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Biomedical subjects

H D Snoddy

Publications and source records attributed to H D Snoddy.

At least 55 records · Page 3Linked to original sources
PubMed1981

Repeated administration of pergolide to rats attenuates the acute elevation of serum corticosterone by pergolide.

A single injection (0.3 mg/kg IP) of pergolide mesylate, a dopamine agonist, increased serum corticosterone concentration several-fold in rats. This increase did not occur or was greatly diminished in rats that had received four previous daily injections of pergolide. The non-responsiveness to pergolide persisted at the second day after the last of 4 daily injections of pergolide, but by the third and fourth days the rats were again responsive to pergolide in terms of serum corticosterone elevation. The lowering of dopamine metabolites (3,4-dihydroxyphenylacetic acid and homovanillic acid) by pergolide occurred in pergolide-pretreated rats to the same extent as in control rats. Serum corticosterone concentration in pergolide-pretreated rats was elevated normally by a serotonin agonist, quipazine. Since the pituitary-adrenocortical system can be activated in pergolide-pretreated rats (indicated by the normal response to quipazine), the insensitivity to pergolide may be due to decreased responsiveness of central dopamine receptors mediating corticosterone elevation by pergolide.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Comparative effects of amantadine and amfonelic acid on dopamine metabolism in rat brain.

Amantadine (50 and 100 mg/kg IP) did not change basal levels of DOPAC (3,4-dihydroxyphenylacetic acid) or HVA (homovanillic acid) in rat brain and did not alter the increase in DOPAC levels resulting from dopamine receptor blockade by spiperone. The increase in HVA levels produced by spiperone was significantly, but only slightly, enhanced by amantadine at these doses. In contrast, amfonelic acid at a dose of 5 mg/kg increased DOPAC and HVA levels and enhanced several-fold the spiperone-induced elevation of DOPAC and HVA levels. Amfonelic acid at at 2.5 mg/kg dose enhanced the turnover of dopamine (measured by the decline in dopamine concentration after inhibition of tyrosine hydroxylation with alpha-methylytyrosine) in spiperone-treated rats, whereas amantadine (100 mg/kg) had a smaller and not statistically significant effect. Neither compound affected significantly dopamine levels in a alpha-methyltyrosine-treated rats not given spiperone. Although amantadine has been observed by earlier workers to enhance the stimulated release of dopamine, it does not appear to act in a manner similar too amfonelic acid.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1981

Sympathetic noradrenergic innervation of guinea-pig liver: histofluorescence and pharmacological studies.

Norepinephrine concentration was higher in guinea-pig liver than in rat or mouse liver and evidence was obtained that the norepinephrine was present within nerves. In guinea pigs, norepinephrine in liver was depleted by reserpine, 6-hydroxydopamine and metaraminol. The depletion by 6-hydroxydopamine and metaraminol was antagonized by prior treatment with desipramine, an inhibitor of uptake into norepinephrine neurons. Guinea-pig liver concentrated metaraminol to a greater extent than did rat liver; the concentration of metaraminol was lowered by desipramine pretreatment and, within three tissues of the guinea pig (heart greater than liver greater than muscle), paralleled the concentration of endogenous norepinephrine. These findings constitute pharmacological evidence for noradrenergic innervation of guinea-pig liver to a greater extent than in other species. Histofluorescence studies confirmed the existence of norepinephrine-containing nerve terminals in guinea-pig liver. Norepinephrine-containing varicosities were seen adjacent to the hepatic artery, portal vein and bile duct in the portal spaces and adjacent to sinusoid capillaries and hepatocytes in the liver parenchyma. These findings strengthen the evidence for sympathetic innervation of liver and suggest the guinea pig as a useful species in exploring physiological roles of noradrenergic innervation of liver.

Animals↗
PubMed1980

Elevation of serum prolactin acutely after administration of p-chloroamphetamine in rats.

p-Chloroamphetamine hydrochloride (0.5-10 mg/kg, i.p.) caused a rapid (within 30 minutes), dose-related increase in serum prolactin concentration in male rats. The effect was antagonized by pretreatment with p-chlorophenylalanine, an inhibitor of serotonin synethesis, or by metergoline, a serotonin receptor antagonist. The acute elevation of serum prolactin may have been mediated by the release of serotonin by p-chloroamphetamine.

Amphetamines↗
PubMed1980

Effect of serotonin-releasing drugs on serum corticosterone concentration in rats.

(+/-)p-Chloroamphetamine hydrochloride, at doses of 1-8 mg/kg i.p. in rats, caused a dose-related increase in serum corticosterone concentration. The increase occurred rapidly, within 30 min, and was over within 4 h. Evidence that the increase was mediated by serotonin release consisted of the following findings: (1) a similar increase did not occur with (+/-)o-chloroamphetamine or (+/-)p-chloro-alpha-methylbenzylamine, analogs of p-chloroamphetamine lacking its ability to deplete serotonin; (2) the increase was prevented by prior treatment with p-chlorophenylalanine, which reduced the brain stores of serotonin available for release by p-chloroamphetamine; (3) the increase was prevented by prior treatment with fluoxetine, an inhibitor of the uptake pump on serotonin neurons, which blocks serotonin release by p-chloroamphetamine, and (4) the increase was mimicked by fenfluramine and norfenfluramine, agents known to release brain serotonin in a manner similar to the action of p-chloroamphetamine. These findings strengthen earlier evidence that brain serotonin neurons have a stimulatory influence on pituitary-adrenocortical function in rats.

Amphetamines↗
PubMed1980

Comparative effects of p-chloroamphetamine and 1-(p-chlorophenyl)piperazine on 5-hydroxyindole concentration in rat brain.

1-(p-Chlorophenyl)piperazine (PCPP), a structural analog of p-chloroamphetamine (PCA), increased serotonin and decreased 5-hydroxyindoleacetic acid (5-HIAA) concentration in rat brain at 6 hours. At one day and one week, serotonin and 5-HIAA concentrations were normal. In contrast, PCA lowered serotonin and 5-HIAA at all three times. These different effects on 5-hydroxyindole concentrations in brain were not due to differences in brain levels of the two compounds, since these were approximately equal. PCPP lacks the ability of PCA to deplete brain 5-hydroxyindoles.

Amphetamines↗
PubMed1979

Effect of mazindol on brain dopamine turnover in spiperone-treated rats.

Mazindol, an anorexic drug, caused a large increase in brain 3, 4-dihydroxyphenylacetic acid (DOPAC) concentration in spiperone-pretreated rats. The increase was dose-related over a 1--10 mg/kg dose range of mazindol and was maximum within 1 hour after maxzindol injection into rats pretreated 1 hour previously with spiperone. In spiperone-pretreated rats, mazindol accelerated the disappearance of dopamine after the inhibition of dopamine synthesis by alpha-methyltyrosine. Mazindol apparently resembles amfonelic acid, methylphenidate, and cocaine in facilitating the impulse-mediated release of dopamine.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1979

Effects of prolintane on 3,4-dihydroxyphenylacetic acid concentration in rat brain after spiperone treatment.

Prolintane (1-[alpha-propylphenethyl]-pyrrolidine) but not l-(alpha-methylphenethyl)-pyrrolidine markedly enhanced the increase in 3,4-dihydroxyphenylacetic acid concentration in the brains of rats treated with spiperone, a neuroleptic drug. This action and other properties of prolintane described in the literature place it in a group of stimulant drugs that includes methylphenidate, cocaine and amfonelic acid with properties that differ from those of amphetamine.

3,4-Dihydroxyphenylacetic Acid↗