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

Behavioral and neuropathological responses to increasing doses of morphine hydrochloride (10-75 micrograms) administered into the rat amygdala were studied. Unilateral microinjections of morphine in doses of 40 and 75 micrograms produced a sequence of behavioral alterations including staring spells, gustatory automatisms, wet dog shakes, motor limbic seizures and limbic status epilepticus. Lower doses of morphine (10 and 20 micrograms) showed different threshold for these behavioral phenomena but a similar time course of development. Histological examination of frontal forebrain sections revealed widespread, apparently seizure-mediated pattern of brain damage. Neuropathological alterations were observed in the olfactory cortex, thalamus, neocortex, hippocampal formation and amygdaloid complex. Pretreatment of animals with diazepam (10 mg/kg i.p.) prevented the development of sustained limbic seizures and brain damage caused by morphine, while pretreatment with naloxone hydrochloride (2-20 mg/kg i.p.) failed to affect morphine-induced convulsant activity and brain damage. These results may suggest that morphine elaborates sustained limbic seizures and widespread brain damage by mechanism underlying the antagonism of inhibitory amino acid neurotransmission and opioid receptors do not seem to be involved.
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PMID:Intraamygdaloid morphine produces seizures and brain damage in rats. 666 39

Kainic acid (KA), a heterocyclic structural analog of the putative excitatory neurotransmitter, glutamate (Glu), powerfully mimics many of the neuroexcitatory and neurotoxic properties of Glu. KA differs from Glu and its straight chain "excitotoxic" analogs, however, in inducing a limbic seizure-brain damage syndrome when administered subcutaneously (12 mg/kg) to adult rats. This syndrome consists of sustained seizures, resembling amygdaloid kindled seizures, and acute destruction of neural elements in limbic brain regions (amygdala, olfactory cortex, hippocampus, lateral septum and several thalamic nuclei). Early changes consist of massive edematous swelling of glia and neuronal dendrites and either swelling or dark cell changes in neuronal somata, with subsequent necrosis of many of the neurons involved. Elsewhere we demonstrated that pretreatment with morphine markedly enhances both the convulsant and brain damaging actions of KA. Here we report that pretreatment with 2 anticonvulsants (diazepam or phenobarbital) markedly reduces both athe seizure and brain damaging actions of KA, whereas, two other anticonvulsants (phenytoin or valproic acid) fail to suppress either phenomenon. Our findings suggest that a seizure mechanism underlies much of the limbic brain damage induced by systemic KA and that the toxic mechanism may have two mutually reinforcing components--a glutamergic excitatory component and a GABAergic disinhibitory component.
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PMID:Only certain anticonvulsants protect against kainate neurotoxicity. 679 81

Long-term records of field potentials during kindling were analysed in 2 preparations: the prepyriform cortex (PPC) in dog and the CA1 subarea of the hippocampus in rat. Besides the occurrence of after-discharges directly following the kindling stimulus, short transients were found to occur spontaneously between seizures: spontaneous inter-ictal transients or SITs. In both the PPC and the hippocampus 2 different types of SITs were encountered. Both types corresponded to a dipole layer centred around the main local pyramidal neurones (PPC or hippocampus). One type occurred early in the course of kindling and had the same polarity as the local evoked potential (EP) produced by stimulation of the lateral olfactory tract in PPC or of the Schaffer collaterals in the hippocampus. The other type occurred at later stages and had a reversed polarity to the EP. These findings were interpreted as indicating that at the onset of kindling spontaneously occurring depolarizations corresponding to the early type of SITs are restricted to the level of the synapses to which the kindling stimulus is applied; at a later stage, when convulsions are likely to occur, large spontaneous depolarizations corresponding to the late type of SITs are generated at the level of the cell bodies.
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PMID:Common aspects of the development of a kindling epileptogenic focus in the prepyriform cortex of the dog and in the hippocampus of the rat: spontaneous interictal transients with changing polarities. 696 23

The relationship between seizure propensity and the vascular anatomy of the anterior cerebral arteries, or stroke induced by unilateral ligation of the common carotid artery, was investigated utilizing well differentiated colonies of seizure-prone (SP) and non-seizure-prone (NSP) gerbils. Twenty SP and 20 NSP gerbils were perfused with a latex dye and the vascular patterns of the anterior cerebral arteries (ACA) were analyzed. In addition, 30 SP and 30 NSP gerbils were subjected to unilateral ligation of the common carotid artery and the number developing stroke (determined by clinical observation as well as by microscopic examination of the brain) was recorded. We found that in all animals the ACAs formed a fused-central vessel which vascularized the olfactory bulbs, as well as two lateral vessels (rostral arteries) that vascularized a previously undescribed nasal plexus. Neither the vascular pattern of the ACA, nor the frequency of occurrence of stroke following unilateral ligation was related to seizure propensity.
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PMID:Brain vasculature and induced ischemia in seizure-prone and non-seizure-prone gerbils. 705 30

The effects of bath-applied 4-aminopyridine on neurones and extracellular potassium and calcium concentrations were recorded in slices of guinea-pig olfactory cortex. Neurones were orthodromically activated by stimulating the lateral olfactory tract. 4-Aminopyridine (3-10 microM) had the following effects: (1) an increase in the frequency and amplitude of spontaneous postsynaptic potentials; (2) a prolongation and oscillatory behaviour of orthodromically evoked postsynaptic potentials; (3) induction of spontaneous or stimulus-evoked seizure-type discharges which were accompanied by large rises in extracellular potassium and falls in calcium concentration; (4) a prolongation of the lateral olfactory tract population fibre spike. Prior to paroxysmal depolarization, membrane potential, input resistance and soma spike duration were unaffected. In the seconds before seizure discharges, a late hyperpolarizing potential (evoked by orthodromic stimulation) was reduced in amplitude or abolished. Diphenylhydantoin (50 microM) or magnesium ions (5 mM) prevented paroxysmal activity. Our results show that 4-aminopyridine can produce seizure-type discharges in a brain slice preparation. The role of increased spontaneous potentials and possible loss of synaptic inhibition as causal factors for such discharges is discussed.
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PMID:Convulsant actions of 4-aminopyridine on the guinea-pig olfactory cortex slice. 710 8

