Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: UMLS:C0038220 (status epilepticus)
7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using focal brain stimulation (kindling), discrete seizures can be triggered from many neuroanatomic sites with varying degrees of facility. From several of these sites, protracted seizures or status epilepticus (SE) also can be triggered. To date, no comparison has been made between different brain sites in their sensitivity both to kindling and to SE development. In this report, we have compared the kindling profiles of three amygdala nuclei, namely the basal (BL), central (CE), and medial (ME) nuclei, to the adjacent piriform (PIR) and perirhinal (PRH) cortices. In addition, three weeks following kindling, the susceptibility of each kindled site to status epilepticus (SE) was assessed by exposing the site to 60 min of electrical stimulation. We observed that (a) during the course of daily kindling, the afterdischarge threshold dropped progressively and significantly in all structures, (b) the rate of kindling in the PRH and PIR cortices and the CE amygdala was significantly faster than either the BL or ME amygdala, (c) when discrete convulsions were triggered, the latency to forelimb clonus in the PRH cortex and CE amygdala was significantly shorter than the other three structures, and (d) despite being slower to kindle than most other sites, stimulation of the BL nucleus most readily triggered SE. The kindling data suggest that discharges triggered from the PRH and CE more readily access motor systems supporting limbic convulsions than discharges triggered from the BL, ME nuclei or the PIR cortex. On the other hand, the SE data indicate that the mechanisms and circuits associated with the development of discrete kindled seizures are not identical to those associated with the induction of limbic SE.
...
PMID:Differential sensitivity of various temporal lobe structures in the rat to kindling and status epilepticus induction. 873 21

Administration of subconvulsive dose of pilocarpine (30 mg/kg s.c.) to rats pretreated with lithium chloride (3 meq/kg i.p.) produced a state of status epilepticus in animals. The animals showed characteristic symptoms of generalized convulsions, wet dog shakes (WDS), forelimb clonus and falling back. The symptoms of status epilepticus (SE) developed within 26.8 +/- 3.6 min after administering pilocarpine and these symptoms continued uninterrupted. The phenomenon was totally reproducible, with a consistent latency of onset of seizures and a high mortality rate. The symptoms were blocked by atropine, scopolamine and the GABAergic agents GABA, sodium valproate, (+)-baclofen and clonazepam when given prior to pilocarpine, but not when administered 30 min after pilocarpine administration.
...
PMID:Protective effects of GABAergic drugs and other anticonvulsants in lithium-pilocarpine-induced status epilepticus. 881 69

Although status epilepticus in children is associated with neuronal pathologies, there are few developmental models of status epilepticus which produce damage in the immature brain. We have developed a new model of status epilepticus using systemically injected pilocarpine in immature rabbits pretreated with lithium. Injected animals demonstrated behavioral and electrographic seizures. Behavioral seizures were characterized by sustained or recurrent bouts of clonus in all limbs. The pilocarpine-induced seizures had a 40% mortality. All animals surviving the status epilepticus had hippocampal lesions when evaluated 48 h after the SE. Within the hippocampus, CA1 pyramidal cells were the most vulnerable cell population. Extrahippocampal damage was seen in the majority of animals. Our results show that severe seizures cause hippocampal lesions in the absence of hypoxemia and suggest that the presumed resistance of the immature brain to seizure-induced damage is not a general rule which can be applied to all models or species.
...
PMID:Lithium-pilocarpine status epilepticus in the immature rabbit. 917 39

Effect of adenosinergic agents were investigated in lithium-pilocarpine-induced status epilepticus (SE) in rats. Adenosinergic agents such as adenosine (50, 100 mg/kg), 2-choloroadenosine (1, 2 mg/kg), carbamazepine (20, 80 mg/kg), N6-cyclohexyladenosine (1, 2 mg/kg) and dipyridamole (10, 20 mg/kg) produced theophylline-sensitive protective effects as they dose-dependently prolonged the latencies for onset of forelimb clonus with rearing. Pretreatment with Ro 5-4864 (20 mg/kg i.p.) did not offer any protection. These results indicate the possible involvement of adenosinergic mechanism in preventing lithium-pilocarpine-induced SE and mortality.
...
PMID:Modulation of lithium-pilocarpine-induced status epilepticus by adenosinergic agents. 937 81

