Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This investigation was carried out to test the hypothesis that amygdaloid epileptiform activity is due to cholinergic hyperactivity. It was designed to study the underlying physiopathology of, and to act as an experimental model for, psychomotor epilepsy. Neostigmine was injected intracerebrally into the amygdala of the cebus monkey with chronically implanted "chemitrodes" fitted with EEG recording electrodes. The injections were made in the basal amygdaloid nucleus which normally shows very high acetylcholinesterase (AChE) enzymatic activity in histochemical preparations. Neostigmine injection resulted in very high amplitude spike activity in the amygdala only. Other brain areas, including the neighboring temporal cortex, did not show any marked EEG changes. In the first day or two, these EEG changes were associated with myoclonus localized in the ipsilateral muscles of facial expression and also associated with masticatory seizures. Subsequently the animal became aggressive and remained so several months after the injection of neostigmine. The EEG changes continued for approximately 6 weeks. Intramuscular injections of atropine diminished the amplitude of the epileptiform EEG discharges and modified slightly the animal's behavior.
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PMID:Neostigmine activated epileptiform discharge in the amygdala: electrographic-behavioral correlations. 10 9

The enzymes of the cholinergic system have been investigated in discrete brain areas in alcohol-dependent rats, which were still intoxicated or were undergoing withdrawal. The ethanol intoxication resulted in a slight, but significant increase in choline acetyltransferase (CAT) activity in the caudate nucleus both 1 and 7 h after the last dose of ethanol. We also found a significant decrease in CAT activity in the temporal limbic cortex while rats were highly intoxicated. All other brain regions investigated, e.g., cerebellum, pons-medulla, frontoparietal cortex, hypothalamus and septum showed unchanged CAT activity. Rats were also analysed immediately following the onset of a withdrawal-induced audiogenic convulsive seizure where, in addition to the striatum, depressed CAT activity was observed in the hippocampus. In all the analysed situations acetylcholinesterase activity remained unchanged. These results show that ethanol intoxication leads to a perturbation in the synthetic capacity of acetylcholine in certain defined brain structures and that this may have some correlation to the observed behavioural impairments.
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PMID:Cholinergic involvement in ethanol intoxication and withdrawal-induced seizure susceptibility. 10 88

The activity of ATP-ase and acetylcholinesterase (AChE) in crude mitochondrial fraction (CMF) and microsomal fraction of rat brain cortex and the spinal cord was studied in clonic seizures evoked by electroshock and 5 min after them. Inhibition of the Na, K-ATP-ase activity of the CMF of the brain at the clonic phase of convulsions and an increase in the activity of this enzyme in all the fractions of the tissues under study at the postconvulsive period were revealed. The activity of Ca-ATP-ase in the CMF of the brain increased during the convulsions and decreased at the postconfulsive period. The activity of Mg-ATP-ase remained unchanged. The AChE activity, as a rule increased during the convulsions, and grew even more during the postconvulsive period; the spinal cord tissue displayed a reduction of the activation effect. A possibility of structural reconstructions in the excitable neuron membranes during the convulsive activity is discussed.
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PMID:[Na, K-ATP-ase and acetylcholinesterase activity of the membrane structures of the rat brain and spinal cord during the seizure process]. 13 79

When the insecticide parathion was administered to awake, unrestrained rats with chronically implanted brain electrodes, it was observed that the latency of the averaged flash-evoked potential in the visual cortex and superior colliculus was increased and the amplitude was decreased 2 to 4 hours later with responses returning to pretreatment levels about 8 hours after administration. Similarly, after administration of several dose levels of parathion in the rat, durations of phases of the maximal electroshock seizure (MES) pattern were altered to the greatest extent 4 hours later, but effects disappeared at 24 hours. These effects of parathion on the MES and evoked potentials coincided with a fall in blood and brain acetylcholinesterase (AChe) activities but disappeared after AChe inhibition had reached its peak and stabilized. Brain AChe activities required 2 to 4 weeks for recovery whereas blood AChe activity recovered in 1 week following inhibition by parathion (at least 2 mg/kg body weight). Studies in the monkey demonstrated similar results. Because these measurements of central nervous system function returned to normal despite continued inhibition of AChe activity, the results are interpreted to mean either that adaptation of evoked potentials or MES responses to prolonged AChe inhibition can occur in the rat and monkey after parathion administration or that some of the effects of parathion do not depend on AChe inhibition. Administration of DDT (100 mg/kg by mouth) to awake, unrestrained rats markedly increased the amplitude of spontaneous electrical activity in the cerebellum, whereas there was much less effect on electrical activity recorded simultaneously in the occipital cortex, reticular formation, and medial geniculate body. Similarly, DDT administration had marked effects on the averaged, sound evoked potential recorded in the cerebellum; DDT caused the appearance and increased the amplitude of an early component of this response not usually present during control recordings. Sound-evoked potentials recorded simultaneously from the frontal and occipital cortex and reticular formation were affected less or were decreased in amplitude by administration of DDT.
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PMID:Some aspects of neurophysiological basis of insecticide action. 18 31

