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

The effects on cortical kindling of atropine (a muscarinic, cholinergic blocking agent) and reserpine (a depleter of catecholamines and 5 hydroxytryptamine) were tested in this study. Atropine, which had previously been found to retard amygdaloid kindling, had similar but somewhat weaker effects on cortical kindling. Reserpine also had similar effects on cortical kindling compared to subcortical kindling in that it potentiated seizure responses.
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PMID:The effects of atropine and reserpine on cortical kindling in the rat. 26 55

Rats were given a single footshock while licking a water tube and tested 24 hr later for retention of the footshock experience. A single bilateral injection of a subseizure dose of physostigmine into the amygdala applied immediately, but not 18 hr, after the footshock imparied retention. This effect appeared to be somewhat localized, as physostigmine injected into the hippocampus or lateral ventricles did not disrupt retention. Conversely, a subseizure dose of atropine sulfate into the amygdala, given immediately or 18 hr after the footshock did not impair retention. Atropine injected concurrently with physostigmine into the same amygdaloid loci counteracted a potential physostigmine-induced retention deficit. Injection of carbachol into the amygdala also impaired retention; however, carbachol precipitated seizures and possibly exerted proactive consequences on performance. The time-dependent nature of the deficit following physostigmine is consistent with the view that injection of cholinergic agonists into the amygdala disrupts memory for the footshock experience.
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PMID:Effects of posttraining injection of cholinergic agonists and antagonists into the amygdala on retention of passive avoidance training in rats. 73 Aug 61

Behavioural analyses have been made of effects brought about by both single and combined injections of dopamine, haloperidol, carbachol and atropine into the caput nuclei caudati of rhesus monkeys. High doses of dopamine produced the subsequent development of three types of behavioural changes: an increase in the number of skilled manipulation movements (the dynamic phase); the appearance of a dystonic torticollis (the dystonic phase); and, finally, the appearance of an oro-lingual-facial dyskinesia and a number of dyskinetic activities in the extremities (the dyskinetic phase); low doses of dopamine solely produced the dynamic phase. Haloperidol only inhibited the dopamine-induced dynamic and dystonic phase: it did not suppress the dyskinetic phase. High doses of carbachol produced the subsequent development of four phases: a dynamic, dystonic, dyskinetic and epileptoid phase; the last one was marked by the appearance of secondary generalized epileptic seizures. Low doses of carbachol solely produced the dynamic phase. Atropine inhibited the carbachol-induced dynamic, dystonic and epileptoid phase; it did not suppress the dyskinetic phase. High doses of dopamine strongly modified the carbachol-induced phases: dopamine intensified the dystonic phase on the one hand, but it abolished the generalized epileptic seizures on the other hand. Apart from the fact that the data presented have confirmed that both dopaminergic and cholinergic mechanisms within the basal ganglia of rhesus monkeys are involved in the elicitation and modulation of both normal and abnormal motor activities, they have also revealed that the simple concept of a stristal acetylcholine-dopamine "see-saw" has to be revised. Furthermore, the data have suggested that development of supersensitive dopamine-sensitive sites is not the only mechanism that underlies the elicitation of the oro-lingual-facial dyskinesia. And finally, the present experiments have given clearcut evidence that an intrastriatal acetylcholine-dopamine "see-saw" fulfils and essential role in the process involved in the generalization of epileptic seizures.
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PMID:The acetylcholine-dopamine balance in the basal ganglia of rhesus monkeys and its role in dynamic, dystonic, dyskinetic, and epileptoid motor activities. 115 71

The behavioural and neuropathological effects of both systemic and intrahippocampal injections of paraquat dichloride (1,1'-dimethyl 4,4'-bipyridinium dichloride) were studied in rats. Paraquat (0.1-1.0 mumol) injected into the dorsal hippocampus, produced limbic motor seizures within a few minutes of injection followed by neuronal damage in the CA1 and CA3 pyramidal cell layers, pyriform cortex, dentate granule cell layer and in the hilus fascia dentata at 24 hr (n = 9 rats). A smaller dose of paraquat (10 nmol) was ineffective. The effects of intrahippocampal injections of paraquat (1 mumol) were prevented by administering it together with atropine (50 nmol; n = 6 rats) or by giving it 60 min. after MK 801 (0.3 mg.kg-1 intraperitoneally). Systemic injections of paraquat (20-100 mg.kg-1) also produced forelimb clonus and rearing in 10 out of 15 animals. Neuronal cell death was found 24 hr later in 9 of these rats and was restricted to the pyriform cortex, the brain region with the highest concentrations of paraquat. Atropine (150 mg.kg-1 intraperitoneally given 60 min. previously) completely prevented the motor seizures but cell death still occurred in 2 of the 6 animals tested. In conclusion, both systemic and intrahippocampal injections of paraquat produced behavioural excitation accompanied 24 hr later by brain damage and antagonist studies suggested involvement of muscarinic and NMDA receptors in the neurotoxic mechanism.
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PMID:Production of limbic motor seizures and brain damage by systemic and intracerebral injections of paraquat in rats. 148 May 53

