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Biomedical subjects

M E Corcoran

Publications and source records attributed to M E Corcoran.

14 recordsLinked to original sources
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↗
PubMed1977

On the role of ascending catecholaminergic systems in intravenous self-administration of cocaine.

The role of ascending noradrenergic (NA) and dopaminergic (DA) systems in intravenous self-administration of cocaine in rats was investigated by examining the effects of 6-hydroxydopamine-induced lesions of these systems on responding for the drug on a FR-1 schedule of reinforcement. Lesions of the dorsal and ventral NA bundles that reduced hippocampal-cortical NA by 96% and hypothalamic NA by 72% failed to have any effects on responding for cocaine. Lesions of the nucleus accumbens that reduced the DA content of this nucleus by 90% resulted in a significant and long-lasting (15 days) reduction in self-administration of cocaine. Apomorphine self-administration was not affected in the same animals. Identical lesions of the n accumbens had only transient (2-3 days) effects on food-reinforced operant responding, suggesting that the prolonged disruption of cocaine self-administration was not the result of motor deficits. The results are discussed with reference to the possibility that DA terminals in the n accumbens may mediate some of the positive reinforcing properties of cocaine.

Animals↗
PubMed1975

Frontal lobe and kindling in the rat.

To test the hypothesis that the cortex participates in amygdaloid kindling in rats, bilateral aspiration lesions were made in various cortical areas in rats prior to kindling. Lesions in orbital cortex (on the dorsal lip of the rhinal sulcus) or prefrontal cortex (area 10) significantly retarded the rate of amygdaloid kindling; lesions in motor cortex, anterior cingulate cortex, or visual cortex were without effect. Detailed analysis indicated that the orbital lesioned and frontal-lesioned rats kindled relatively normally up to the second-last stage of amygdaloid kindling, in which stage they perseverated significantly longer than the controls and the other lesioned rats. These results suggest that areas of the frontal lobe participate in the elaboration and generalization of amygdaloid seizures in rats. Although retarded in rate, kindling nonetheless occurred in the lesioned rats, indicating that these cortical areas are not essential for the development of amygdaloid seizures.

Action Potentials↗