of libido. Epilepsy itself, antiepileptic drugs (AEDs), and psychosocial factors are believed to contribute to impaired sexuality. We studied luteinizing hormone (LH) pulsatile secretion, gonadotropin, and prolactin (PRL) responses to LH-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) in 37 adult male epileptic patients receiving AED monotherapy who were seizure-free and had normal EEGs. Sexuality was assessed by psychological interview. Impotence was diagnosed in 8 patients (in 2 combined with loss of sexual desire). The occurrence of hyposexuality (approximately 20%) was independent of epilepsy syndrome or AED. No change in total testosterone (T) level was observed. Free T (fT) and dihydrotestosterone (DHT) levels were lower and sex hormone binding globulin (SHBG) levels were higher in epileptic subjects than in healthy controls, but a statistically significant difference was not observed between hypo- and normosexual patients. In impotent epileptic patients, estradiol (E2) levels were significantly increased as compared with those of patients with preserved sexuality and of healthy controls. The unbalanced relation between androgen and E2 levels was emphasized by decreased T/E2, fT/E2, and DHT/E2 ratios obtained in hyposexual epileptic patients. In this group, LHRH induced blunted LH peaks. No changes were noted in LH pulsatility features. These findings of higher E2 levels and of decreased LH response to LHRH administration in some epileptic patients with impaired sexuality, may suggest they have subclinical hypogonadotropic hypogonadism.
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PMID:Sex hormones and pituitary function in male epileptic patients with altered or normal sexuality. 760 14

We produced limbic status epilepticus in rats by injecting a combination of dibutyryl-cAMP (db-cAMP) and ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM). Thirty minutes after intra-AM db-cAMP/EDTA injection, thyrotropin-releasing hormone (TRH) was administered intravenously or intracerebroventricularly. Intravenous TRH (3, 25, 50 mg/kg) produced immediate activation of electroclinical seizures, lasting for 25-45 min. In some animals which showed this seizure activation, complete seizure suppression occurred 55-70 min after the TRH treatment. Similar activation of ictal seizures with delayed seizure suppression was obtained after intracerebroventricular TRH (25, 50 micrograms). The findings suggest that the effects of intravenous TRH are due to its central action and that the use of intravenous TRH is not a promising approach for the treatment of status epilepticus.
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PMID:The effect of thyrotropin-releasing hormone (TRH) on limbic status epilepticus in rats. 780 43

Tolerance to carbamazepine's anticonvulsant effects on amygdala kindled seizures occurs contingently, that is, only when carbamazepine is given prior to, but not after the seizure occurs. Biological correlates of contingent tolerance were examined using in situ hybridization and receptor binding techniques for thyrotropin-releasing hormone (TRH) mRNA and TRH receptor binding. Rats were fully kindled and given daily injections of carbamazepine (15 mg/kg, i.p.) either 15 min before (CBZ-before) or after (CBZ-after) amygdala stimulation until the CBZ-before rats became tolerant. Kindled rats were matched so that the two groups had an equal number of seizures and doses of CBZ. Three other groups were also used for comparison: kindled rats that received vehicle injections, and sham-kindled animals treated with either vehicle or CBZ. Rats were sacrificed 4 h after the last seizure or sham stimulation. Both sham-kindled rat groups had barely detectable levels of TRH mRNA. In the CBZ-after (non-tolerant) and vehicle-kindled rats, TRH mRNA levels were increased in the dentate gyrus, pyriform, entorhinal, and perirhinal cortices. In contrast to the other kindled animals, the CBZ-before rats (tolerant) had dramatically diminished TRH mRNA levels bilaterally in the dentate gyrus and pyriform cortex, and ipsilateral to the stimulation in the entorhinal cortex. Decreases in TRH receptor binding were demonstrated autoradiographically in the dentate gyrus and perirhinal cortex in all of the kindled groups with no differences between tolerant and non-tolerant rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contingent tolerance to carbamazepine: alterations in TRH mRNA and TRH receptor binding in limbic structures. 792 72


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