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

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

Fourteen days administration of haloperidol (1 mg/kg daily) prevented the motor depressant effect of caerulein (an agonist at cholecystokinin receptors, 15 micrograms/kg) and the antagonistic effect of caerulein (100 micrograms/kg) against (+)-amphetamine (5 mg/kg) induced hyperlocomotion in mice. The antiaggressive effect of caerulein (40 micrograms/kg) in saline-treated mice was replaced by increased aggressiveness after long-term haloperidol and diazepam (5 mg/kg daily) treatment. The anticonvulsant effect of caerulein (125 micrograms/kg) against picrotoxin (10 mg/kg) induced seizures was abolished after 14 days diazepam, but not after haloperidol, treatment. The above described changes in the mouse behaviour are probably related to the development of subsensitivity at CCKA receptors, whereas the CCKB receptor subtype becomes more sensitized to the action of caerulein after long-term haloperidol and diazepam treatment.
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PMID:Changes at cholecystokinin receptors induced by long-term treatment with diazepam and haloperidol. 149 96

Utilizing audiogenic seizure-prone P77PMC rats, the effects of cholecystokinin octapeptide (CCK-8) on genetic seizure susceptibility were studied in vivo, in cerebral cortical synaptosomes, and in cortical neuronal cell cultures. The results showed that CCK-8 could decrease seizure susceptibility, and that the K(+)-stimulated release of GABA in cerebral cortex synaptosomes from seizure-prone animals was depressed. The presence of exogenous CCK-8 (10(-7) M) together with elevated K+ (25 mM) causes a higher increased magnitude in GABA release from synaptosomes (enhanced by 100%) and cell cultures (17 days in vitro, increased by 177%) derived from seizure-prone rats than the controls (increased by 42%, in synaptosomes; and 107% in cell cultures). These preliminary results raise the possibility that the developmental abnormalities in modulation effect of CCK-8 on GABA release in central nervous system may play a role causing greater seizure susceptibility in genetic seizure-prone rats. The analysis of the brain tissue level and gene-expression of CCK-8 will be the important step of further investigation.
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PMID:Effects of cholecystokinin octapeptide on genetically determined seizure susceptibility. 159 69

Rats were submitted to single or repeated (7 days, one session for each day) sessions of electroconvulsive shock. A computer-assisted morphometric and microdensitometric analysis of glial fibrillary acidic protein-, ornithine decarboxylase-, somatostatin- and cholecystokinin-like immunoreactivities was performed in the hippocampal formation and other brain areas. The results of the study showed a significant increase of the intensity of the immunostaining for glial fibrillary acidic protein, ornithine decarboxylase, somatostatin and cholecystokinin in the hippocampal formation and distinctively in the dentate gyrus following repeated, but not single, electroconvulsive shock. No significant change was found in the number of somatostatin- and cholecystokinin-like immunoreactive cell bodies in any hippocampal subregion and in the number of glial cells in the hilus of dentate gyrus in rats treated with single or repeated electroconvulsive shock. It is a distinct possibility that the observed increase in the content of the neuropeptides in the hippocampal formation reflects a compensatory response of the brain to seizure-inducing stimuli and that such an increase may play a role in the therapeutic effect of electroconvulsive shock.
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PMID:Repeated electroconvulsive shock increases glial fibrillary acidic protein, ornithine decarboxylase, somatostatin and cholecystokinin immunoreactivities in the hippocampal formation of the rat. 170 56

As neuropeptides may play a role in the electrical kindling model of epileptogenesis, hippocampal somatostatin, Met-enkephalin and cholecystokinin were studied by immunocytochemistry in rats 24 h following full hippocampal kindling (three stage 5 seizures). As control animals we used sham-kindled rats, unoperated rats and rats subjected to a single electroshock-induced seizure. In addition, the distribution of septohippocampal, cholinergic fibers and hippocampal mossy fibers were studied by histochemistry. The important finding was that after kindling there was, as compared to unoperated control, (1) a marked increase of somatostatin immunoreactivity in cell bodies in the dentate hilus and their presumed projections area in the outer parts of the dentate molecular layer, and (2) a marked increase of Met-enkephalin immunoreactivity in hippocampal mossy fiber terminals. We found no evidence of aberrant sprouting of mossy fiber collaterals in the fascia dentata.
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PMID:Increased somatostatin and enkephalin-like immunoreactivity in the rat hippocampus following hippocampal kindling. 197 72