The report pertains to some data on the cholinesterase activity in the blood serum and CSF of 62 patients with epilepsy, in correlation with different clinical characteristics (the severity of the disease, the character of the EEG, frequency of seizures, treatment efficacy, etc). In 86,8% of the cases there was a significant increase in the activity of serum cholinesterase. Increased cholinesterase activity correlated only with pronounced pathological changes in the EEG (reverse correlation) and the efficacy of treatment (direct correlation). After surgical treatment of 9 cases there was a drop in the cholinesterase activity of the blood serum and CSF, which correlated with an improvement in the general state of the patients. On the basis of personal experience, as well as literary data, it is assumed that an increase in the cholinesterase activity in epileptic patients is not related to the main etiological factors of this disease but is rather a secondary change, a peculiar "symptom" of the disease.
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PMID:[Role of the acetylcholine--cholinesterase system in the development of epilepsy]. 47 14

In rats with cobalt implanted in the right frontal cerebral cortex, acetylcholine (ACh) levels were depressed in the visually non-necotic, surrounding cortex at 7 and 14 days after surgery in comparison with values for controls treated with glass. At 21 days post-implantation, ACh levels were not different for glass and cobalt treatments. Effects of drugs affecting cholinergic function on electro-corticographic (ECoG) epileptiform activity were determined in rats implanted bilaterally with cobalt. The cholinesterase inhibitors, physostigmine and diisopropylfluorophosphate reduced both seizure activity and interictal spiking in these cobalt-treated rats. Hemicholinium-3 (HC-3), given subacutely initially inhibited seizures, but seizure frequency increased later during treatment. HC-3 did not appear to inhibit interictal spiking. These results suggest an involvement of brain cholinergic system in chronic cobalt experimental epilepsy. Seven days after cobalt implantation, HC-3 was less effective in depleting ACh in cerebral cortex adjacent to the cobalt-lesion than in similar tissue from rats with no cobalt implants. This suggests that the cholinergic neurons adjacent to the implant are not highly active at a time when seizure frequency is maximal.
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PMID:Cholinergic involvement in cobalt-induced epilepsy in the rat. 91 28

Physostigmine salicylate, a cholinesterase inhibitor, has been shown to reverse the effects of certain drugs with anticholinergic properties. The paper provides a brief historical account of physostigmine, reviews the cholinergic drugs and their effects and suggests a management protocol based on physiologic criteria. Twenty-six overdose cases, recently treated with physostigmine, are summarized. The controversy regarding the etiology of seizures following physostigmine administration is discussed.
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PMID:Physostigmine--its use and abuse. 93 11

The activity of acetylcholinesterase and butyrilcholinesterase was studied during prolonged seizures developing from a primary-cortical focus. The activity was found to spread both along the wide limbic system, which indicates to participation of cholinergic agents in processes of "recurrent generalization" of excitations, and along the horizontal system of fibers connecting both hemispheres. This latter finding indicates to participation of cholinergic mediatory mechanisms in formation of seizures.
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PMID:[Cerebral cholinesterase under conditions of a generalized convulsive seizure]. 102 30

The effects of tacrine (5 mg/kg i.p.), a potent acetylcholinesterase inhibitor, were studied in rats pretreated (24 h beforehand) with a single dose (12 mEq/kg i.p.) of LiCl. Tacrine and LiCl were ineffective when given individually. Tacrine elicited seizures and brain damage in 90% of the rats treated. The intracerebroventricular microinfusion of N omega-nitro-L-arginine methyl ester (300 micrograms given 24 h after LiCl administration) significantly reduced the seizures and brain damage produced by tacrine (given 15 min later). These experiments suggest that the seizures and brain damage elicited by tacrine may be due, in part, to increased nitric oxide production in the brain.
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PMID:Tacrine-induced seizures and brain damage in LiCl-treated rats can be prevented by N omega-nitro-L-arginine methyl ester. 132 16

The changes in extracellular acetylcholine and glutamate levels were determined, during the course of seizures induced by soman, an irreversible inhibitor of acetylcholinesterase, in the CA1 hippocampal area of rats previously injected with atropine or normal saline into septum. The marked increases observed in soman-treated animals were abolished in rats receiving atropine. These data strongly suggest that, during soman intoxication, septal cholinoceptive cells play a key role in controlling the release of acetylcholine and glutamate in hippocampus. The mechanisms underlying this phenomenon are discussed.
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PMID:Changes in hippocampal acetylcholine and glutamate extracellular levels during soman-induced seizures: influence of septal cholinoceptive cells. 135


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