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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The release of somatostatin (somatostatin-like immunoreactivity) from hippocampal slices during the development of hippocampal kindling in rats was measured under resting and depolarizing conditions. Preliminary experiments in naive rats showed that the spontaneous efflux of somatostatin (4.0 +/- 0.3 fmol/ml every 10 min) was independent of external Ca2+ but was reduced to 71.5 +/- 6% of baseline (P < 0.05) during 20 min incubation with 5 microM tetrodotoxin. Neuronal depolarization with 25, 50 and 100 mM KCl induced a Ca(2+)-dependent somatostatin release, respectively 4.3 +/- 0.4, 16.7 +/- 1.6 and 22.0 +/- 1.3 times baseline (P < 0.01). Veratridine caused a dose-dependent Ca2+ and tetrodotoxin (5 microM) sensitive release ranging from 6.5 +/- 0.1 to 13.0 +/- 1.4 times baseline at 1.4 microM and 50 microM respectively (P < 0.01). One week after the last of three consecutive stage 5 seizures (full seizure expression) or 48 h after the last stage 2 stimulation (preconvulsive stage), 50 mM KCl-induced somatostatin release was significantly higher (1.8 +/- 0.1, P < 0.01) than in shams (animals implanted with electrodes but not stimulated) in the stimulated and contralateral hippocampus. Somatostatin release measured under resting conditions was increased by 1.5 times in the stimulated hippocampus at stage 2 (P < 0.05) and by 2.2 and 1.7 times in both hippocampi at stage 5 (P < 0.01). Forty-eight hours after the induction of a single afterdischarge no significant changes were found in either spontaneous or 50 mM KCl-induced release of somatostatin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Somatostatin release is enhanced in the hippocampus of partially and fully kindled rats. 136 Dec 18

Patients with medically intractable temporal lobe epilepsy (TLE) undergo medial temporal lobectomy with hippocampectomy for one of two reasons. (1) A lesion (tumor or arteriovenous malformation) adjacent to, but not invasive of, the hippocampus, results in the removal of the lesion and adjacent hippocampus in order to ensure a tumor-free margin. This group will be referred to as tumor-related TLE (TTLE) patients. (2) The operation is performed when depth electrode recordings and other evaluative techniques point to the hippocampus as the focus of seizure initiation. This group will be referred to as cryptogenic TLE (CTLE) patients. Analysis of the hippocampi of these two groups of patients reveals that the TTLE hippocampus is quite similar to that of autopsy subjects in its chemical neuroanatomy. However, the dentate gyrus of the CTLE patients shows considerable morphological and cytochemical reorganization. This reorganization is characterized by a number of features. (1) There is a loss of granule cells which occurs either as a patchy loss and/or a thinning of the granule cell layer. (2) Remaining granule cells which contain dynorphin appear to produce recurrent collaterals into the inner molecular layer of the dentate gyrus. (3) In the subgranular region of the hilus (the polymorphic layer) there is a selective loss of interneurons immunoreactive for somatostatin, neuropeptide Y and substance P. (4) There appears to be an increase in fibers immunoreactive for somatostatin and neuropeptide Y which extend throughout the dentate molecular layer. Somatostatin fibers being less numerous than neuropeptide Y fibers (5). The distributions of a number of neurotransmitter receptors also show striking reorganization in the dentate gyrus of the CTLE hippocampus. (6) Second messenger systems protein kinase C and adenylate cyclase, and Na+, K(+)-ATPase activity, as determined by ouabain binding, is increased in the molecular layer of CTLE. This remodeling of the CTLE hippocampus may hold the key to the mechanisms of hyperexcitability of the granule cells in the hippocampus of this group, and consequently the generation of seizures. The removal of the hippocampus in CTLE patients results in good control of seizures, whereas removal of hippocampi that do not show such reorganization, in a group of patients classified as atypical CTLE patients, results in inadequate seizure control. These findings suggest a complex series of processes in converting the properly regulated granule cells into hyperexcitable ones.
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PMID:Neurotransmitters and their receptors in human temporal lobe epilepsy. 136 31

A selective loss of somatostatin- and neuropeptide Y-immunoreactive neurons has been reported in the dentate gyrus of rats with cerebral ischemia, following sustained electric stimulation, and in patients with non-tumor-related temporal lobe epilepsy. Three theoretical possibilities were tested that may explain why these neurons are more vulnerable than others, such as the cholecystokinin- and calcium-binding protein-containing cells: (1) the seizure-sensitive neurons are more involved in specific excitatory circuitry than are the seizure-resistant cells; (2) the somatostatin- and neuropeptide Y-immunoreactive neurons are less protected by inhibitory GABAergic inputs than cells immunoreactive for cholecystokinin; and (3) the seizure-sensitive neurons do not contain calcium-binding proteins. The present results of light and electron microscopic, single and double, immunostaining experiments and co-localization studies performed on the hippocampal formations of rats and non-human primates, support the idea that the calcium-binding protein content of a neuron defines its seizure sensitivity.
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PMID:Synaptic connections of seizure-sensitive neurons in the dentate gyrus. 136 32

