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E A Cavalheiro

Publications and source records attributed to E A Cavalheiro.

At least 37 records · Page 2Linked to original sources

Ricinine-elicited seizures. A novel chemical model of convulsive seizures.

The present investigation introduces ricinine-elicited seizures as a novel chemical model of convulsive seizure. Ricinine, a neutral alkaloid obtained from the plant Ricinus communis, induces seizures when administered to mice at doses higher than 20 mg/kg. Animals presenting seizures showed a marked preconvulsive phase followed by short duration hind limb myoclonus, respiratory spasms, and death. The lethal nature of ricinine seizures is also pointed out as a good model to study the events causing death in clonic seizures, particularly those related to respiratory spasms, which are also observed in some types of human epilepsy. The behavioral signs of ricinine-elicited seizures are accompanied by electrographic alterations more evident during the preconvulsive phase in the cerebral cortex and more intense during the ictal phase both in the cortex and in the hippocampus. The ricinine-elicited seizures may be inhibited by diazepam but not by phenobarbital, phenytoin, or ethosuximide. Micromolar concentrations of ricinine cause a small decrease in the binding of [3H]-flunitrazepam to cerebral cortex membranes, but do not alter the binding of other radioligands to AMPA, 5-HT(1A), muscarinic, and alpha(1)-adrenergic receptors. Although ricinine presents a cyanide radical, only higher doses of ricinine (4 mM) caused a small impairment of mitochondrial respiration. These results suggest that the mechanism of action of ricinine probably involves the benzodiazepine site in the GABA(A) receptor. This may represent a new mechanism of drug-elicited seizures that may contribute to a better understanding of epilepsy and to new therapeutic approaches to this disease.

Alkaloids↗

Epileptogenesis in immature rats following recurrent status epilepticus.

Strong evidences link status epilepticus (SE) in childhood with the later development of epilepsy. Pilocarpine-induced SE in developing rats leads to late appearance of spontaneous epileptic seizures only when SE is induced after the 18th day of life. We examined the possibility that 3 consecutive episodes of pilocarpine-induced SE on postnatal days 7, 8 and 9 could induce behavioral, electrographic and histological epileptic changes in adult life. The animals also underwent behavioral tests (inhibitory step-down avoidance, skinner box, rota-rod, open field and elevated plus-maze). EEG recordings made at the age of 30, 60 and 90 days showed the occurrence of several episodes of spikes and/or polyspikes appearing simultaneously in hippocampus and cortex. Only three isolated spontaneous seizures were observed during the whole period of observation (120 days). The long-term effects of three consecutive episodes of SE include increased spontaneous exploratory activity, learning impairment, and reduced anxiety when tested on P60. Our findings provide evidence for EEG changes and cognitive deficits in adult life following recurrent SE on postnatal days 7-9.

Age Factors↗

Changes in synaptosomal ectonucleotidase activities in two rat models of temporal lobe epilepsy.

Adenosine has been proposed as an endogenous anticonvulsant which can play an important role in seizure initiation, propagation and arrest. Besides the release of adenosine per se, the ectonucleotidase pathway is an important metabolic source of extracellular adenosine. Here we evaluated ATP diphosphohydrolase and 5'-nucleotidase activities in synaptosomes from hippocampus and cerebral cortex at different periods after induction of status epilepticus (SE) by intraperitoneal administration of pilocarpine or kainate. Ectonucleotidase activities from synaptosomes of hippocampus and cerebral cortex of rats were significantly increased at 48-52 h, 7-9 days and 45-50 days after induction of SE by pilocarpine. In relation to kainate model, both hippocampal enzymes were enhanced at 7-9 days and 45-50 days, but only 5'-nucleotidase remained elevated at 100-110 days after the treatment. In cerebral cortex, an increase in ATP diphosphohydrolase was observed at 48-52 h, 7-9 days and 45-50 days after induction of SE by kainate. However, 5'-nucleotidase activity only presented significant changes at 45-50 and 100-110 days. Our results suggest that SE can induce late and prolonged changes in ectonucleotidases activities. The regulation of the ectonucleotidase pathway may play a modulatory role during the evolution of behavioral and pathophysiological changes related to temporal lobe epilepsy.

5'-Nucleotidase↗

Multiple pilocarpine-induced status epilepticus in developing rats: a long-term behavioral and electrophysiological study.

