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Results for “METRAZOL”

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At least 73 records · Page 4Linked to original sources

PubMed1981

Effect of antiepileptic drugs on metrazol convulsions during ontogenesis in the rat.

The effect of ethosuximide, dipropylacetate and clonazepam on metrazol convulsions induced by a dose of 80 mg/kg was studied in 314 male albino rats aged from 5 days to adult. In a standard dose of 125 mg/kg, ethosuximide reliably protected only adult and 25-day-old rats, i.e. the age groups in which a mature minimal seizure was the only type of convulsion induced; in younger animals, not even a much higher dose (tested in 12-day-old rats) afforded reliable protection. Dipropylacetate and clonazepam had a manifest protective effect in all age groups, irrespective of the type of seizure. Isolated myoclonic jerks were less sensitive to antiepileptics and only dipropylacetate blocked them in the youngest age groups. In 21-day-old and older animals dipropylacetate induced stereotype head movement reminiscent of the serotonergic stereotypy described in the literature.

Age Factors↗

PubMed1983

Localization of the origin of metrazol-induced rhythmic electrocorticographic activity in rats.

In acute experiments we studied the structures essential for the genesis of rhythmic electrocorticographic activity composed of spike-and-wave rhythm of 5 Hz frequency evoked in rats by the systemic administration of pentamethylenetetrazol. Brain stem transection at intercollicular level did not prevent this rhythmic activity from developing. Episodes of this activity were suppressed during a wave of thalamic spreading depression--in every case on the side of depression and in more than half the cases also in the contralateral hemisphere. We further observed that the effect on rhythmic activity in the sensorimotor and visual region was unequal. It can be concluded that the thalamocortical system is essential for the development of rhythmic metrazol spike-and-wave activity, but that this system is not functionally homogeneous.

Animals↗

PubMed1980

Electrocorticographic activity elicited by metrazol during ontogenesis in rats.

Electrocorticographic changes induced by intraperitoneal injections of metrazol were studied in 72 male rats aged from 4 to 29 days. The initial paroxysmal signs varied according to age; 4- to 7-day-old rats: discharges of waves in the alpha and theta range; 11- to 20-day-old rats: spikes in the frontal area; rats aged 24 days and more: theta waves discharges (of about 5Hz) in the occipital area, i.e. a typical mature reaction. In 4- and 5-day-old rats, generalized seizures were manifested as slow waves only. A shift towards fast frequencies was observed during further development; a substantial part of this shift took place before the 14th day. After this age, bilateral synchrony of long-lasting seizure discharges was also present.

Aging↗

PubMed1993

Metrazole induces the sequential activation of c-fos, proenkephalin, and tyrosine hydroxylase gene expression in the rat adrenal gland: modulation by glucocorticoid and adrenocorticotropic hormone.

The immediate-early gene c-fos (a nuclear transcription factor) has been viewed as a nuclear "third messenger" or cellular "master switch." Both in vitro and in vivo studies have suggested that the proenkephalin (Penk) and tyrosine hydroxylase (TH) genes are potential targets of this immediate-early gene. We investigated the relationships between the activation of the c-fos gene and the activation of the Penk and TH genes in both rat hippocampus and adrenal using a commonly used model, metrazole (MTZ)-induced convulsions. The administration of MTZ produced a sequential elevation in c-fos, preproenkephalin (PPenk), and TH mRNAs. One hour after MTZ administration, c-fos mRNA was increased about 10-fold in rat hippocampus and about 5-fold in rat adrenal, without a significant change in spinal cord levels. Immunocytochemistry revealed that Fos-like immunoreactivity was greatly increased in both hippocampus and adrenal medulla at 3 hr after MTZ administration. The levels of PPenk and TH mRNAs were significantly increased (5-fold and 3-fold, respectively) in the adrenal 6 hr after MTZ treatment. The effects of MTZ on c-fos, PPenk, and TH mRNAs were dose dependent in both adrenal and hippocampus. In the adrenal, both the basal levels and the MTZ induction of PPenk mRNA were significantly attenuated by hypophysectomy (hypox) and were partially reinstated by adrenocorticotropic hormone (ACTH) replacement. In contrast, the basal levels of c-fos and TH mRNAs were not altered in hypox rat adrenal. ACTH treatment completely blocked the MTZ induction of adrenal c-fos mRNA and the subsequent induction of Fos-like immunoreactivity, whereas MTZ increased PPenk and TH mRNAs nearly 3-fold. Thus, in hypox rats MTZ can increase adrenal c-fos and TH mRNA levels without a corresponding increase in PPenk mRNA, whereas in ACTH-treated rats PPenk and TH mRNA levels in adrenal can be increased by MTZ without a preceding increase in c-fos mRNA. The MTZ induction of c-fos appears neither sufficient nor always necessary for the subsequent MTZ induction of Penk and TH gene expression. We conclude that c-fos, Penk, and TH genes can be differentially regulated in the adrenal of hypox rats or animals treated with ACTH, although they are co-localized in the same medullary cells.

Adrenal Glands↗

PubMed1950