Gamma-hydroxybutyrate (GHB) was intracortically applied in two doses (first 10 and then 20 mg/ml) to awake Wistar rats using microdialysis. Simultaneously, EEG and the release of somatostatin-like immunoreactivity (SLI) were measured from the frontal cortex. Intracerebrally administered GHB induced cortical epileptogenic spikes, but not high voltage spindles (HVS) as reported after systemic administration, and seizures with myoclonic jerks and contraversive head movements. Compared to the basal level, GHB (10 mg/ml) initially increased the release of SLI (p < 0.05). However, when the frequency of spikes and seizures rose rapidly (p < 0.001), SLI release decreased significantly (p < 0.001). Minimum release of SLI occurred when seizures were most frequent (during perfusion with 20 mg/ml GHB), while after removal of the drug it rose above the basal level (p < 0.05). According to these results, intracortically applied GHB increases the release of SLI in the surrounding tissue. However, further exposure of GHB leads to a manifestation of epileptic spikes and seizures, during which the release of SLI is significantly attenuated. This suggests that release of somatostatin is affected during epileptic phenomena induced also by intracortical GHB application.
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PMID:Somatostatin release in rat neocortex during gamma-hydroxybutyrate-provoked seizures: microdialysis combined with EEG recording. 136 75

A number of pharmacological evidence supports the view that somatostatin (SS) may be importantly involved in the seizure susceptibility both in humans and in laboratory animals. In a previous report the Authors have provided the finding that a short-term carbamazepine (CBZ) administration is able to reduce SS-CSF-IR in epileptic patients. The present study has been carried out to investigate whether a long-term treatment with CBZ affects in a similar way SS-IR content in CSF from temporal lobe epileptics (CPS). The results confirm and expand previous evidence suggesting that CBZ lowering effect on CSF-SS-IR may be relevant to its anticonvulsivant action.
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PMID:Long-term treatment with carbamazepine affects CSF somatostatin immunoreactivity in epileptic patients. 136 57

Previous studies have demonstrated that the dentate granule and the CA3 pyramidal cells of the rat hippocampal formation are neuronal populations vulnerable to the toxic effects of ethanol. It also has been shown that the resulting alterations do not end after withdrawal from ethanol. As the neurons in the dentate hilus are heavily interconnected with the dentate granule cells, the authors decided to examine the fate of the hilar neurons after chronic alcohol consumption and withdrawal, inasmuch as the hilar somatostatin-immunoreactive (SS-I) neurons were found to be sensitive to cerebral ischemia and to seizures. The following groups of adult rats were studied: (1) alcohol-fed for 6 and 12 months; (2) alcohol-fed for 6 months and then switched to water for a further 6 months; (3) pair-fed controls; and (4) controls fed ad libitum. The authors determined the numerical density of hilar neurons and the number of its SS-I subpopulation. These were found to be significantly reduced in both the alcohol-fed and withdrawal groups when compared with the respective age-matched controls. The consequent loss of the integrative action of the hilar neurons, including the SS-Is, could explain some of the alcohol-related functional deficits as well as their persistence after withdrawal.
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PMID:Effects of chronic alcohol consumption and withdrawal on the somatostatin-immunoreactive neurons of the rat hippocampal dentate hilus. 136 47

This paper reviews chemical models of epilepsy and their relevance in the identification and characterization of anticonvulsants. For each convulsant we discuss possible modes of administration, clinical type(s) of seizures induced, proposed mechanism(s) of epileptogenesis and, where available, responsiveness of the induced seizures to anticonvulsants. The following compounds are reviewed: pentylenetetrazol, bicuculline, penicillin, picrotoxin, beta-carbolines, 3-mercaptopropionic acid, hydrazides, allylglycine; the glycine antagonist strychnine; gamma-hydroxybutyrate; excitatory amino acids (glutamate, aspartate, N-methyl-D-aspartate, quisqualate, kainate, quinolinic acid); monosubstituted guanidino compounds, metals (alumina, cobalt, zinc, iron); neuropeptides (opioid peptides, corticotropin releasing factor, somatostatin, vasopressin); cholinergic agents (acetylcholine, acetylcholinesterase inhibitors, pilocarpine); tetanus toxin; flurothyl; folates; homocysteine and colchicine. Although there are a multitude of chemical models of epilepsy, only a limited number are applied in the routine screening of potential anticonvulsants. Some chemical models have a predictive value with regard to the clinical profile of efficacy of the tested anticonvulsants. Some chemical models may contribute to a better understanding of possible mechanisms of epileptogenesis.
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PMID:Chemical models of epilepsy with some reference to their applicability in the development of anticonvulsants. 139 44