PURPOSE: Animal models are useful for the study of status epilepticus (SE)-induced epileptogenesis and neurological sequelae, especially during early brain development. Here, we show several permanent abnormalities in animals subjected to multiple SE during early development. METHODS: Wistar pup rats (7 to 9 days old) were subjected to three consecutive episodes of SE induced by systemic pilocarpine injections. To study the long-lasting consequences of early-induced SE. chronic electroencephalographic recordings were made from the hippocampus and cortex and several behavioral tests (inhibitory step-down avoidance, rota-rod, open field, elevated plus-maze, and Skinner box) were performed at postnatal days 30 to 90. We also investigated in vitro electrophysiological responses of the CA1 area using extracellular recordings in hippocampal slices. A histological analysis was done using cresyl violet staining 24 hours and several months after SE induction. Apoptotic cell death was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL staining) 24 hours after the last SE episode. RESULTS: Electroencephalographic recordings from 30- to 90-day-old rats that had been subjected to multiple SE episodes in early life showed marked changes compared with those from nontreated controls. These included frequent episodes of continuous complex spiking activity and high-voltage ictal discharges, with a small percentage of these rats presenting spontaneous behavioral seizures. These animals also presented evidence of severe cognitive deficit in adulthood. In vitro, a persistent hyperexcitability of the CA1 area was detected in experimental animals. Histological analysis of the brains did not reveal any major long-term pathological changes. Nevertheless, an increased number of TUNEL-positive nuclei were present in some animals in both the hippocampus and the thalamus. CONCLUSIONS: These data show persistent abnormalities in animals subjected to multiple SE episodes during early postnatal development. SE may result in important plastic changes in critical periods of brain maturation leading to long-lasting epileptogenesis, as manifested by electrographic epileptiform discharges, behavioral deficits, and in vitro hyperexcitability of hippocampal networks.

Age Factors↗

Catecholamine response to exercise in individuals with different levels of paraplegia.

The purpose of this study was to investigate the effect of the level of injury on the serum level of norepinephrine (Nor) and epinephrine (Epi) at rest and after maximal exercise in individuals with paraplegia. Twenty-six male spinal cord-injured subjects with complete paraplegia for at least 9 months were divided into two groups of 13 subjects each according to the level of injury, i.e., T1-T6 and T7-T12. Serum Nor and Epi concentrations were measured by HPLC-ECD, at rest (PRE) and immediately after a maximal ergospirometric test (POST). Statistical analysis was performed using parametric and non-parametric tests. Maximal heart rate, peak oxygen uptake, and PRE and POST Nor were lower in the T1-T6 than in the T7-T12 group (166 +/- 28 vs 188 +/- 10 bpm; 18.0 +/- 6.0 vs 25.8 +/- 4.1 ml kg(-1) min(-1); 0.54 +/- 0.26 vs 0.99 +/- 0.47 nM; 1.48 +/- 1. 65 vs 3.07 +/- 1.44 nM). Both groups presented a significant increase in Nor level after exercise, while only the T7-T12 group showed a significant increase in Epi after exercise (T1-T6: 0.98 +/- 0.72 vs 1.11 +/- 1.19 nM; T7-T12: 1.24 +/- 1.02 vs 1.89 +/- 1.57 nM). These data show that individuals with paraplegia above T6 have an attentuated catecholamine release at rest and response to exercise as compared to subjects with injuries below T6, which might prevent a better exercise performance in the former group.

Adolescent↗

Selective alterations of glycosaminoglycans synthesis and proteoglycan expression in rat cortex and hippocampus in pilocarpine-induced epilepsy.

