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Biomedical subjects

M E Corcoran

Publications and source records attributed to M E Corcoran.

At least 73 records · Page 4Linked to original sources
PubMed1980

Kindling of seizures with low-frequency electrical stimulation.

Repeated application of electrical stimulation to the amygdala at a frequency of 3 Hz resulted in the development of afterdischarge and behavioral seizures. The rate of low-frequency kindling was faster than that of kindling with conventional 60 Hz stimulation, but the form of the seizures kindled with the two frequencies of stimulation was identical. Low-frequency kindling was obtained only when pulses of sufficient duration and intensity were administered.

Amygdala↗
PubMed1980

Role of forebrain catecholamines in amygdaloid kindling.

The rate and pattern of seizure development provoked by repeated electrical stimulation of the amygdala (kindling) was assessed in rats that had been pretreated with intracerebral injections of the selective catecholaminergic neurotoxin 6-hydroxy-dopamine. Rats with selective depletion of forebrain noradrenaline displayed a highly significant facilitation of both primary-site and secondary-site kindling, whereas no such effect occurred in rats with selective depletion of forebrain dopamine. The facilitative effects of noradrenaline depletion were apparently related to disinhibition of the spread of seizure discharge from the stimulated site rather than to increased epileptogenicity in the stimulated site itself. These results are consistent with previous evidence that noradrenaline reduces the susceptibility of the central nervous system to epileptiform activity, and they suggest that a lessening of seizure-suppressant noradrenergic function in the forebrain might be part of the mechanism underlying kindling.

Amygdala↗
PubMed1980

Kindling in the seizure-prone and seizure-resistant Mongolian gerbil.

The kindling response in the amygdala of each of two strains of Mongolian gerbil bred for resistance to and suceptibility to stress-precipitated seizures was assessed. Seizure-prone gerbils had a lower afterdischarge threshold, a longer initial afterdischarge duration, and required fewer sessions to develop generalized kindled convulsions. Following kindling, the precipitated seizure pattern was exacerbated in both groups. These results suggest that the naturally occurring and kindled seizure states may depend in part on a common neural mechanism in this species.

Amygdala↗
PubMed1979

Catecholamines and convulsions.

Severe depletion of brain noradrenaline and separately of brain dopamine was induced in rats by intracerebral injection of the selective neurotoxin 6-hydroxydopamine, and the susceptibility of the treated animals to various seizure-inducing manipulations was examined. A significant potentiation of the seizures induced both by Metrazol and by electroconvulsive shock was found in animals depleted of brain noradrenaline, but no alteration was seen after depletion of brain dopamine on either measure. The catecholaminergic drug cocaine also induced seizures, but these were found not to depend on either brain noradrenaline or dopamine as they continued to occur in the virtual absence of either catecholamine. It is concluded that cocaine induces seizures by a non-specific toxic mechanism and that noradrenaline, but not dopamine, is involved in reducing the suceptibility of the central nervous system to the several distinct forms of seizure induction examined.

Animals↗
PubMed1979

Noradrenergic processes involved in the locomotor effects of ethanol.

Male albino Wistar rats were depleted of forebrain noradrenaline by intracerebral injection of 4 microgram of 6-hydroxydopamine into the noradrenaline bundles in the mesencephalon. The locomotor response was examined in response to intraperitoneal injection of ethanol. The locomotor stimulation by 0.1 g/kg ethanol was not altered by the lesion, whereas the sedation found in response to 1 g/kg in controls failed to occur in the lesioned rats and instead a stimulation was seen.

Animals↗
PubMed1979

Noradrenaline and ethanol intake in the rat.

Intracerebral injection of 4 microgram of the neurotoxin 6-hydroxydopamine (6-OHDA) was used to deplete forebrain noradrenaline (NA) in rats to less than 5% of control values without affecting brain dopamine (DA) and the oral consumption of ethanol examined. Control rats showed a progressive increase in their intake of a 15% ethanol solution and after 15 days were consuming large quantities. This increase did not occur in NA depleted rats, which after 15 days had consumed no more than a few millilitres of the solution in total. The results are discussed in terms of a central noradrenergic basis of ethanol reward.

Alcohol Drinking↗
PubMed1979

Photically induced seizures in the yellow baboon, Papio cynocephalus.

Significant susceptibility to photically induced seizures has in the past been observed only in Senegales baboons (Papio papio) and epileptic humans. However, we have unexpectedly observed a photomyoclonic response to intermittent photic stimulation in 5 of a sample of 6 yellow baboons (Papio cynocephalus).

Animals↗
PubMed1979

Depletion of brain noradrenaline, but not dopamine, by intracerebral 6-hydroxydopamine potentiates convulsions induced by electroshock.

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 electroconvulsive shock-induced convulsions was examined, and a significant potentiation of the response was seen in the rats depleted of noradrenaline but not in those depleted of dopamine. The duration of the convulsion was significantly increased as a result of loss of forebrain noradrenaline.

Animals↗