Despite intensive study, the neurobiological basis of epilepsy and persistent memory impairment following traumatic head injury remains unknown. Since abnormalities of the hippocampus are known to be associated with temporal lobe seizures and memory dysfunction, we investigated the effects of experimental traumatic brain injury on hippocampal structure and function in the rat. Using a model of fluid-percussion injury, we have discovered that neurons of the dentate hilus are vulnerable to a brief, unilateral impact to the extradural surface of the brain. One week after trauma, there was a dramatic reduction in hilar neurons ipsilateral to the impact, and a milder but significant decrease in neurons on the contralateral side as well. This neuronal loss was highly selective since adjacent dentate granule and pyramidal neurons appeared relatively unaffected. Immunocytochemistry showed that the hilar cell loss included a loss of somatostatin-immunoreactive neurons, and degeneration stains provided evidence that irreversible hilar injury occurred within 4 hr of impact. To assess the functional effects of the hilar damage, dentate granule cell field potentials were measured in response to perforant path stimulation. This revealed abnormal dentate granule cell hyperexcitability at 2.0 Hz stimulation in many of the injured animals. The presence of abnormal hyperexcitability correlated with the loss of hilar neurons. Thus, a momentary impact to the surface of the brain can cause selective, bilateral hippocampal injury with associated abnormalities in dentate gyrus physiology. Furthermore, the pattern of cell loss is similar to that observed in some patients with temporal lobe epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective vulnerability of dentate hilar neurons following traumatic brain injury: a potential mechanistic link between head trauma and disorders of the hippocampus. 146 70

We tested the hypothesis that brain somatostatin levels modify two motor behaviors evoked by ICV infusions of nicotine. Unrestrained, awake rats were given fixed-concentration infusions of nicotine until the prostration/immobility (PI) syndrome and convulsions were produced. Infusion duration ranged from 0.9 to 1.2 min for the PI syndrome and 2.5 to 4.9 min for the convulsions. Octreotide, a stable somatostatin analog (4.5 micrograms, ICV), significantly raised the threshold for nicotine convulsions 1.0 and 5.5 h after pretreatment but not at 24 or 48 h. Cysteamine, a somatostatin releaser and depletor (0.35-0.75 mg/rat, ICV), also caused a dose-dependent increase in seizure threshold. Similarities in the response to octreotide and cysteamine suggest that depression of nicotine convulsions by cysteamine may be mediated by release of endogenous somatostatin. Neither octreotide nor cysteamine altered the threshold for the PI syndrome. These results support the view that one motor behavior evoked by nicotine is subject to control by somatostatin whereas another is not.
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PMID:Differential effects of octreotide on motor responses to nicotine in rats. 147

The inducible 72 kDa heat shock protein (HSP72) has been shown to be protective in non-neuronal cells and neurons in culture, but its function and the control of its expression in the CNS are poorly understood. Although HSP72 is induced in neurons in vivo by neurotoxic compounds that produce seizures and neuronal damage, it is unknown if its expression is a specific response to excitation per se or to "stressful" or potentially injurious excitation, or if it is a marker or mediator of irreversible injury. We have attempted to identify the nature of the stimulus for HSP72 expression by utilizing focal electrical stimulation that can either excite or destroy postsynaptic cells, depending on the duration of afferent stimulation. Previous studies have demonstrated that intermittent stimulation of the main hippocampal afferent pathway for 24 hr evokes synchronous discharges in dentate granule cells but does not injure them. However, the same stimulation irreversibly destroys three of the four cell populations innervated by the granule cells. The three vulnerable populations are the dentate hilar mossy cells, the somatostatin/neuropeptide Y (NPY)-immunoreactive hilar neurons, and the CA3c pyramidal cells. The fourth and relatively resistant population is the GABA-immunoreactive dentate basket cells. In this study, we have localized HSP72 expression immunocytochemically in the hippocampal dentate gyrus in response to nontoxic durations of potentially neurotoxic afferent stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Heat shock protein expression in vulnerable cells of the rat hippocampus as an indicator of excitation-induced neuronal stress. 149 43


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