The atypical antipsychotic clozapine treatment (at high doses) has been reported to be associated with tremors. However, antitremor effects of clozapine have also been reported in Parkinsonian patients. Recently, we reported the protective effects of acute clozapine against pilocarpine-induced status epilepticus (SE). With this background, this study was designed to investigate the possible protective effect of clozapine against acute chemoconvulsions and kindling seizures produced by pentylenetetrazol (PTZ) in mice. Various doses of clozapine (1.0, 2.5, 5.0 and 7.5 mg) offered different degrees of protective effects against PTZ (80 mg) challenge, and the maximum protection was observed with the 2.5 mg dose as it delayed the onset of jerks, clonus, tonic extensor phase and reduced mortality. Animals chronically pretreated with clozapine (2.5, 7.5 and 15.0 mg) for 8 days when challenged by PTZ (50 and 80 mg) on the 8th day also showed protection. Repeated administration of PTZ at a subconvulsive dose (30 mg/kg, i.p, three times a week, for 9 weeks) produced kindled seizures in over 80% of the mice. Pretreatment with clozapine (1 or 5 mg) prevented the behavioral manifestations (motor seizures) as well as the development of kindling. The effect was compared with GABA (200 mg) and diazepam (1 mg), a known anticonvulsant drug.
...
PMID:Protective effect of clozapine against pentylenetetrazol convulsions and kindling. 970 77

Although the immature brain is highly susceptible to seizures, it is more resistant to seizure-induced neuronal loss than the adult brain. The developing brain contains high levels of neurotrophins which are involved in growth, differentiation and survival of neurons. To test the hypothesis that neurotrophins may protect the developing brain from seizure-induced neuronal loss, brain-derived neurotrophic factor up-regulation was blocked by intracerebroventricular infusion of an 18mer antisense oligodeoxynucleotide sequence to brain-derived neurotrophic factor in 19-day-old rats using micro-osmotic pumps. Control rats were infused with sense or missense oligodeoxynucleotide. Status epilepticus was induced by intraperitoneal administration of kainic acid 24 h after the start of oligodeoxynucleotide infusion. Seizure duration was significantly increased in the antisense oligodeoxynucleotide plus kainic acid group compared to groups that received kainic acid alone or kainic acid plus sense or missense oligodeoxynucleotide. There was no difference between groups in the latency to forelimb clonus. A twofold increase in brain-derived neurotrophic factor levels was observed in the hippocampus 20 h following kainic acid-induced seizures. This kainic acid-induced increase was absent in animals receiving infusion of antisense oligodeoxynucleotide to brain-derived neurotrophic factor at time of seizure induction. Hippocampi of rats in this group (antisense oligodeoxynucleotide plus kainic acid) showed a loss of CA1 and CA3 pyramidal cells and hilar interneurons. This neuronal loss was not dependent upon seizure duration since animals injected with diazepam to control seizure activity in the antisense plus kainic acid group also showed similar neuronal loss. Administration of kainic acid or infusion of antisense alone did not produce any cell loss in these regions. Induction of seizures at postnatal day 20, in the presence or absence of antisense oligonucleotide, did not produce an impairment in learning and memory when tested 15 days later in the Morris water maze. The hippocampi of these animals did not show any synaptic reorganization as assessed by growth-associated protein-43 immunostaining and Timm staining. Our findings confirm prior studies demonstrating that seizures in the immature brain are associated with little, if any, cell loss. However, when seizure-induced increase in brain-derived neurotrophic factor is blocked, seizures do result in neuronal loss in the developing brain. Thus, brain-derived neurotrophic factor appears to provide protection against kainic acid seizure-induced neuronal damage in the developing brain.
...
PMID:Neuroprotective effects of brain-derived neurotrophic factor in seizures during development. 1033 79

Pregnenolone sulfate (PS) is an endogenous neurosteroid known to antagonize GABA(A) receptor-mediated inhibitory responses and potentiate NMDA receptor-mediated excitatory responses in vitro. To assess the actions of the steroid as a modulator of seizure susceptibility in vivo, PS (30-300 nmol) was administered intracerebroventricularly in mice. At doses of 50 to 150 nmol, PS elicited seizures characterized by head jerks, rearing and falling, severe forelimb and hindlimb clonus, opisthotonos and explosive running. The seizures increased in severity and frequency with time and eventually progressed to status epilepticus, tonic hindlimb extension and death. The doses producing convulsions in 50% (CD(50)) and 97% (CD(97)) of animals were 92 and 205 nmol, respectively. A subconvulsant dose of PS (50 nmol) significantly increased the convulsant potencies of systemically administered pentylenetetrazol (30-50 mg/kg) and NMDA (50-100 mg/kg). Systemically administered PS at doses as high as 100 mg/kg failed to induce seizures or alter the convulsant potencies of pentylenetetrazol and NMDA. Protection against PS (205 nmol)-induced seizures and lethality was conferred by the GABA(A) receptor positive allosteric modulators clonazepam and allopregnanolone, and by the NMDA receptor antagonists dizocilpine and (R)-CPP. The overall pharmacological profile suggests that the convulsant actions of PS are mediated predominantly via its effects on GABA(A) receptors, and also possibly by effects on NMDA receptors.
...
PMID:Convulsant actions of the neurosteroid pregnenolone sulfate in mice. 1041 90