Recent studies have demonstrated that the regulation of neuropeptide expression in forebrain neurons is responsive to external influences including changes in physiological activity. This has been demonstrated most clearly in studies of hippocampus where the synthesis and resting levels of several neuropeptides, localized within well-characterized components of hippocampal circuitry, have been shown to be selectively influenced by seizure activity. In studies described here, we examined the influence of recurrent limbic seizures on the expression of enkephalin, dynorphin, cholecystokinin, and neuropeptide Y (NPY) in rat and mouse hippocampus using immunohistochemical, in situ hybridization and blot hybridization techniques. The data demonstrate that seizures differentially influence the expression of each peptide as a part of a broader cascade of changes in genomic expression within individual hippocampal neurons. In particular, seizures increase preproenkephalin mRNA and enkephalin peptide but decrease dynorphin peptide in the dentate gyrus granule cell/mossy fiber system. Seizure-induced decreases in the concentration of preprodynorphin mRNA in the granule cells have been reported by others. Immunoreactivity for CCK, which is codistributed with the opioid peptides in the mossy fiber system of mouse, is also dramatically reduced in the granule cell axons by seizure. Recurrent seizures induce two temporally distinct changes in NPY expression in hippocampus. First, there is an increase in hybridization to preproNPY mRNA within scattered, probable local circuit neurons in all subfields. This is followed by the seemingly novel appearance of preproNPY mRNA within the dentate gyrus granule cells and pyramidal cells of field CA1. Clues about mechanisms of neuropeptide regulation have come from observations of other, more rapid, transcriptional events induced by seizure. Most notably, our results and those of others demonstrate that seizures increase the expression of messenger RNAs from immediate-early genes (c-fos, c-jun, and NGFI-A) which encode proteins that may mediate neuropeptide gene regulation. In addition, mRNA for nerve growth factor is dramatically increased in the dentate gyrus granule cells by seizure; increased production of this trophic factor might mediate the more delayed changes in genomic expression and growth responses observed to occur in hippocampus and other forebrain areas following seizure activity.
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PMID:Seizures, neuropeptide regulation, and mRNA expression in the hippocampus. 220 4

A behavioral analysis of intracranial self-stimulation (ICSS) was provided for mesolimbic/mesocortical, nigrostriatal, hypothalamic and extrahypothalamic sites in the CD-1 mouse. Robust responding and rapid acquisition of mesocortical ICSS appeared dorsally along notably fluorescent sites in rostral and caudal planes. ICSS was diminished demonstrably in medial and ventral positions in posterior planes. Mesolimbic ICSS from the medial and ventral nucleus accumbens (Nas), was accompanied by significant elevations in locomotor activity, corresponding to regions of dopamine (DA) and cholecystokinin co-localization. Stimulation-induced seizures appeared from both the Nas as well as the mesocortex. ICSS from the ventral tegmental field (VTA) was evident along its medial, lateral and dorsal borders with longer pulse durations more likely to elicit responding. Seizure activity was absent from the VTA. Striatal ICSS was conspicuously poor in dorsal and medial locations; regions presumably devoid of tegmental innervation. ICSS emerged from both the ventrocaudal and anteromedial striatum; regions linked to innervation by the dorsolateral and ventromedial VTA. The red nucleus, a previously neglected self-stimulation site supported marked responding for ICSS. Regions supporting rubral ICSS were correlated with thalamic innervation sites; notably the ventrolateral thalamic nucleus and the parafascicular nucleus, regions found to support ICSS. The substantia nigra supported high rates of responding for ICSS when electrode placement was restricted to the dorsomedial portion of the pars compacta. Electrode deviations lateral and dorsal to the substantia nigra pars medialis induced a progressive decline in responding. Hypothalamic sites were found to support significant responding for ICSS, although such performance was frequently associated with seizure induction. Taken together these data (1) provide the first behavioral analysis of ICSS in mice responding from previously unexamined DA sites in the mesolimbic (e.g. VTA, Nas) and nigrostriatal systems (e.g. caudate, red nucleus) (2) suggest an anatomical reconsideration of the assumptions underlying the elicitation of ICSS from the frontal cortex (3) suggest that the neural circuitry underlying thalamic, caudate, rubral and frontal cortical ICSS are interrelated and (4) suggest that the Nas and the frontal cortex, like the hypothalamus, in the mouse appear to be particularly sensitive to stimulation-induced seizures.
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PMID:Behavioral characterization of intracranial self-stimulation from mesolimbic, mesocortical, nigrostriatal, hypothalamic and extra-hypothalamic sites in the non-inbred CD-1 mouse strain. 231 Apr 89

