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Biomedical subjects

R H Roth

Publications and source records attributed to R H Roth.

At least 271 records · Page 15Linked to original sources
PubMed1980

Chronic haloperidol or fluphenazine: effects on dopamine metabolism in brain, cerebrospinal fluid and plasma of Cercopithecus aethiops (vervet monkey).

Chronic treatment with haloperidol for 3 to 5 weeks (0.5 mg/kg, daily) resulted in significant increases of homovanillic acid (HVA) content in dorsal and orbital frontal cortex and in cingulate cortex. No change in HVA was seen in the olfactory cortex, basal ganglia, cisternal cerebrospinal fluid or plasma of animals chronically treated with haloperidol. Treatment with a single weekly dose of fluphenazine decanoate (5 mg/kg) for 3 weeks resulted in increased HVA levels in all the above brain regions, cisternal cerebrospinal fluid and plasma. Moreover, the fluphenazine-treated group had a significantly higher incidence of extrapyramidal side effects than the haloperidol-treated group. It is concluded that chronically increased dopamine metabolite production in the basal ganglia but not in cortex is reflected by increases in the HVA level of cerebrospinal fluid and plasma and is accompanied by severe extrapyramidal side effects.

Animals↗
PubMed1980

Correlation of cerebrospinal fluid serotonin and altered spinal cord blood flow in experimental trauma.

Serotonin levels in the cerebrospinal fluid (CSF) were determined at various time intervals following experimental spinal cord trauma and correlated with alterations in the intramedullary blood flow. At one hour after injury, a significant elevation of CSF serotonin was noted to parallel a marked reduction in white matter perfusion. The correlation between elevated CSF serotonin and decreased blood flow in the traumatized spinal cord suggests that serotonin may have pathogenetic importance relative to posttraumatic alterations in the intramedullary microcirculation. The possible role of serotonin in the pathophysiology of blood flow changes following experimental spinal cord injury are discussed as are the therapeutic implications.

Animals↗
PubMed1979

Denervation supersensitivity to serotonin in rat forebrain: single cell studies.

To investigate the development of denervation supersensitivity to serotonin (5-hydroxytryptamine, 5-HT) in the amygdala (AMYG) and the ventral lateral geniculate nucleus (vLGN), single cell recordings, microiontophoretic, histochemical and biochemical techniques were used in the present study. 5-HT projections to the vLGN and the AMYG were destroyed by 5,7-dihydroxytryptamine (5,7-DHT, a relatively selective toxin for 5-HT neurons) injected directly into the lateral ventricle or the ascending 5-HT pathway in the ventromedial tegmentum area. Enhanced responsiveness of cells to the inhibitory effect of microiontophoretically applied 5-HT (ionto-5-HT) began to develop within 24 h and approached a maximum 7 days after 5,7-DHT pretreatment. In general, the time courses for the reduction in both the density of 5-HT fluorescent varicosities and synaptosomal 5-HT uptake activity paralleled the time course for the development of denervation supersensitivity to 5-HT. During the first 2 days after 5,7-DHT, the enhanced sensitivity was selective for 5-HT; responses to D-lysergic acid diethylamide (LSD), norepinephrine (NE) and gamma-aminobutyric acid (GABA) were unchanged. Seven or more days after 5,7-DHT there was a marked increase of the responsiveness of neurons in the vLGN and the AMYG to both 5-HT and LSD (a 5-HT agonist which is not a substrate for the high affinity 5-HT uptake system). At these later times, the responsiveness of cells in the AMYG to NE and to a lesser extent GABA was also increased. In contrast to the marked supersensitivity seen after 5,7-DHT induced denervation, chronic administration of parachlorophenylalanine, a 5-HT synthesis inhibitor, failed to induce 5-HT supersensitivity.

5,7-Dihydroxytryptamine↗
PubMed1979

Antipsychotic drug action in schizophrenic patients: effect on cortical dopamine metabolism after long-term treatment.

In the brains of deceased schizophrenics who underwent long-term treatment with antipsychotic drugs, the concentration of homovanillic acid (a dopamine metabolite) was significantly increased in the orbital frontal, cingulate, and temporal tip areas of the cortex, but not in the putamen or the nucleus accumbens. The concentration of homovanillic acid was normal in the brains of schizophrenics who were not treated with drugs.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Clonidine reversal of increased norepinephrine metabolite levels during morphine withdrawal.

The production of the norepinephrine metabolite 3-methoxy-4-hydroxyphenethyleneglycol (MHPG) in brain regions innervated by the locus coeruleus was increased during naloxone-precipitated withdrawal from chronic morphine treatment. This MHPG increase was reversed by subcutaneous administration of clonidine. Changes in MHPG levels paralleled the elctrophysiological changes found by Aghajanian (1978) in locus coeruleus firing rate with similar treatments, demonstrating the usefulness of MHPG changes as an index of central noradrenergic function.

Animals↗
PubMed1979

3,4-Dihydroxyphenylacetic acid and homovanillic acid in rat plasma: possible indicators of central dopaminergic activity.

The concentrations of dopamine (DA) metabolites (free and conjugated) was measured in plasma and brain regions of rats by the mass spectrometric method of selected ion monitoring. Experimental treatments which altered the function of central dopamine neurons also induced concomitant changes in plasma 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Stimulation of the nigrostriatal pathway increased plasma DOPAC and HVA whereas lesion of the pathway decreased plasma metabolites. Several drug treatments induced parallel changes in brain and plasma concentrations of DA metabolites. It is suggested that changes in the concentration of DOPAC and HVA in rat brain are reflected by parallel changes in plasma. No conjugated forms of DOPAC and HVA were found in plasma and brain tissue of vervet monkeys (Cercopithecus aethiops).

3,4-Dihydroxyphenylacetic Acid↗