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At least 19 recordsLinked to original sources
PubMedDate not supplied

Correlation between effects of acute acetazolamide administration to mice on electroshock seizure threshold and maximal electroshock seizure pattern, and on carbonic anhydrase activity in subcellular fractions of brain.

The relationships between inhibition of carbonic anhydrase (CA) activity in cytoplasmic, microsomal, and myelin subcellular fractions obtained from cerebral cortex, subcortex, and cerebellum and electroshock seizure threshold (EST) and modification of the extension/flexion (E/F) ratio following maximal electroshock seizures (MES) were ascertained in Swiss-Webster mice given 40 and 200 mg/kg acetazolamide. The parameters were determined at 1, 4, and 24 h after administration of acetazolamide. The results showed that changes in the E/F ratio induced by acetazolamide correlated linearly (r = 0.90) with changes in CA activity in the cytoplasm of the subcortex. However, there was an inverse power function correlation (r = 0.92) between EST and CA activity in the myelin fraction of the cerebral cortex. The time course of acetazolamide inhibition of CA activity in these two fractions also paralleled the time course of its effects on EST and E/F ratio. Thus, acetazolamide decreases susceptibility to seizures (raises EST) by inhibiting myelin CA and prevents spread of seizure activity by inhibiting CA in the cytoplasm of glial cells. The CO2 that accumulates as a result of CA inhibition in these two fractions causes profound changes in brain function.

Acetazolamide↗
PubMed2000

The lesional and epileptogenic consequences of lithium-pilocarpine-induced status epilepticus are affected by previous exposure to isolated seizures: effects of amygdala kindling and maximal electroshocks.

In temporal lobe epilepsy, the occurrence of seizures seems to correlate with the presence of lesions underlying the establishment of a hyperexcitable circuit. However, in the lithium-pilocarpine model of epilepsy, neuronal damage occurs both in the structures belonging to the circuit of initiation and maintenance of the seizures (forebrain limbic system) as in the propagation areas (cortex and thalamus) and in the circuit of remote control of seizures (substantia nigra pars reticulata). To determine whether or not we could protect the brain from lesions and epileptogenesis induced by status epilepticus and identify cerebral structures involved in the genesis of epilepsy, we studied the effects of the chronic exposure to non-deleterious seizures, either focalized with secondary generalization (amygdala kindling, kindled-pilocarpine rats), or primary generalized (ear-clip electroshocks, electroshock-pilocarpine rats) on neuronal damage and epileptogenesis induced by lithium-pilocarpine status epilepticus. These animals were compared to rats subjected to status epilepticus but not pretreated with seizures (sham-kindled-pilocarpine or sham-electroshock-pilocarpine rats). Compared to sham-pilocarpine rats, neuronal damage was prevented in the limbic system of the kindled-pilocarpine rats, except in the hilus of the dentate gyrus and the entorhinal cortex, while it was enhanced in rats pretreated with electroshocks, mainly in the entorhinal and perirhinal cortices. Most sham-kindled- and sham-electroshock-pilocarpine rats (92-100%) developed recurrent seizures after a silent period of 40-54days. Likewise, all kindled-pilocarpine rats developed spontaneous seizures after the same latency as their sham controls, while only two of 10 electroshock-pilocarpine rats became epileptic after a delay of 106-151days. The present data show that the apparent antiepileptic properties of electroshocks correlate with extensive damage in midbrain cortical regions, which may prevent the propagation of seizures from the hippocampus and inhibit their motor expression. Conversely, the extensive neuroprotection of the limbic system but not the hilus and entorhinal cortex provided by amygdala kindling does not prevent epileptogenesis. Thus, the hilus, the entorhinal and/or perirhinal cortex may be key structure(s) for the establishment of epilepsy.

Amygdala↗
PubMed1999

Electroshock seizures protect against apoptotic hippocampal cell death induced by adrenalectomy.

Seizures evoked by electroshock induce rapid changes in the expression of several genes in the adult brain, including those encoding for neurotrophic factors. Some of the neurotrophic factors induced by brief seizures such as basic fibroblast growth factor and nerve growth factor have been shown to have neuroprotective action. We reasoned therefore that these seizures may protect against neural injury. To test this hypothesis, we examined the effect of electroshock-induced seizures on the vulnerability to cell death in the hippocampus. Cell death was induced by adrenalectomy, which results in a highly selective apoptotic neuronal death in the dentate granule cell layer of the hippocampus. Daily electroshock seizures were administered for seven days to sham-operated and adrenalectomized rats. Neuronal degeneration was evaluated by the highly sensitive and reliable cupric-silver impregnation method. Animals experiencing electroshock seizures were completely protected against adrenalectomy-induced cell death, whereas adrenalectomized animals not exposed to electroshock seizures exhibited substantial neuronal cell degeneration in the dentate granule cell layer. Daily restraint stress did not prevent the adrenalectomy-induced neuronal death, indicating that the neuroprotective effect of the seizure treatment is not accounted for by stress. We conclude that brief controlled seizure-evoked neural activation may allow the sparing of otherwise vulnerable neuronal populations in the injured adult brain. This prompts a need to explore the possibility that controlled administration of electroshock seizures may have therapeutic potential in treating neurodegenerative disorders.

