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)

It is now a recognized principle that various neuropeptides are neuronally co-localized with biogenic amine or aminoacid neurotransmitters. In the rat CNS it has previously been shown that TRH is co-localized with 5-HT (and also with substance P) in cell bodies of the posterior raphe that project to the spinal cord. Although TRH cell bodies are known to be widely distributed throughout the forebrain there is no other known co-localization with 5-HT. In this study we further specify the forebrain there is no other known co-localization with 5-HT. In this study we further specify the anatomical relationship of TRH with 5-HT by use of surgical and neurotoxic lesioning with reference to limbic forebrain regions wherein TRH is greatly increased following seizures. In groups of rats, the fimbria-fornix was lesioned alone, or combined with a lesion of the dorsal perforant path or the ventral perforant path. There was a sham lesioned control group. Additional groups were lesioned with 5,7 dihydroxytryptamine, 100 micrograms i.v.t., 45 min. after i.p. desipramine, 25 mg/kg. All rats were sacrificed three weeks after lesions. Indoleamines were determined by HPLC in left anterior cortex, left pyriform/olfactory cortex, left dorsal hippocampus and left ventral hippocampus. TRH was determined by specific RIA in the corresponding right brain regions. The modal n was 7 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Some regional anatomical relationships of TRH to 5-HT in rat limbic forebrain. 138 39

There is an international consensus on the indications of electroconvulsive treatment (ECT): they result in particular from the limitations of antidepressant drug treatment. Even though the global effect of ECT is considered as satisfactory, 10 to 20% of depressed patients eligible for ECT are treatment refractory. This warrants a search for factors predicting efficacy or lack of efficacy of ECT. Predicting factors prior to ECT: Usual clinical criteria, such as the presence of delusional thoughts, are generally classified with endogenous signs of depression. Among biological criteria, EEG data, tests assessing reactivity of autonomous nervous system, plasma measures of catecholamines, calcium and cortisol do not seem relevant parameters. Dexamethasone suppression test and stimulation of TSH by TRH have no more predictive value. Predictive indices during treatment: Empirically clinicians identified a sequence in the response of depressive symptoms, although no conclusion can be drawn from these clinical impressions. Among biological factors some authors stress the importance of the epileptogenic threshold and of measuring plasma levels of peptides released by the posterior lobe of hypophysis. Such data have to be confirmed and their physiopathological value better understood. Actually some parameters representing good therapeutic practices are valued by physicians using ECT: sufficient duration of electrical crisis, total seizure time during the series of electroshocks. Those conceptions are close to the classical emphasis on the adequate number of ECTs and to the discussion on the comparative efficacy of unilateral and bilateral ECT. After ECT most authors shift to antidepressants, although data about medium and long term outcome prediction with this approach are also lacking.
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PMID:[Predictive factors of response to electronarcosis]. 180 65

Effects of YM-14673 (N alpha-[( (S)-4-oxo-2-azetidinyl]-carbonyl]-L- prolinamide dihydrate), a new TRH analogue, on the development of kindling and the duration of afterdischarge (AD) were observed in amygdaloid-kindled rats in comparison with those of TRH. The right medial amygdaloid nucleus was electrically stimulated once a day for establishment of kindling. YM-14673 and TRH were administered intraperitoneally 15 and 30 min prior to electrical stimulation from 2 days after the first stimulation, respectively, and the number of stimulations required for the development of generalized seizures was measured. YM-14673 (1 mg/kg) showed tendency to suppress the development of kindling (p less than 0.1), but TRH even at high dose (10 mg/kg) showed little effect on it. In addition, the experiment for the AD duration was conducted in full-kindled rats from one day after at least 3 reproducible generalized seizures were elicited by electrical stimulation of the medial amygdaloid nucleus once a day. Both YM-14673 (1 mg/kg) and TRH (10 mg/kg) administered 15 and 30 min prior to electrical stimulation of the amygdala, respectively, significantly shortened the AD duration in full-kindled rats. At these doses, both drugs desynchronized spontaneous cortical electroencephalogram (EEG) in normal rats. These results indicate that YM-14673 seems to possess anticonvulsive property in rats.
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PMID:Anticonvulsive properties of YM-14673, a new TRH analogue, in amygdaloid-kindled rats. 206 5

In a previous study we reported significant elevations of TRH in neocortex, hippocampus and combined amygdala/pyriform cortex in rats 48 h after the last of a series of stage 5 kindled seizures. In the present study, to determine whether the increases in TRH were proportional to the intensity of the convulsions, and the degree of development of the kindling process, we compared the effects of partially kindled (stage 2) vs fully kindled (stage 5) seizures. As a further refinement, we examined separately the TRH responses in the pyriform, cingulate and frontal cortices. The responses were especially marked in the pyriform cortex, where TRH increased 7-fold after stage 5 kindled convulsions, compared with 2-fold increases after stage 2-3 seizures. Increases were seen in other cortical regions, as well, but only after stage 5 seizures. These findings are consistent with reports suggesting that the increases in brain TRH occurring after convulsions are aftereffects of the seizures, possibly representing homeostatic anticonvulsant responses, and that the pyriform cortex is a site that is uniquely activated by convulsions.
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PMID:Elevated TRH levels in pyriform cortex after partial and fully generalized kindled seizures. 212 20