Effects of various calcium channel inhibitors have been studied in lithium-pilocarpine model of status epilepticus. Status epilepticus was induced by administration of lithium chloride (3 meq/kg) followed 21 hr later by pilocarpine (30 mg/kg). Diltiazem (5 and 10 mg/kg) was not effective in delaying onset of convulsions. Verapamil (20 mg/kg) showed protection against lithium-pilocarpine-induced convulsions. The dihydropyridine nifidepine (2.5 and 5 mg/kg) did not show any protection in this model. Amlodipine (5 and 10 mg/kg) as partially protective. Flunarizine (10 and 20 mg/kg) delayed the onset of forelimb clonus and rearing and only 60% of the rats underwent status in the 20 mg/kg group. Pre-treatment of MK-801 led to a potentiation of the antiseizure activity of calcium channel inhibitors. The percent increase in amplitude at various time points with amlodipine pretreatment was significant only at the 30th min recording, and at the rest of the time frames was practically similar as the controls. It can be concluded that the anticonvulsant action of MK-801 can be enhanced by centrally acting calcium channel inhibitors.
...
PMID:Motor and electrographic response of refractory experimental status epilepticus in rats and effect of calcium channel blockers. 1121 25

Since the dorsal and ventral hippocampus in the rat may act differently from one another in limbic seizures, we studied effects of orthogonal transection between the dorsal and ventral hippocampus upon kainic acid-induced amygdalar seizures. A total of 26 rats were divided into three groups. Ten rats underwent transection using a modified wire knife (transection group); 16 others were untransection group (n=10) and controls (n=6). All the rats then underwent stereotactic implantation of electrodes in the left amygdala (LA), left dorsal hippocampus (LdH), left ventral hippocampus (LvH), and the left sensorimotor cortex (LCx). A stainless steel cannula also was introduced into the LA. Rats except controls later received 1.0 microg of kainic acid (KA) via the cannula. Controls received phosphate buffer solution alone. In the untransection group, multiple spike discharges in the LA immediately propagated concurrently to the LvH and LdH. Propagation involved the LCx to become status epilepticus 1 to 2 h after KA injection. Seizures, characterized by mastication, salivation, facial twitching, forelimb clonus, and sometimes rearing and falling, lasted 1 to 2 days. Microscopic examination revealed severe neuronal cell damage in the LA, LvH, and LdH. In the transection group, multiple spike discharges initiated from the LA and were propagated to LvH, but LdH as well as LCx involvement was slight. Status epilepticus involved only the LA and LvH 1 to 2 h following KA injection. Seizures subsided within 24 h, showing no ictal manifestations except for aggressiveness. Overall, seizures were weak and transient compared with those in controls. Histologically, hippocampal neuronal damage was slight, but damage to amygdalar neurons was similar to that in untransection group. No electroclinical and histological changes were seen in controls. These results indicated that connections between the dorsal and ventral hippocampus are important for full development of KA-induced amygdalar seizures.
...
PMID:Hippocampal transection attenuates kainic acid-induced amygdalar seizures in rats. 1128 62

Estrogens protect ovariectomized rats from hippocampal injury induced by kainic acid-induced status epilepticus (SE). We compared the effects of 17beta-estradiol in adult male and ovariectomized female rats subjected to lithium-pilocarpine-induced SE. Rats received subcutaneous injections of 17beta-estradiol (2 microg/rat) or oil once daily for four consecutive days. SE was induced 20 h following the second injection and terminated 3 h later. The extent of silver-stained CA3 and CA1 hippocampal neurons was evaluated 2 days after SE. 17beta-Estradiol did not alter the onset of first clonus in ovariectomized rats but accelerated it in males. 17beta-Estradiol reduced the argyrophilic neurons in the CA1 and CA3-C sectors of ovariectomized rats. In males, estradiol increased the total damage score. These findings suggest that the effects of estradiol on seizure threshold and damage may be altered by sex-related differences in the hormonal environment.
...
PMID:Estradiol reduces seizure-induced hippocampal injury in ovariectomized female but not in male rats. 1275 99


<< Previous 1 2 3 Next >>

---