Proteoglycans and glycosaminoglycans are elements of matrix. In the nervous system, glycosaminoglycans modulate neurite outgrowth and are co-receptors for growth factors playing a crucial role in cell differentiation and synaptogenesis. The receptor of protein tyrosine phosphatase beta (RPTPbeta) is a chondroitin sulphate proteoglycan which plays an important role in neural morphogenesis and axon guidance mechanisms. Pilocarpine-treated rats present status epilepticus, which is followed by a seizure-free period (silent), by a period of spontaneous recurrent seizures (chronic), and the hippocampus of these animals exhibits cell loss and mossy fiber sprouting. Thus, the synthesis of heparan sulphate and chondroitin sulphate and the time course of RPTPbeta immunoreactivity were studied in the hippocampus and cerebral cortex during these phases of pilocarpine-induced epilepsy. The results showed decreased synthesis of heparan sulphate during the acute phase and an increased synthesis of chondroitin sulphate during the silent period in the cortex and hippocampus. In control rats RPTPbeta immunoreactivity was detected only in glial cells. After 6 h of status epilepticus the RPTPbeta immunoreactivity was no longer detectable in the glial cells in both tissues and intense staining became evident in the matrix, surrounding CA3 and dentate gyrus and piriform cortex neurones. In the silent and chronic periods RPTPbeta immunoreactivity was mainly detected in neuronal somata and fibers of neurones of hippocampus and cortex. These changes show a selective variation of synthesis and expression of glycosaminoglycans and RPTPbeta in relation to epilepsy suggesting a molecular interplay between glia and neurones during seizures.

Animals↗

Growth-associated phosphoprotein expression is increased in the supragranular regions of the dentate gyrus following pilocarpine-induced seizures in rats.

Neuroplasticity has been investigated considering the neuronal growth-associated phosphoprotein as a marker of neuronal adaptive capabilities. In the present work, studying the hippocampal reorganization observed in the epilepsy model induced by pilocarpine, we carried out quantitative western blotting associated with immunohistochemistry to determine the distribution of growth-associated phosphoprotein in the hippocampus of rats in acute, silent and chronic periods of this epilepsy model. The fibers and punctate elements from the inner molecular layer of the dentate gyrus were strongly immunostained in animals killed 5 h after status epilepticus, compared with the same region in control animals. Rats presenting partial seizures showed no alterations in the immunostaining pattern compared with saline-treated animals. The hippocampal dentate gyrus of animals during the seizure-free period and presenting spontaneous recurrent seizures was also characterized by strong growth-associated phosphoprotein immunostaining of fibers and punctate elements in the inner molecular layer, contrasting with the control group. As determined by western blotting analysis, growth-associated phosphoprotein levels increased following status epilepticus and remained elevated at the later time-points, both during the silent period and during the period of chronic recurring seizures. Pilocarpine-treated animals, which did not develop status epilepticus, showed no change in growth-associated phosphoprotein levels, indicating that status epilepticus is important to induce growth-associated phosphoprotein overexpression. The measurement of this overexpression could represent one of the early signals of hippocampal reorganization due to status epilepticus-induced damage.

Animals↗

The course of untreated seizures in the pilocarpine model of epilepsy.

The course of untreated epilepsy is not well established. This study uses a model of chronic limbic epilepsy (pilocarpine model of epilepsy) to determine the pattern of occurrence of seizures in untreated animals. Following pilocarpine administration, 21 rats were monitored continuously with a video system for 135 days after the first spontaneous seizure. Animals showed a great variability in seizure numbers and were divided in two subgroups presenting either a low frequency of seizures (n = 9 animals presenting ten or less seizures in the first 15 days of observation) or a high frequency of seizures (n = 12 animals presenting more than ten seizures during this period). Animals with low number of seizures during the first 15 days of observation showed a significant increase in seizure frequency in the following period of analysis (until 105 days). On the other hand, those with initial high number of seizures showed significant changes in seizure frequency only in the first 2 months. The duration of each spontaneous seizure did not change significantly over time. These findings show that in untreated epilepsy there is a maturation process in the early stages and this accelerating process can be of predictive value for the treatment of epilepsy.

Animals↗

Effect of physical exercise on seizure occurrence in a model of temporal lobe epilepsy in rats.

Although the favorable effect of physical fitness on general health is unquestionable, physical exercise and fitness programs in patients with epilepsy are still a matter of controversy. Little objective evidence regarding the effect of exercise on seizure frequency and severity has been reported. One sought to clarify the relationship between exercise and epilepsy in an animal model of temporal lobe epilepsy (the pilocarpine model of epilepsy). To evaluate the effect of an aerobic physical program on seizure frequency, 29 epileptic animals were continuously monitored during 24 h for 135 days after the first spontaneous recurrent seizure (SRS) and divided into three groups. The first group (N = 14) was submitted to an aerobic exercise program (training group). The second group (N = 7) was maintained in the treadmill for the same time as the training group without being submitted to physical exercise (sham group). The third group (N = 8) served as control. The behavioral observation was divided in three periods of 45 days. The first period was used to determine the number of seizures before physical training program. The second period was utilized to determine the number of seizures during the physical training program. The third period was used to analyze the frequency of seizures after the physical training program. The mean frequency of seizures in the control and sham groups increased significantly from period 1 to period 2 and from period 1 to period 3. However, in the training group, the frequency of seizures did not change significantly between the three periods of 45 days of observation. When the same periods of the three groups were analyzed together, a significant reduction in seizure frequency was observed comparing the training group with the control and sham groups during the period of physical training. The data presented in this study suggest that physical exercise is not a seizure-inducing factor in this experimental model of epilepsy.

