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noradrenaline/seizures
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 248 rezultatus
Alpha-noradrenaline modulation of D,L-allylgycine seizures.
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The preferential alpha 2-noradrenergic agonist clonidine dose-relatedly increased the onset of seizures and mortality times, and decreased severity in rats treated with D,L-allylglycine. These effects were reduced by a dose (2.5 mg/kg) of the preferential alpha 2-antagonist yohimbine, which was
A possible role for spinal noradrenaline in the mechanisms of 6-hydroxydopamine against pentylenetetrazol induced convulsions in rats.
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The threshold of the generalized clonic convulsions induced by intravenous infusion of pentylenetetrazol (PTZ) was significantly increased by the intraperitoneal administration of noradrenaline (NA) neurotoxin, 6-hydroxydopamine, which produced no changes in the levels of catecholamines in discrete
Seizure development and noradrenaline release in kindling epilepsy after noradrenergic reinnervation of the subcortically deafferented hippocampus by superior cervical ganglion or fetal locus coeruleus grafts.
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Solid pieces of fetal locus coeruleus (LC) or superior cervical ganglion (SCG) were placed into a fimbria-fornix lesion cavity in 6-hydroxydopamine-treated, noradrenaline (NA)-denervated rats. Six to 8 months later, all animals were subjected to electrical kindling stimulations in the hippocampus
Regional concentrations of GABA, serotonin and noradrenaline in brain at onset of seizures induced by lindane (gamma-hexachlorocyclohexane).
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The main objective of this study was to determine the modifications induced by the pesticide lindane (gamma-hexachlorocyclohexane) in the regional concentration of neurotransmitters in brain, taking the tonic-clonic seizure as the main sign of its neurotoxic action. The animals were given lindane
Selective depletion of spinal noradrenaline inhibits post-decapitation convulsions in rats.
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Local administration of 6-hydroxydopamine in the subarachnoidal space of the spinal cord in rats resulted in a selective long-lasting depletion of spinal noradrenaline, but not of dopamine, and prevented the occurrence of post-decapitation convulsions.
Brain noradrenaline concentration in seizure-prone chicks, Gallus domesticus.
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The mutant, sex-linked recessive px (paroxysm) gene, expressed in female White Leghorn chicks (Gallus domesticus), causes seizures beginning on approximately day 9 after hatching. In an attempt to determine possible central nervous system involvement in the seizures, brain levels of the putative
Paradoxical effect of noradrenaline-mediated neurotransmission in the antinociceptive phenomenon that accompanies tonic-clonic seizures: role of locus coeruleus neurons and α(2)- and β-noradrenergic receptors.
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The postictal state is generally followed by antinociception. It is known that connections between the dorsal raphe nucleus, the periaqueductal gray matter, and the locus coeruleus, an important noradrenergic brainstem nucleus, are involved in the descending control of ascending nociceptive
Synaptosomal high-affinity noradrenaline uptake does not differ between mice susceptible (DBA/2J) and resistant (C57 BL/6) to audiogenic seizures.
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Abnormalities in noradrenaline-mediated neurotransmission have been advocated as a basis of the age-related susceptibility of DBA/2J mice to generalised convulsions induced by auditory stimulation. We have measured the kinetics of synaptosomal high-affinity noradrenaline uptake in 5 brain regions of
Plasma concentrations of prolactin, noradrenaline, vasopressin and oxytocin during and after a prolonged epileptic seizure.
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The time course and extent of changes in plasma prolactin, noradrenaline, vasopressin and oxytocin levels is reported following serial observations of a prolonged epileptic seizure arising in the temporal lobe, recorded by video-EEG-telemetry, in which the epileptic activity evolved from a simple
Depletion of noradrenaline fails to affect kindled seizures.
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Convulsive seizures were kindled in rats by repeated stimulation of the amygdala, and the subjects then received intracerebral injections of 6-hydroxydopamine into the dorsal noradrenergic bundle. Although this treatment severely depleted noradrenaline, there was no effect on the intensity or
Host regulation of noradrenaline release from grafts of seizure-suppressant locus coeruleus neurons.
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Intrahippocampal implants of noradrenaline-rich neural tissue from the fetal locus coeruleus region suppress development of seizures induced by hippocampal kindling stimulation in hyperexcitable, noradrenaline-depleted rats. In the present study the intracerebral microdialysis technique has been
Age- and seizure-related changes in noradrenaline and dopamine in several brain regions of epileptic El mice.
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Noradrenaline (NA) and dopamine (DA) levels in six brain regions of stimulated and nonstimulated El (El[s] and El[ns]) mice and their maternal ddY mice were determined at various ages and various times after a convulsion. The NA levels in the striatum and hippocampus of 12-week-old El[s] and El[ns]
Physiological function of descending noradrenaline projections to the spinal cord: role in post-decapitation convulsions.
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Destruction of the descending noradrenergic innervation to the spinal cord, but not that to the cerebellum or the forebrain, by the use of intracerebral injection of 6-hydroxydopamine completely prevented the occurrence of the usual itation convulsion. Depletion of brain noradrenaline by synthesis
Effects of AT1 receptor antagonism on kainate-induced seizures and concomitant changes in hippocampal extracellular noradrenaline, serotonin, and dopamine levels in Wistar-Kyoto and spontaneously hypertensive rats.
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In the management of epilepsy, AT1 receptor antagonists have been suggested as an additional treatment strategy. A hyperactive brain angiotensin (Ang) II system and upregulated AT1 receptors are implicated in the cerebrovascular alterations in a genetic form of hypertension. Uncontrolled
Depletion of brain noradrenaline, but not dopamine, by intracerebral 6-hydroxydopamine potentiates convulsions induced by electroshock.
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Intracerebral injection in rats of 4 microgram of the catecholamine neurotoxin 6-hydroxydopamine was used to deplete forebrain noradrenaline to less than 10% of control values and separately to deplete brain dopamine to less than 15% of control. The susceptibility of these animals to
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