Seizures induced by three convulsant treatments produced differential effects on the concentration of acetylcholine in rat brain. Status epilepticus induced by (i) coadministration of lithium and pilocarpine caused massive increases in the concentration of acetylcholine in the cerebral cortex and hippocampus, (ii) a high dose of pilocarpine did not cause an increase of acetylcholine, and (iii) kainate increased acetylcholine, but the magnitude was lower than with the lithium/pilocarpine model. The finding that the acetylcholine concentration increases in two models of status epilepticus in the cortex and hippocampus is in direct contrast with many in vitro reports in which excessive stimulation causes depletion of acetylcholine. The concentration of choline increased during seizures with all three models. This is likely to be due to calcium- and agonist-induced activation of phospholipase C and/or D activity causing cleavage of choline-containing lipids. The excessive acetylcholine present during status epilepticus induced by lithium and pilocarpine was responsive to pharmacological manipulation. Atropine tended to decrease acetylcholine, similar to its effects in controls. The N-methyl-D-aspartate (NMDA) receptor antagonist, MK-801, reduced the excessive concentration of acetylcholine, especially in the cortex. Inhibition of choline uptake by hemicholinium-3 (HC-3) administered icv reduced the acetylcholine concentration in controls and when given to rats during status epilepticus. These results demonstrate that the rat brain concentrations of acetylcholine and choline can increase during status epilepticus. The accumulated acetylcholine was not in a static, inactive compartment, but was actively turning-over and was responsive to drug treatments. Excessive concentrations of acetylcholine and/or choline may play a role in seizure maintenance and in the neuronal damage and lethality associated with status epilepticus.
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PMID:Seizures increase acetylcholine and choline concentrations in rat brain regions. 181 38

Investigations were made of the action of ACTH and LH-RH on a number of behavioural paradigms and the possible involvement of neurotransmitters or opiates by pretreatment of receptor blockers in rats and mice. ACTH delayed the extinction of active avoidance behaviour. Atropine and haloperidol blocked this action, whereas phenoxybenzamine and propranolol were ineffective. LH-RH or a highly potent analogue of LH-RH (D-Trp6-LH-RH) decreased the rate of disappearance of dopamine in the hypothalamus following alpha-methyl- paratyrosine inhibition of catecholamine synthesis, and blocked the accumulation of serotonin following MAO inhibition. LH-RH or the analogue attenuated the consolidation of passive avoidance learning. Apomorphine-induced cage-climbing was also inhibited by the LH-RH analogue, but this action was not influenced by naloxone. Open-field activity (ambulation, rearing and grooming) was decreased by the analogue peptide. Naloxone blocked the action on ambulation and rearing, but was ineffective on grooming. The LH-RH analogue caused a dose-dependent increase in cataleptogenic activity. This action could not be blocked with naloxone. The LH-RH analogue suppressed picrotoxin-induced seizures. Naloxone restored the situation to the control level. The data suggested that the effects of some neurohormones are mediated by transmitters or endogenous opiates, and that both peptide-transmitter and peptide-peptide interactions have to be considered in the action of neurohormones.
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PMID:Involvement of neurotransmitter and neuropeptides in behavioural action of some neurohormones. 198 90

A unique type of limbic seizures, maximal dentate activation, was used to examine the effects of cholinergic and adrenergic agents on the processes involved in epileptogenesis. The time to onset of maximal dentate activation was used to monitor the initiation of seizures while the duration of maximal dentate activation monitored termination of seizures. The cholinergic agonist pilocarpine shortened maximal dentate activation at 20 mg/kg and lengthened maximal dentate activation at 50 mg/kg, while both doses delayed the onset of maximal dentate activation. Atropine, a cholinergic antagonist, at 50 mg/kg, slowed the rate of lengthening of maximal dentate activation that occurred with repeated stimulation. The beta-adrenergic antagonist propranolol also slowed the rate of lengthening of maximal dentate activation at 3 mg/kg and shortened maximal dentate activation at 10 mg/kg. The alpha 2-agonist clonidine, at 0.5 mg/kg, shortened maximal dentate activation and increased the time to onset; at 0.1 mg/kg, clonidine did not affect maximal dentate activation. Pretreatment with reserpine had no effect on either the time to onset or duration of maximal dentate activation. These results indicate that both cholinergic and adrenergic mechanisms play important roles in the initiation and termination of limbic seizures.
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PMID:Cholinergic and adrenergic agents modify the initiation and termination of epileptic discharges in the dentate gyrus. 204 80