Animals↗

Increased sensitivity to seizures in mice lacking cellular prion protein.

PURPOSE: The physiologic role of the cellular prion protein (PrPc) is unknown. Mice devoid of PrPc develop normally and show only minor deficits. However, electrophysiologic and histologic alterations found in these mice suggest a possible role for PrPc in seizure threshold and/or epilepsy. METHODS: We tested the sensitivity of PrPc knockout mice to seizures induced by single convulsant or repeated subconvulsant (kindling) doses of pentylenetetrazol (PTZ), and to status epilepticus (SE) induced by kainic acid or pilocarpine. RESULTS: In PTZ kindling, seizure severity progressed faster in the PrPc knockout group, in which 92.8% reached stage 5 or death after 4 days of stimulation, as opposed to 38.4% in wild-type animals. After 10 injections, mortality was 85.7% among knockouts and 15.3% among controls. After a single PTZ injection (60 mg/kg), overall mortality due to seizures was 91% in knockout mice, but only 33% among wild-type animals. Pilocarpine-induced SE (320 mg/kg) caused an 86.7% mortality in knockouts, as opposed to 40% in wild-type animals. Finally, after kainic acid injections (10 mg/kg), 70% of the knockouts developed at least one severe seizure, and 50% showed repetitive seizures, whereas no wild-type animal exhibited observable seizures. CONCLUSIONS: Animals lacking cellular prion protein expression are more susceptible to seizures induced by various convulsant agents. This is perhaps the most striking alteration yet found in PrPc-null mice, who at first analysis appeared to be completely normal. A possible role for PrPc in chronic and idiopathic (familial), secondary, or cryptogenic epilepsies in humans remains to be investigated.

Animals↗

Prevalence of epileptic seizures along the wakefulness-sleep cycle in adult rats submitted to status epilepticus in early life.

In 70 adult Wistar rats submitted to pilocarpine-induced status epilepticus in early life the electro-oscillograms were recorded from neocortical areas 10, 3 and 17, from CA1 and CA3 hippocampal fields and, in 10 rats, also from the ventrolateral nuclei and amygdala. Head, eye, rostrum + vibrissae, ear and forelimb movements were recorded as well. Fifty rats were subjected to 4-hour daily recording sessions and 20 to continuous 24-hour recordings. In all the rats spike-wave discharges (SWD) were found in every site from which the electro-oscillograms were recorded, and clonic seizures were also displayed by all the animals. Most seizures (83.75%, mean = 6.59 fits/h) were concentrated in nearly 9 h and 16.25% (mean = 0. 77 fits/h) in the remaining 15 h. Eye movements occurred during 49. 2% of the total duration of motor events, the head moved in 42.8% and the rostrum + vibrissae in 8.1% of the time, departing from normal rats. Therefore, pilocarpine-induced status epilepticus produces striking changes in the wakefulness-sleep cycle characteristics.

Aging↗

Persistence and atrophy of septal/diagonal band neurons expressing the p75 neurotrophin receptor in pilocarpine-induced chronic epilepsy in the rat.