Recently, several systems of neuropeptides have been demonstrated to have anticonvulsant action in some forms of epilepsy to some extent. However, considerably less knowledge has been taken to their involvement in convulsive disorders either with regard to the development, expression or control of seizures. In this study, therefore, we examined the influence of amygdaloid kindling, an experimental model of temporal lobe epilepsy, on thyrotropin-releasing hormone (TRH), somatostatin (SS), cholecystokinin (CCK) and substance P (SP) content in the amygdala/piriform cortex and hippocampus. Male Sprague-Dawley rats were implanted bipolar electrodes into the left amygdala under pentobarbital anesthesia. Daily kindling stimulation was made to the left amygdala with 1 sec, 60 Hz, 400 microA, until 5 consecutive fully kindled generalized convulsive seizures were elicited. Subsequently, amygdaloid kindled rats were decapitated 30 min, 24 hrs, 48 hrs, 7 days and 21 days after the last amygdaloid stimulation, and the amygdala/piriform cortex and hippocampus were dissected. Control animals only received chronic electrodes, but no stimulation was delivered. The immunoreactivity of TRH, SS, CCK and SP was examined by methods of specific radioimmunoassay. The TRH content in these two brain regions significantly increased 24 hrs after the last kindled convulsion. This increase became maximal 48 hrs after the last convulsion: about 3-fold and 4-fold of the control in the amygdala/piriform cortex and hippocampus, respectively. Such increases in the TRH content tended to persist for 7 days, but returned to the control level 21 days after the last convulsion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of amygdaloid kindling on thyrotropin-releasing hormone, somatostatin, cholecystokinin and substance P contents of the amygdala/piriform cortex and hippocampus of rats]. 246 12

Electrolytic lesions of the dentate gyrus hilus have been demonstrated to induce behavioral seizure activity and to result in perturbations in the amount of enkephalin, cholecystokinin, and dynorphin immunoreactivity in the hippocampal mossy fiber system. In the present study, electroencephalographic (EEG) recordings, made from hippocampus contralateral to a hilus lesion in mouse, demonstrate the presence of recurrent hippocampal seizure activity which begins approximately one hour postlesion and continues for several hours thereafter. Behavioral seizures were found to correspond to periods of epileptiform hippocampal EEG. Immunocytochemical analyses of enkephalin-(ENK-I) and cholecystokinin-immunoreactivity (CCK-I) in contralateral hippocampus of animals sacrificed at various postlesion intervals revealed that both ENK-I and CCK-I were depleted from the mossy fibers at 6 and 12 hr postlesion, and that ENK-I rebounded to supranormal levels by 27 hr. In two animals sacrificed 60 days following lesions which induced extreme behavioral seizure activity, ENK-I was still elevated while CCK-I was completely absent from the mossy fiber system. These data suggest that heightened physiological activity, in the form of recurrent limbic seizures, induces long-lasting but quite different alterations in enkephalin and CCK concentration in the hippocampal mossy fiber system.
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PMID:Focal hippocampal lesions induce seizures and long-lasting changes in mossy fiber enkephalin and CCK immunoreactivity. 285 53

Amygdaloid kindling of rats produced an increase in hippocampal Met5-enkephalin-Arg6-Gly7-Leu8 and cholecystokinin immunoreactivities and simultaneously a decrease in dynorphin A1-8 content. In substantia nigra Met5-enkephalin-Arg6-Gly7-Leu8 was increased and no change was observed in dynorphin A1-8 content. These data suggest that specific alterations of neuropeptides in limbic and extrapyramidal circuits are prominent manifestations of the kindling process or kindled seizures.
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PMID:Changes in dynorphin, enkephalin and cholecystokinin content of hippocampus and substantia nigra after amygdala kindling. 286 84


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