Serum cortisol, prolactin (PRL), TSH, GH, LH and FSH levels were measured before and immediately after daily ACTH-Z therapy (0.01 mg/kg/day, 1-2 weeks) for 5 patients with infantile spasms and one patient with myoclonus epilepsy. Total number of ACTH-Z therapy were 8 times, and all patients became seizure free after ACTH-Z therapy. In 6 occasions, TRH, LH-RH and insulin tolerance tests were performed before and after daily ACTH-Z therapy. Serum cortisol levels were significantly increased after daily ACTH-Z therapy but all other hormone levels were significantly decreased. In TRH and LH-RH tolerance tests, peak levels and increments of PRL, LH and FSH were significantly decreased after daily ACTH-Z therapy and those of TSH were mildly decreased. In one case insulin tolerance test revealed an adequate decrease of blood glucose before and after ACTH-Z therapy, and there was a poor GH response after ACTH-Z therapy. Daily ACTH-Z therapy was thought to suppress secretion of anterior pituitary hormones.
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PMID:[Changes in anterior pituitary function during ACTH therapy of patients with infantile spasms]. 280 96

The present study showed that DN-1417 had a dose-dependent anticonvulsant activity on El mouse seizure. This finding is consistent with other reports using the kindling model of epilepsy. Since both the El mouse and kindling preparations have been regarded as complex partial seizure with secondary generalization, endogenous brain TRH, as well as exogenous TRH, may act as an anticonvulsant substance to such a seizure type of epilepsy. Moreover, this study showed IR-TRH of the El mouse changed significantly in the striatum or hippocampus genetically or postictally without a change in the TRH receptor binding. A transient decrease in hippocampal IR-TRH after convulsion shown in this study may suggest an increased release of TRH during and after the seizure. Further studies are required to clarify the relationship between a change in the brain TRH system and seizure susceptibility in the El mouse.
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PMID:Changes in brain thyrotropin-releasing hormone (TRH) of El mice. 283 94

We investigated effects of TRH on glutamate-induced seizures in rats. Rats were injected intraperitoneally with sodium glutamate in a dose (22.3 mmole/kg) equivalent to ED95 for generalized convulsions. Twenty five min later TRH in a dose of maximum effect (40 micrograms in the tartrate form) was injected intracerebroventricularly in order that the time of peak effect was simultaneous with the onset of seizure which was anticipated from the preliminary study. TRH delayed the onset of initial seizures significantly, though neither occurrence nor incidence of various seizure activities was affected. A trend of delay in the mean time of death was also observed. These results suggest that TRH has an inhibitory action against glutamate-induced seizures in rats, albeit mild.
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PMID:Effects of thyrotropin releasing hormone (TRH) on glutamate-induced seizures in rats. 288 80

We assessed the acute effects of various drugs on amygdaloid kindled seizures induced with low-frequency stimulations. We used the number of stimulating pulses required for the induction of epileptic afterdischarge (pulse-number threshold; PNT) as an indicator of the seizure generating threshold and the duration of induced seizures (AD duration; ADD) as an indicator of the seizures. TRH increased the PNT without affecting the ADD at a high dose (1.2 mg/kg). Flunarizine decreased the PNT and ADD simultaneously at a high dose (50 mg/kg). Lithium increased the PNT without affecting the ADD at two doses (100 mg/kg, 200 mg/kg). Zotepine decreased the PNT without affecting the ADD at two doses (8 mg/kg, 16 mg/kg). We propose that the technique of low-frequency kindling is a useful experimental model in assessing the effects of antipsychotic or antiepileptic drugs on the excitability of the limbic regions.
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PMID:Acute effect of TRH, flunarizine, lithium and zotepine on amygdaloid kindled seizures induced with low-frequency stimulation. 289 77

A large pituitary tumour was discovered in a 20 year old man who came to medical attention because of grand-mal seizures. The tumour produced biologically active LH as demonstrated by supranormal plasma LH and plasma testosterone values. Free alpha-subunit values were also elevated. In contrast, plasma FSH was in the lower normal range. Transsphenoidal operation failed to remove all tumour tissue. Detailed studies were carried out in the postoperative period. TRH and GnRH administration were associated with a rise of plasma LH and alpha-subunit, whereas plasma FSH was low and unresponsive. Bromocriptine treatment was ineffective. In contrast, both during and after treatment with SMS 201-995 for 6 weeks, a decrease of basal plasma LH values was observed. Furthermore, the administration of a single dose of SMS 201-995 reproducibly induced a decrease of plasma LH lasting for a period of about 6 h. The study suggests that SMS 201-995 may be useful in the treatment of patients with gonadotrope cell adenomas.
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PMID:Response of luteinizing hormone secreting pituitary adenoma to a long-acting somatostatin analogue. 289 40

We report here an autopsy case, an 8-year-old boy diagnosed as having infantile striatal necrosis, characterized by a preceding febrile illness followed by acute encephalopathy with abrupt obtundation, seizures and dystonia, with remarkable improvement of the disturbed consciousness and intelligence after TRH-T therapy. These clinical symptoms were linked with bilateral necrosis of the striata on CT scanning. The presented case belonged to a newly described subgroup of the heredogenous disorders that produce necrosis of the putamina in children.
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PMID:A case report of infantile striatal necrosis with an acute onset. 310 77


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