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Biomedical subjects

J A McCaughran

Publications and source records attributed to J A McCaughran.

35 records · Page 2Linked to original sources
PubMed1982

Changes in the convulsive threshold in the developing rat following chronic administration of pentylenetetrazol.

The acute and chronic effects of pentylentetrazol (PTZ) on convulsive behavior in the developing rat pup were investigated. Acute treatment at 10 or 15 days of age with 50 or 80 mg/kg evoked clonic or tonic-clonic convulsions from all rats. However, daily administration of equivalent dose levels from 5 to 16 days of age was associated with a marked reduction in the incidence of these convulsions. Alternate day treatment from 5 to 16 days of age with 80 mg/kg or an ascending series of dose levels (10 mg/kg/day increments) was not accompanied by a reduction in convulsive behavior. The present results indicate that treatment of infant rats with PTZ is followed by a 24-48 h increase in convulsive threshold. This phenomenon may be associated with a developmental process since daily treatment past 15 days of age was characterized by a gradual reappearance of convulsive behavior.

Age Factors↗
PubMed1980

The effect of kainic acid on cholinergic enzymes and receptors in the amygdala complex of the rat.

Kainic acid (KA) was injected into the amygdala (AM) complex of the rat and its effect on the cholinergic enzymes, choline acetyltransferase (CAT) and acetylcholinesterase (AChE), and the binding of the muscarinic ligand, [3H]quinuclidinyl-benzilate (QNB) and the nicotinic ligand [125I]alpha-bungarotoxin (aBuTX) was investigated. Ka produced a loss of approximately 35% of the CAT activity in the AM. However, no effect on AChE activity was observed. A 30--50% decrease in the number of muscarinic and nicotinic receptor sites was also found. CAT, AChE and QNB binding in the AM contralateral to the injection did not change. However, the binding of aBuTX was found to decrease by approximately 40%. The present results suggest that the loss of CAT activity in the AM after treatment with KA is due to the destruction of cholinergic neurons within the AM. The lack of effect on AChE suggests that the major cholinergic input to the AM is not affected by KA. In addition, the loss of nicotinic receptors in the contralateral AM may reflect anterograde degeneration of terminals that have nicotinic sites located on them, or may be secondary to the elicitation of intense seizure activity evoked by the KA.

Acetylcholinesterase↗
PubMed1979

Behavioural effects of 6-hydroxydopamine-induced depletion of spinal noradrenaline.

Bilateral injection of 6-hydroxydopamine (4 micrograms/2 microL) into the caudal medulla of rats reduced spinal noradrenaline (NA) to 6% of control values. No significant NA depletion was observed in the hippocampus, cortex, or cerebellum, and a small loss of NA was found in the hypothalamus. These lesions were found to elevate significantly threshold shock levels necessary to elicit jump responses, and they also abolished the reflexive alternating motor movements produced by decapitation. These data support the hypothesis that spinal NA mechanisms modulate reflexive motor movements. However, no significant effect of these lesions was found on either spontaneous or amphetamine-induced locomotor activity, suggesting that spinal NA does not play a significant role in these behaviours.

Amphetamine↗
PubMed1978

Antiepileptic and prophylactic effects of tetrahydrocannabinols in amygdaloid kindled rats.

The antiepileptic and prophylactic effects of delta9-tetrahydrocannabinol (delta9-THC) and delta8-THC were examined in rats that developed generalized seizures in response to intermittent electrical stimulation of the amygdala (kindling). Both isomers of the THC were able to acutely suppress kindled seizures, but consistent antiepileptic effects were obtained only with high, toxic dosages. Tolerance to the antiepileptic effects of THC developed very rapidly when the drugs were give repeatedly, and there was evidence that the repeated administration of a high dosage of delta9-THC resulted in a state of acute physical dependence. Administration of the isomers of THC during seizure development resulted in a suppression of kindling, suggestive of a prophylactic effect. The rate of rekindling after withdrawal of the drugs was not significantly different from that of vehicle-treated control rats, however, indicating that a genuine prophylactic effect was not obtained.

Amygdala↗
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↗
PubMed1975

Cortical electrographic correlates of convulsive seizure development induced by daily electrical stimulation of the amygdala in rats and cats.

Increasing complexity of neocortical AD morphology was associated with clinical seizure development of amygdaloid origin in both rats and cats. Chronological examination of cortical AD and IID patterns in cats suggests very early involvement of basal cortical areas. Delayed but progressive ictal participation of anterior neocortical areas with eventual development of IID was coincident with eventual development of IID was coincident with recruitment of ictal motor manifestations while neocortical asymmetry with contralateral "desynchronization" pattern persisted throughout seizure development. It is suggested that anterior neocortex participates in the clinical expression of seizure development while verticle ictal propagation into the brain stem is responsible for seizure generalization.

Amygdala↗
PubMedDate not supplied

Participation of the central cholinergic system in blood pressure regulation in the Dahl rat model of essential hypertension.

Participation of the cholinergic system in the regulation of blood pressure (BP) in the Dahl salt-sensitive (DS) and salt-resistant (DR) rat model of essential hypertension was investigated. It was found that systemic administration of 0.25 or 0.50 mg/kg physostigmine (PSTG) to unanesthetized, normotensive DS and DR rats caused a significant elevation in BP but did not affect heart rate. At both dose levels, the pressor response was markedly greater and significantly longer in DS rats than in DR rats. The response in both DS and DR rats was blocked by pretreatment with atropine sulfate but not with atropine methylnitrate. These results suggest that the pressor effects of PSTG are mediated by central cholinergic mechanisms, and enhanced central cholinergic activity may participate in the pathogenesis of hypertension in the DS rat.

Animals↗