Systemic administration of pilocarpine, which results in status epilepticus followed by recurrent seizures in rats, is a widely used experimental model of chronic limbic epilepsy. Marked structural alterations have been documented in pilocarpine-induced epilepsy, and these include cell loss in the hippocampus and other brain areas, and sprouting of mossy and cholinergic fibers in the hippocampus. Evidence is accumulating that neurotrophins and neurotrophin receptors are involved in the cascade of these events. Two and 4 months after pilocarpine-induced epilepsy, neurons containing the 75-kDa low affinity neurotrophin receptor (p75NTR) were investigated with immunohistochemistry in the medial septal and diagonal band nuclei. No significant differences in the distribution and number of immunoreactive neurons were found in the epileptic rats compared to control saline-treated animals. However, in the epileptic animals, a significant decrease in the perikaryal size of p75NTR-immunoreactive neurons of the septal/diagonal band region was found by 60 days, and such atrophic changes were more marked in the diagonal band nuclei by 120 days. These findings indicate that the p75NTR-containing cell bodies, which include the neurons projecting to the hippocampal formation and are cholinergic in the normal brain, survive after months of spontaneous recurrent seizures, during which, therefore, a supply of p75NTR to target regions is maintained in the chronic epileptic brain. However, the present data point out that these p75NTR-containing neurons undergo a significant shrinkage in pilocarpine-induced chronic epilepsy, thus indicating that they are involved in the brain pathology of temporal lobe epilepsy.

Animals↗

Tyrosine phosphorylation is increased in the rat hippocampus during the status epilepticus induced by pilocarpine.

Phosphorylation of tyrosine residue in proteins is an important modulatory process for membrane transduction and cell signaling and for several cellular functions. The concentration and distribution of phosphotyrosine proteins were analyzed in the hippocampi of rats in the model of epilepsy induced by pilocarpine using Western blotting and immunohistochemistry. The concentration of several phosphotyrosine proteins increased during status epilepticus. During the seizure-free period and the chronic period of this epilepsy model, the hippocampi of rats did not exhibit changes in the expression of these proteins. Immunohistochemistry showed an increased immunoreactivity throughout the hippocampal formation of rats 1 h after status epilepticus that was acutely induced by pilocarpine. Animals killed after 3 h of status epilepticus showed an increased expression of phosphotyrosine in the hippocampal hilus and CA3 regions. After 5 h of status epilepticus, phosphotyrosine immunoreactivity persisted only in the CA3 region. After 12 h of status epilepticus, the hippocampal formation exhibited a normal phosphotyrosine immunostaining, showing that the increased expression of these proteins is related to the acute phase and that several intracellular events could undergo modifications during the status epilepticus induced by pilocarpine.

Animals↗

Mitogen-activated protein kinase is increased in the limbic structures of the rat brain during the early stages of status epilepticus.

Systemic administration of pilocarpine (PILO) in adult rat produces acute limbic seizures leading to status epilepticus. Recent studies have shown the activation of mitogen-activated protein kinase (MAPK) cascades during experimentally induced seizures. MAPK activation may be triggered by glutamatergic stimulation and may play a key role in signal transduction pathways. In the present study, immunocytochemistry was used to analyze the spatiotemporal distribution pattern of the MAPK protein and its active form (A-MAPK) following PILO-induced status epilepticus. MAPK and A-MAPK immunoreactivities exhibited different patterns of distribution in the brain of normal and epileptic rats. The saline-treated rats, as well as the animals that received PILO but did not evolve to status epilepticus, showed a weak but selective MAPK immunoreactivity, detected in the hippocampal pyramidal neurons, dentate gyrus, hilus, CA3, CA1, and entorhinal, piriform, and cingulate cortices. A-MAPK immunoreactivity was instead observed only in neurites of the CA3 and hilus and in cells of the entorhinal and piriform cortices. In PILO-treated rats, between 30 and 60 min after status epilepticus there was an increase of the immunoreactivity to both antibodies, which were differently distributed throughout several structures of the limbic system. The immunostaining showed a slight decrease after 5 h of status epilepticus. However, MAPK and A-MAPK immunopositivities decreased markedly after 12 h of status epilepticus, returning almost to the basal expression. These findings are consistent with a spatial and time-dependent MAPK expression in selected limbic structures, and its activation could represent an initial trigger for neuronal modifications that may take part in the mechanism underlying acute epileptogenesis and in long-lasting neuropathological changes of the PILO model of epilepsy.

Animals↗

Effect of physical exercise on kindling development.