This study shows our clinical and therapeutical experience in 48 cases of infant COFA intoxication admitted in the Intensive Care Unit of "Emilio Civit Children Hospital", Mendoza, Argentina in a periode of seven years. They were investigated to determine the presence of Parathion in blood and gastric washing with the sodium hydroxide qualitative method, and also cholinesterase was detected in blood with a colorimetric method (the monotest cholinesterase). Age range from one to ten years with predominance from 3 to 4 years; 27 were males and 21 females. In almost all the cases (90%) the toxic ingressed through several ways, and from 10 to 30 minutes appeared the characteristic signs: miosis and bronchorrhea. Clinically in 30 cases the intoxication was considered dangerous and mild in the others. The data obtained by laboratory techniques were diagnostic only in half of the cases. Atropine's sulphate was done to all cases until their recuperation, in doses from 2.5 mg to 20 mg. The evolution was highly satisfactory, only two died and two remained with seizures. Always had thanklessness and carelessness with the child from living together adults, who playing handle and waste the toxic. In two occasions the intoxication was familiar by contaminated food.
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PMID:[Parathion poisoning]. 275 76

Rats were injected in the amygdala and other forebrain sites with nmolar amounts of the highly toxic organophosphate 'nerve agent' compounds soman or VX (O-ethyl-S-(2-diisopropylaminoethyl)-methylphosphonothioate) in an attempt to determine the mechanism(s) responsible for the permanent brain pathology that has been observed following systemic intoxication with these agents. Injections were performed using a stereotaxically guided microsyringe in animals maintained under halothane/oxygen anesthesia or using chronically implanted cannulae in conscious animals. Bilateral microsyringe injections of up to 11.0 nmol soman into the amygdala failed to evoke abnormal behavior or brain pathology. When rats were pretreated with lithium chloride, or when carbachol was coadministered, soman injections evoked repetitive clonic convulsions and neuropathology. Unilateral injections of 3.4 nmol of VX into the amygdala elicited convulsions and brain damage in 67% of the animals tested. Atropine pretreatment (15.0 mg/kg, i.p.) prevented the development of convulsions and brain damage. Neuropathology was observed only in animals that developed repetitive convulsions; the piriform and entorhinal cortex, amygdala, hippocampus and thalamus were the brain structures most consistently damaged. With unilateral injections, the damage was more severe on the side ipsilateral to the injection. The behavioral topography of the convulsions and the neuroanatomical distribution and nature of the subsequent pathology closely resemble that observed with systemic administration of these compounds. The results indicate that the nerve agents are not directly neurotoxic, that peripherally induced hypoxia or anoxia are unlikely mechanisms of the neuropathology, and that the brain damage produced by these compounds is primarily seizure-mediated.
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PMID:Direct microinjection of soman or VX into the amygdala produces repetitive limbic convulsions and neuropathology. 342 47

The ability of various drugs to prevent the onset of status epilepticus induced by administration of the muscarinic agonist, pilocarpine, to lithium-pretreated rats was determined. Motor limbic seizures and status epilepticus occurred in 100% of rats administered pilocarpine (30 mg/kg, s.c.) 20 h after pretreatment with lithium (3 meq/kg, i.p.). The latency to spike activity and to status epilepticus was 20 +/- 1 min and 24 +/- 1 min, respectively. Atropine, diazepam, phenytoin, carbamazepine, phenobarbital, paraldehyde, and L-phenylisopropyladenosine (L-PIA) prevented all phases of seizure activity induced by lithium/pilocarpine treatment. The initiation of status epilepticus was significantly prolonged by pretreatment with sodium valproate. These findings indicate that the seizures induced by administration of lithium and pilocarpine accurately model generalized tonic-clonic epilepsy. The anticonvulsant activity of L-PIA was prevented by prior treatment with the adenosine antagonist, theophylline. The latency to spike and seizure activity was decreased by theophylline, indicating that endogenous adenosine may have a tonic inhibitory influence on cholinergic neurons. Atropine, diazepam, phenobarbital, phenytoin, sodium valproate, L-PIA, and carbamazepine did not interrupt seizure activity when administered 60 min after pilocarpine (approximately 35 min after initiation of status epilepticus). When rats were administered paraldehyde at this time, status epilepticus was rapidly terminated and all rats survived. Thus, status epilepticus induced by lithium and pilocarpine provides a seizure model that is not responsive to conventional anticonvulsants.
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PMID:Effects of drugs on the initiation and maintenance of status epilepticus induced by administration of pilocarpine to lithium-pretreated rats. 358 62


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