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Biomedical subjects

C D Marsden

Publications and source records attributed to C D Marsden.

At least 811 records · Page 45Linked to original sources
PubMed1982

The mode of action of sulpiride as an atypical antidepressant agent.

It can be said that sulpiride exerts a disinhibitory effect in both depression and schizophrenia but this is not associated with mechanisms through which typical antidepressant or anxiolytic agents act. Sulpiride acts selectively as a dopamine receptor antagonist in the brain, its effects on other neuronal systems being extremely limited. Indeed, it may act even selectively within the dopamine systems in that it would appear it specifically interacts with one sub-population of cerebral dopamine receptors. Within a given dopamine receptor system sulpiride may exert a differential pre-synaptic action on dopamine neurones although the evidence for this remains controversial. The disinhibitory effects in depression may be due to a preferential pre-synaptic action of the drug on dopamine neurones causing over-activation of cerebral dopamine post-synaptic receptors causing behavioural arousal and motor facilitation. On the other hand, the disinhibitory effect of sulpiride in schizophrenia may also involve the preferential pre-synaptic action of the drug coupled with the specificity of post-synaptic action to result in little sedation or motor retardation. Sulpiride may also differentially antagonise post-synaptic dopamine receptors in different brain areas and this may also be critically involves in its unusual spectrum of neuroleptic action.

Animals↗
PubMed1982

Morphologic studies on adult neuronal-ceroid lipofuscinosis (NCL).

This report concerns morphologic findings in two middle-aged women, who died of sporadic adult neuronal ceroid-lipofuscinosis (NCL) and whose brains were studied histologically, by electron microscopy and by pigmentoarchitectonic techniques. In addition, the brain of a 35-year-old woman, who died of familial protracted juvenile NCL, was also investigated using pigmentoarchitectonic methods. Clinical, light and electron microscopic findings were compatible with the above-mentioned diagnosis. Pigmentoarchitectural analysis of homotypical isocortex in these three brains revealed (1) loss of pigment-laden stellate cells in layer II, (2) axonal enlargements of layer IIIab-pyramidal cells, and (3) considerable cell loss in layer Va. The changes were more pronounced in the brain affected by protracted juvenile NCL than in the two brains affected by adult NCL. The study emphasizes the value of the pigmentoarchitectonic technique, both in diagnostic neuropathology and in ascertaining patients afflicted with adult NCL. The ultrastructure of the lipopigments showed a motley spectrum of membrane formation such as curvilinear, fingerprint, or straight membranes and was less granular than regular senile lipofuscin.

Adult↗
PubMed1981

Circling behavior following unilateral kainic acid injections into rat striatum.

Unilateral injection of kainic acid (2.5-25 nmol) into rat anterior caudate putamen induced dose-related circling behaviour. Kainic acid (10 nmol) consistently caused initial weak ipsiversive circling lasting 1 h followed by prolonged strong contraversive rotation lasting in excess of 10 h. Unilateral intrastriatal administration of L-glutamic acid, or of monosodium L-glutamate, to normal rats, or administration of monosodium L-glutamate to rats with extensive decortication, did not induce circling behaviour. The simultaneous unilateral injection of monosodium L-glutamate (1 mumol) with kainic acid (10 nmol) did not modify circling behaviour induced by kainic acid. However, extensive decortication greatly reduced circling induced by unilateral intrastriatal kainic acid (10 nmol), and effect not reversed by the simultaneous administration of monosodium L-glutamate (1 mumol). Unilateral 6-hydroxydopamine lesions of the left nigrostriatal pathway abolished the initial ipsiversive rotation and potentiated the subsequent contraversive rotation for up to 4 h after intrastriatal injection of kainic acid (10 nmol). Peripheral administration of haloperidol (1 mg/kg i.p.) also abolished initial ipsiversive rotation and decreased the subsequent contraversive rotation. Electro-coagulation of the ipsilateral strio-nigral pathway prolonged the initial ipsiversive rotation produced by kainic acid, but markedly attenuated contraversive rotation. These findings suggest that circling induced by intrastriatal administration of kainic acid depends on intact corticostriate pathways, but it cannot be reproduced or modified by intrastriatal administration of glutamate. Kainic acid circling appears to be mediated via strio-nigral pathways, and to be modulated by dopaminergic function.

Animals↗
PubMed1981

Hypophysectomy does not prevent development of striatal dopamine receptor supersensitivity induced by repeated neuroleptic treatment.

Hruska et al. (1980) reported that hypophysectomy prevented the onset of dopamine receptor supersensitivity. We have repeated this investigation administering haloperidol (0.75 mg/day) or sulpiride (2 X 15 mg/day) or saline for 17 days, followed by a 3 day drug washout period, to sham-operated or hypophysectomised rats. Haloperidol or sulpiride pretreatment caused an enhancement of apomorphine-induced stereotyped behaviour and increased the number of specific striatal [3H]spiperone binding sites (Bmax) in both hypophysectomised and sham-operated animals compared to their respective saline controls. We conclude that hypophysectomy does not prevent the onset of striatal dopamine receptor supersensitivity induced by repeated neuroleptic treatment in the rat.

Animals↗
PubMed1981

Behavior of the long-latency stretch reflex prior to voluntary movement.

Attempts to elicit stretch reflexes from the 'relaxed' human long thumb flexor were made at various times prior to the onset of a voluntary contraction of that muscle. When the muscle was fully relaxed, there were no short or long-latency responses at the rates of stretch employed (about 600 degrees/sec). Without complete relaxation there was a small long-latency response, which occasionally increased in amplitude as the time for voluntary activation approached. This augmentation seemed to be a result of a subtle parallel augmentation of background EMG, anticipating the major voluntary contraction, thereby increasing the gain of the long-latency stretch response.

Electroencephalography↗