In this experiment, a new model of partial status epilepticus (SE) is described which is based on the antecedent development of a kindled focus. Following kindling, the amygdala was stimulated continuously for 60 min with the previous kindling stimulus (60 Hz sine wave, 50 microA peak-to-peak). This treatment provoked SE in 22 of 35 rats. Without drug intervention, rats spontaneously recovered (SR group) from the seizure between 10 and 24 h. After recovery from SE, after discharge (AD) thresholds were elevated and remained so for the 2 weeks before sacrifice. The histologies of these SR rats indicated massive gliosis and degeneration of the ipsilateral hemisphere, extending from the medial olfactory bulb, through the amygdala-pyriform cortex to the ventral hippocampus. Damage was observed frequently in the midline thalamic nuclei and hippocampal CA1 fields. Interruption of the SE with Nembutal 30 min after the stimulation offset (30 Min group) was occasionally associated with slight gliosis at the kindled electrode, whereas interruption after 4 h of SE (4 Hr group) resulted in more extensive cell loss. The AD thresholds of the 30 Min group, like those of the rats which did not develop SE (NSE group), returned to near-normal values by 2 weeks after SE; only the NSE rats exhibited generalized seizures to their AD threshold stimulus. This model of SE results in brain pathology similar to that found in other models, but has the advantage of being uncontaminated by exogenous chemicals and toxins.
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PMID:A new model of partial status epilepticus based on kindling. 713 21

Ingestion of palatable and unpalatable solutions was measured in adult mice in which had been administered the common parasite of the dog, Toxocara canis alone, or in combination with lead. In addition, response to hot plate and susceptibility to electroconvulsive seizure were also measured. Results from the palatability test indicated that either lead or Toxocara may alter the mouse's mode of interacting with its environment. However, the two agents in combination interacted in their effects on consummatory behavior. Results from the hot plate and ECS measures were less clear with respect to how lead and/or Toxocara influence temperature reactivity and seizure susceptibility. Histological examination of the CNS in parasite infected animals revealed Wallerian Type degeneration of fiber pathways including the corpus callosum, olfactory tract, and cerebellar penduncles.
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PMID:Toxocara canis and lead alter consummatory behavior in mice. 727 5

Repeated audiogenic seizures (4 times a day for 14 days), in genetically selected sensitive mice, induce a significant decrease in GABA level in the following brain areas: nucleus caudatus, posterior colliculus, occipital and frontal cortex, cerebellum, substantia nigra, hippocampus, amygdala, and temporal cortex. No variations were observed in olfactory bulbs, pons medulla, hypothalamus, thalamus, or cochlear area.
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PMID:Effect of repeated convulsive seizures on brain GABA levels. 727 6

The effects of some gamma-aminobutyric acid (GABA) antagonists and other "convulsants" have been tested on neurones of the isolated olfactory cortex slice preparation of the guinea-pig using single cell intracellular and gross extracellular recording techniques. Bicuculline, picrotoxin, strychnine, leptazol, bemegride, and also theophylline and d-tubocurarine all increased the duration and amplitude of the excitatory postsynaptic potential, thereby producing a seizure-like discharge. These drugs reduced and shortened the peak conductance increase during the inhibitory postsynaptic potential (i.p.s.p.) in normal solution and after the i.p.s.p. had been prolonged by the presence of a barbiturate. The results suggested that these drugs antagonise synaptic inhibition through a common mechanism, perhaps by reducing the effect of neurally released GABA.
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PMID:Convulsants antagonise inhibition in the olfactory cortex slice. 744 24

We have previously reported that focally evoked limbic motor seizures rapidly increase levels of mRNA encoding nerve growth factor (NGF) and basic fibroblast growth factor (bFGF) in specific limbic system areas of the adult rat brain. The present studies examined the effect of both minimal and maximal electroconvulsive shock, applied via corneal electrodes, on NGF and bFGF mRNA levels in several limbic (entorhinal cortex, hippocampus, olfactory bulb) and extralimbic (striatum and cerebellum) brain regions. By 5 h following limbic motor seizures induced by low-intensity (minimal) electroshock (LES) (0.2 s, 50-70 mA; three times over a 1-h period), bFGF mRNA was significantly increased in entorhinal cortex and hippocampus, but not in the other regions examined. In contrast, tonic extensor seizures evoked by maximal electroshock (MES) (0.2 s, 150 mA; three times over a 1-h period) were associated with a significant increase in bFGF mRNA in all limbic and extralimbic regions examined. In the same animals, increases in NGF mRNA were limited to entorhinal cortex and hippocampus. Adrenal steroids were not required for the seizure-induced increase in NGF or bFGF mRNAs, based on the finding that adrenalectomized rats exhibited electroshock-induced increases in both NGF and bFGF mRNAs equivalent to the increase observed in sham-operated rats. It is suggested that the increase in mRNA levels for the neurotrophic factors occurs selectively in those regions which are especially activated by the specific seizure model, and represents an adaptive response to repeated noninjurious neuronal stimulation.
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PMID:Regional and temporal pattern of expression of nerve growth factor and basic fibroblast growth factor mRNA in rat brain following electroconvulsive shock. 751 52


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