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H C Fibiger

Publications and source records attributed to H C Fibiger.

At least 37 records · Page 2Linked to original sources
PubMed1979

Avoidance, operant and locomotor behavior in rats with neostriatal injections of kainic acid.

Compared with saline injected controls, rats with bilateral injections of kainic acid (KA) in the dorsal neostriatum showed increased locomotor response to d-amphetamine, increased resistance to extinction and impaired acquisition and retention of passive avoidance. The KA injection resulted in loss of local neurons in the dorsal neostriatum, with no appreciable damage either to dopaminergic terminals or to extrinsic myelinated axons, thus supporting both the selective neurotoxic action of KA on neuronal perikarya and the proposed similarity of KA-induced neostriatal lesions with those found in the caudate-putamen of patients with Huntington's disease. Although loss of hippocampal neurons was occasionally observed, the behavioral results could not be wholly attributed to hippocampal damage, since rats with no demonstrable extrastriatal lesions were not less impaired than those with hippocampal damage. An altered arousal reaction to stressful situations might account for the learning and memory impairments of the KA neostriatal rats.

Animals↗
PubMed1979

Neurochemical basis of the dorsal bundle extinction effect.

Injection of 6-hydroxydopamine into the mesencephalon of the rat has been found to cause resistance to extinction on continuously reinforced schedules. The neurochemical basis of this effect was investigated by using another concentration of 6-hydroxydopamine and by another position of injection. Severe depletion of forebrain noradrenaline was found after these injections with no change in dopamine, serotonin, cholinergic or GABAergic parameters in any brain area measured. The noradrenergic nature of the effect was further shown by the reversal fo the usual behavioural effect following pretreatment with a noradrenaline uptake inhibitor (desimipramine, 25 mg/kg 30 min prior to intracerebral injection of 6-hydroxydopamine). This rules out non-specific damage caused by the 6-hydroxydopamine as the neurochemical basis of the dorsal bundle extinction effect. Failure to find resistance to extinction after either kainic acid or 5-7 dihydroxytryptamine injection seems also to exclude respectively cell body loss at the injection site or damage to serotonergic systems. It is concluded that the dorsal bundle extinction effect is noradrenergic in nature.

5,7-Dihydroxytryptamine↗
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

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

Noradrenergic influences on catalepsy.

Widespread depletion of forebrain noradrenaline, produced by the intracerebral injection of 4 microgram of 6-hydroxydopamine into the fibres of the dorsal noradrenergic bundle, potentiated the catalepsy induced by 20 mg/kg of morphine and severely attenuated the catalepsy induced by two separate cholinergic agonists, arecoline and pilocarpine. It did not, however, affect haloperidol catalepsy at any of the four doses tested. These results suggest that cholinergic catalepsy may be critically dependent on an intact noradrenergic substrate, perhaps through cholinergic receptors located either presynaptically on noradrenergic terminals or on the cell bodies of origin in the locus coeruleus. Noradrenaline appears to play a modulatory role in morphine catalepsy, although other sites of action must also be involved. Ascending noradrenergic systems do not appear to influence haloperidol catalepsy.

Animals↗
PubMed1978

6-OHDA lesion to the dorsal noradrenergic bundle alters morphine-induced locomotor activity and catalepsy.

Rats show an initial depression in locomotor activity in response to doses of morphine greater than 5 mg/kg during the first hour after injection which is followed by a prolonged hyperactive phase. The effect of bilateral 6-hydroxydopamine (6-OHDA) lesions to the dorsal noradrenergic bundle on this biphasic action of morphine was studied. These lesions were found to significantly potentiate the locomotor depressant effects of morphine at 10.0 and 20.0 mg/kg while leaving the subsequent stimulant action of morphine unchanged. The cataleptic action of morphine at 20.0 mg/kg as measured in a separate test was also potentiated. These lesions were found to deplete hippocampal and cortical noradrenaline (NA) to 3% and hypothalamic NA to 32% of control values and also to cause significant increases in cerebellar and spinal NA. These data suggest a role for NA in the depressant effects of morphine but not in its subsequent stimulant actions which appear to be mediated by other neurochemical systems.

Animals↗
PubMed1978

Kainic acid lesions of the striatum: behavioural sequalae similar to Huntington's chorea.

Kainic acid (3 nmoles bilaterally) was injected into the dorsal striatum of the rat producing virtually complete destruction of cell bodies in this structure but without directly affecting the dopamine terminals ascending from the substantia nigra and terminating in the striatum. Other fibres of passage, such as the internal capsule, were also spared. The locomotor and stereotypy responses to doses of amphetamine, a dopamine releasing agent, were found to be consistently enhanced after this lesion. The stereotypy and locomotor activity in response to the direct receptor agonist, apomorphine, however were not consistently affected. The results are interpreted in terms of a functional dichotomy between dorsal and ventral striatum and in terms of previously demonstrated electrophysiological alterations in the striatonigral feedback loop after kainic acid injection. Similarities are noted with the effects of these two stimulant drugs in human patients with Huntington's disease, thus strengthening the kainic acid animal model of this disease, first proposed on biochemical grounds.

Animals↗