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Biomedical subjects

P Jenner

Publications and source records attributed to P Jenner.

At least 469 records · Page 26Linked to original sources
PubMed1977

Behavioural and biochemical effects of chronic reduction of cerebral noradrenaline receptor stimulation.

Mice were given various 7-day treatments designed to reduce cerebral noradrenergic function. Following these treatments, alterations in the sensitivity of limbic forebrain adenylate cyclase to noradrenaline (NA), and in the locomotor response of the mice to dopaminergic and noradrenergic agonists were studied. An enhanced response of the NA-sensitive adenylate cyclase to 1-NA(10-5 M), in comparison to control mice, was demonstrated after treatments producing a chronic reduction in stimulation of alpha-adrenergic receptors (phenoxybenzamine 10 mg/kg per day), beta-adrenergic receptors (propranolol, 0.05% diet), all noradrenergic receptors (reserpine 5 mg/kg, followed by FLA-63, 25 mg/kg per day), and dopaminergic as well as noradrenergic receptors (chlorpromazine, 5 mg/kg per day). Sensitivity of the NA-stimulated adenylate cyclase was not altered by chronic treatment with FLA-63 alone as a 0.05% diet. However, none of the chronic treatments except chlorpromazine administration increased the locomotor activity recorded for 2 h following apomorphine (1 mg/kg, s.c.) and none of the treatments altered the locomotor activity recorded in the 2 h following administration of the alpha-adrenergic agonist clonidine (1mg/kg, i.p.), or a combination of apomorphine (1 mg/kg, s.c.) plus clonidine (1 mg/kg, i.p.) The results support the hypothesis that noradrenergic stimulation plays a role secondary to that of dopamine in the production of locomotor activity.

Adenylyl Cyclases↗
PubMed1977

Clinical, biochemical, and physiological features distinguishing myoclonus responsive to 5-hydroxytryptophan, tryptophan with a monoamine oxidase inhibitor, and clonazepam.

Fifteen patients with a variety of myoclonic syndromes were studied clinically, pharmacologically, and physiologically. CSF tryptophan, 5HIAA, and HVA were also measured. Of these patients, 8 were improved to varying degrees by therapy with 5HTP, tryptophan in combination with MAOI (but not tryptophan alone), and clonazepam. This group included 6 cases of post-anoxic myoclonus, one case of post-traumatic myoclonus and one undiagnosed case of non-progressive focal myoclonus and epilepsy. In this group low levels of CSF 5HIAA were found compared to non-responsive cases and controls. Two cases of dysynergia cerebellaris myoclonica, 2 cases of undiagnosed aetiology, 2 cases of essential myoclonus, and one case of palatal myoclonus failed to respond to drug therapy. However, even amongst the responsive group the improvement varied. The most dramatic responses were seen in those patients in whom physiological study suggested that myoclonus was mediated by brain-stem structures. Less dramatic responses were seen in patients in whom the myoclonus appeared to originate from cortical structures. The neurochemical basis of myoclonus responding to 5HT precursors and clonazepam is discussed. It is suggested that such myoclonus arises from a relative hypoactivity of the 5HT neuronal system which results in a release of abnormal responses to sensory stimuli which characterize this type of myoclonus.

5-Hydroxytryptophan↗
PubMed1977

Amphetamines, growth hormone and narcolepsy.

1 Plasma amphetamine and growth hormone levels have been measured in eight normal and twenty-six narcoleptic subjects following a single dose of (+)-amphetamine (20 mg) or (-)-amphetamine (20 mg) by mouth. 2 Peak plasma levels and the shape of the plasma amphetamine-time curve were similar with both isomers in normal and narcoleptic subjects. 3 In most normal subjects both (+)-and (-)-amphetamine (20 mg) caused an increase in the plasma concentration of growth hormone. The two isomers were approximately equipotent in this respect. Neither (+)- nor (-)-amphetamine (20 mg) caused an increase in plasma growth hormone concentration in narcoleptics. 4 Following amphetamine (30 mg), two of six narcoleptic subjects had an increase in plasma growth hormone concentration. 5 Levodopa (250 mg) with (-)-alpha-methyldopa hydrazine 25 mg (Sinemet) by mouth, caused a rise in plasma growth hormone concentration in most normal subjects. The magnitude of the Sinemet-induced rise in plasma growth hormone concentration in narcoleptics was less than in normal subjects.

Adult↗
PubMed1977

Plasma DOPA levels and growth hormone response to levodopa in parkinsomism.

It has been suggested that the therapeutic response to levodopa in patients with Parkinson's disease may be related to changes in plasma growth hormone concentration. In order to examine this problem, we have determined plasma DOPA and growth hormone levels after a standard oral levodopa load in 32 patients with Parkinson's disease. Levodopa caused an increase in plasma growth hormone concentration in 30 subjects. The magnitude and timing of this growth hormone response was not related to the clinical response, the presence or absence of response swings, or the occurrence of dyskinesias. The growth hormone response to levodopa is normal in patients with Parkinson's disease and not altered by long-term levodopa treatment.

Adult↗
PubMed1976

The roles of noradrenaline and dopamine in contraversive circling behaviour seen after unilateral electrolytic lesions of the locus coeruleus.

Unilateral electrolytic lesions of the locus coeruleus in rats result in spontaneous ipsiversive rotation, which is then replaced by contraversive rotation. One week after lesioning, when spontaneous turning ceases, apomorphine and d-amphetamine elicit contraversive circling behaviour, which was not affected by noradrenergic receptor blockade but was abolished by dopamine receptor blockade. The drug-induced contraversive circling response was also reproduced by piribedil but not clonidine. Combined unilateral electrolytic locus coeruleus and substantia nigra lesions on the same side resulted in apomorphine- and d-amphetamine-induced ipsilateral rotational behaviour which was indistinguishable from that seen with substantia nigra lesions alone. In rats with unilateral locus coeruleus lesions, the dose of intrastriatally injected apomorphine required to produce circling was less on the lesioned than the non-lesioned side. Direct injection of noradrenaline into one substantia nigra caused contraversive circling. Direct injection of phenoxybenzamine into one substantia nigra followed by apomorphine caused ipsiversive circling. The results suggest that the circling behaviour seen after unilateral locus coeruleus lesions depends on an asymmetry of striatal dopamine receptor activity and are consistent with a proposed coeruleus-nigral noradrenergic pathway, which enhances impulse flow in the dopaminergic nigrostriatal system.

Animals↗