Adrenalectomy↗
PubMedDate not supplied

Electroshock- and pentylenetetrazol-induced seizures in genetically epilepsy-prone rats (GEPRs): differences in threshold and pattern.

Using facial and forelimb (F&F) clonus (a proposed forebrain marker) and running-bouncing (R/B) clonus and tonus (proposed brain-stem markers), the responsiveness of forebrain and brain-stem to electroshock or pentylenetetrazol seizures was assessed in GEPRs. The most striking finding was the failure of GEPR-9s to display F&F clonus in response to transcorneal electroshock at any stimulus intensity. Indeed, GEPR-9s displayed only R/B clonus or tonus indicative of brain-stem seizure discharge. GEPR-3s and normal rats, on the other hand, displayed F&F clonus in response to the least effective electroshock stimulus, and R/B clonus and tonus at higher stimulus intensities. After treatment with phenytoin (50 mg/kg) to inhibit the tonic seizure, the least effective electroshock stimulus also produced F&F clonus in GEPR-9s. These findings suggest that the threshold for triggering brain-stem seizure discharge by electroshock is lower than that for triggering forebrain seizure discharge in GEPR-9s, whereas the reverse relationship is true in normal rats and GEPR-3s. The rank ordering of the electroshock thresholds was: normals greater than GEPR-3s greater than GEPR-9s. Both GEPR-3s and GEPR-9s were found to be hyper-responsive to pentylenetetrazol as evidenced by shorter latency for the tonic seizure and a greater seizure severity than normal rats. The rank ordering of seizure severity in response to pentylenetetrazol was: GEPR-9 greater than GEPR-3 greater than normal rats.

Animals↗
PubMed1984

Inhibition of seizures induced by picrotoxin and electroshock by cholecystokinin octapeptides and their fragments in rats after intracerebroventricular administration.

The anticonvulsive activity of cholecystokinin octapeptide sulphate ester (CCK-8-SE), non-sulphated cholecystokinin octapeptide (CCK-8-NS) and three different N- and C-terminal fragments were investigated against seizures induced by picrotoxin and electroshock in rats after intracerebroventricular administration. Doses of 0.8 and 80 pmol of CCK-8-SE and CCK-8-NS significantly enhanced the latency of seizures induced by picrotoxin and shortened the duration of the clonic phase of the seizures induced by electroshock. Only CCK-8-SE shortened the recovery time and only 0.8 pmol of CCK-8-SE could shorten the duration of the tonic phase of convulsions induced by electroshock. Doses of the octapeptides of 8000 pmol were ineffective, with the exception of CCK-8-NS in the picrotoxin test. Of the fragments tested, the C-terminal tetrapeptide, CCK-5-8, enhanced the latency of seizures induced by picrotoxin in a dose of 0.8 pmol, and had a dose-dependent biphasic effect on the duration of the clonic phase of seizures induced by electroshock. Intracerebroventricular administration of diazepam enhanced only the latency of tremor and clonic seizures induced with picrotoxin in a dose of 40 nmol. Twelve nmole of diazepam shortened the clonic phase of convulsions induced by electroshock. The peptides tested were much more active than diazepam, and their effective doses were comparable to the amounts of cholecystokinin octapeptide found in brain structures.

Animals↗
PubMed1985

Dexamethasone differentially alters naltrexone effects on vasopressin and oxytocin release during tail electroshock.

The origin of endogenous opioid peptides that inhibit release of vasopressin (VP) and oxytocin (OT) into the bloodstream after tail electroshock was investigated. We hypothesized that endogenous opioid peptides derived from the anterior pituitary reduced secretion of VP and OT during this stimulus. To test this hypothesis, dexamethasone (DEX) was used to preferentially suppress release of endorphins with ACTH from the anterior pituitary. We evaluated the effects of an opiate receptor antagonist, naltrexone, on the rise in plasma [VP] and [OT] after tail electroshock in male Sprague-Dawley rats given DEX either chronically or acutely before the shock. In the chronic study rats were injected SC daily with saline (3.2 ml/kg) or DEX (0.2 mg/kg) for 17 days. In the short term study, rats were injected IP with saline (5 ml/kg) or DEX (0.5 mg/kg) the day before and again 105 min prior to tail electroshock. Thirty min (chronic study) or 90 min (acute study) after saline or DEX was given on the last day, rats were injected SC with saline (1 ml/kg) or naltrexone (1 mg/kg). Fifteen min later, animals received tail electroshock (41 V, 30 sec) and were decapitated 15 sec after shock was completed. Control animals were treated similarly but not shocked. Amounts of VP and OT in plasma and the neurointermediate lobe were quantified by RIA. [VP] and [OT] were elevated in plasma of all rats given tail electroshock. Greater increases (p less than 0.05) in hormone concentrations were measured in plasma of shocked rats treated with DEX.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