The relationship between epilepsy and exercise is a subject of controversy and needs more investigation. We report a study of the effect of physical activity on the development of amygdala kindling in rats. To analyze the acute and chronic effects of exercise on kindling development, 45 rats were divided randomly into three groups. The first group (acute group, n=15) was submitted to a daily bout of aerobic exercise (40 min running on the treadmill at 20 m/min) and kindling stimulated 1 min post-exercise; the second group (chronic group, n=15) was submitted to an aerobic training program (40 min running on the treadmill at 20 m/min, 7 days per week, for 45 days) and then submitted to the same procedure as the first group (daily bout of aerobic exercise -- 40 min running on the treadmill at 20 m/min and kindling stimulated 1 min post-exercise); and the third group (n=15) served as control. All groups were kindling stimulated until they reached stage 5 of kindling. The number of stimulations required to reach stage 5 was statistically higher for the chronic exercise group when compared to the acute exercise group and the control group. A longer time spent in stage 1 and a shorter after-discharge duration in stage 1 was observed in the acute and chronic exercise groups in relation to the control group. This finding suggests that chronic physical exercise inhibits development of amygdala kindling in rats.

Amygdala↗

Hormonal and gestational parameters in female rats submitted to the pilocarpine model of epilepsy.

Endocrine and reproductive alterations are frequently reported to occur in women with temporal lobe epilepsy as well as in female rats in different experimental models of limbic seizures. As previously reported, women with epilepsy have lower fertility rates than women without epilepsy (Tanganelli, P., Regesta, G., 1992. Neurology (suppl.) 42 (5), 89-93; Cummings, L.N., Guidice, L., Morrel, M.J., 1995. Epilepsia 36, 355-359). In order to investigate the possible substrate of endocrine alterations in epilepsy, hormonal and gestational parameters were studied in female rats submitted to the pilocarpine model of epilepsy. The results demonstrated that the oestrus cycle is altered following pilocarpine-induced status epilepticus and such alteration lasted for several weeks. Progesterone, LH and FSH levels decreased and estradiol levels increased significantly during the period of spontaneous and recurrent seizures. The frequency of seizures during pregnancy and lactation decreased. These results document that significant changes in gonadal, hypophyseal and hypothalamic hormones, as well as in sexual behaviour, occur following status epilepticus induced by pilocarpine administration.

Animals↗

Serum level of serotonin during rest and during exercise in paraplegic patients.

The purpose of this study was to evaluate the serum level of serotonin (5-HT) during rest and response to exercise in subjects with spinal cord injury (SCI) with different levels of physical activity. Twenty-five male subjects with traumatic paraplegia, the neurological levels being between T1 and T12, volunteered for the study. They were divided into two groups matched for age, weight and time since injury, according to the level of physical activity: 14 inactive and 11 subjects regularly involved in sports activity and considered active. They all performed a maximal spiroergometric test with an arm crank ergometer. Two samples of blood were collected for 5-HT determination, during rest (PRE) and immediately after exercise test (POST). Serum 5-HT concentration was measured by high performance liquid chromatography using electrochemical detection (HPLC-ED). The results showed that peak oxygen uptake (VO2peak) was higher in the active group (27.08 +/- 2.60 vs 18.89 +/- 5.58 mL.kg-1.min-1, P < 0.001). There were no significant differences between the inactive and active groups for the 5-HT PRE (respectively 176.96 and 193.73 ng.mL - 1, P > 0.05) or POST values (275.44 vs 311.05 ng.mL-1, P > 0.05). Both groups showed an increment in 5-HT after maximal exercise, but only in the active group it reached statistical significance (Wilcoxon test, P < 0.02). Our results show that chronic paraplegic individuals have normal resting serum serotonin levels and normal response to exercise. The relationship between training status, mood elevation and 5-HT in SCI could not be established in the present study, and further investigation is needed to clarify this issue.

Adult↗

Glucose utilization during interictal intervals in an epilepsy model induced by pilocarpine: a qualitative study.

PURPOSE: Interictal intervals in pilocarpine-induced chronic epilepsy are characterized by apparent normal electrographic activity and longer sleep periods or drowsiness or both. Sparse information exists concerning the neural network activity during these seizure-free intervals. In our research, a [14C]2-deoxy-D-glucose (2DG) autoradiographic technique was used to investigate interictal changes in the metabolism of the epileptic rat brain. METHODS: Epileptic rats were monitored by video-EEG for approximately 120 days, with [14C]2DG injected after a seizure-free interval of > or = 24 h. RESULTS: Autoradiographic analysis revealed an increase in glucose utilization by several brain regions; the most consistent increase was found in the lateral posterior thalamic nucleus and pretectal region. CONCLUSIONS: These findings suggest that the lateral posterior thalamic nucleus and the pretectal region may be involved in cerebral circuits inhibiting epileptic activity during interictal intervals.

Animals↗