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Biomedical subjects

K W Perry

Publications and source records attributed to K W Perry.

At least 19 recordsLinked to original sources
PubMed1992

Effect of fluoxetine on serotonin and dopamine concentration in microdialysis fluid from rat striatum.

Fluoxetine injected i.p. into rats at a dose of 10 mg/kg rapidly increased serotonin concentration in microdialysis fluid from the striatum by at least 4-fold, an increase that was maintained throughout the 3 hr observation period. Dopamine concentration in the microdialysis fluid did not change. The concentration of the two dopamine metabolites, 3,4-dihydroxyphenylacetic acid and homovanillic acid, was not changed in the microdialysis fluid, whereas the concentration of the serotonin metabolite, 5-hydroxyindoleacetic acid, was significantly decreased after fluoxetine injection. The increased extracellular concentration of serotonin no doubt resulted from inhibition of the serotonin uptake carrier by fluoxetine, and the lack of change in dopamine is evidence for the specificity of action of this uptake inhibitor.

Animals↗
PubMed1992

Supersensitization of the oral response to SKF 38393 in neonatal 6-OHDA-lesioned rats is mediated through a serotonin system.

To study possible interactions between dopamine (DA) and serotonin (5-HT) neurochemical systems in the D-1 supersensitized induction of oral activity in neonatal 6-hydroxydopamine (6-OHDA) lesioned rats, the effects of a series of 5-HT agonists and antagonists were determined. At 3 days after birth rats were treated with desipramine HCl (20 mg/kg i.p., base form, 1 hr) and 6-OHDA HBr (100 micrograms, salt form, in each lateral ventricle). Rats were observed individually as adults, once a minute every 10 min over a 1-hr period after challenge with a DA or 5-HT receptor agonist. The respective 5-HT1A and 5-HT1B agonists, (+/-)-8-hydroxydipropylaminotetralin (0.50 mg/kg s.c.) and CGS 12066B maleate (7-trifluoromethyl-4(4-methyl-1-piperazinyl)-pyrrolo[1, 2-alquinoxaline], 1:2 maleate salt; 3.0 mg/kg i.p.), did not increase oral activity. The mixed 5-HT1C and 5-HT2 receptor agonist, m-chlorophenylpiperazine (m-CPP), produced a slight increase in oral activity in control rats and a marked increase in oral activity in 6-OHDA-lesioned rats. In the 6-OHDA group the peak effect of 76.5 +/- 4.1 oral movements occurred with an m-CPP 2-HCl dose of 4.0 mg/kg. Pindolol (1.0 mg/kg i.p.), ketanserin tartrate (5 mg/kg i.p.) and MDL-72222 (3-tropanyl-3,5-dichlorobenzoate; 10 mg/kg s.c.), antagonists with high affinity for 5-HT1A,1B, 5-HT2 and 5-HT3 receptors, respectively, did not attenuate m-CPP actions. However, mianserin HCl (1.0 mg/kg s.c.), an antagonist with high affinity for 5-HT1C and 5-HT2 receptors, attenuated the oral response to m-CPP.(ABSTRACT TRUNCATED AT 250 WORDS)

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1978

Effect of lergotrile on 3,4-dihydroxyphenylacetic acid (DOPAC) concentration and dopamine turnover in rat brain.

Lergotrile, a dopamine agonist, lowered whole brain DOPAC (3,4-dihydroxyphenylacetic acid) concentration in rats. At low doses down to 0.5 mg/kg of lergotrile mesylate, this effect occurred within 30 min, whereas at higher doses (20 mg/kg) the decline in DOPAC was delayed. The decrease in DOPAC persisted for several hours and presumably resulted from a compensatory decrease in brain dopamine turnover secondary to receptor stimulation by lergotrile. Other indications of decreased brain dopamine turnover after lergotrile included (a) a slower decline in dopamine concentration after synthesis inhibition by alpha-methyltyrosine, (b) a slower decline in alpha-methyl-m-tyramine, a false transmitter that is stored and released by dopamine neurons, and (c) a decreased accumulation of dopamine in response to gamma-butyrolactone, an agent that blocks firing and dopamine release by dopamine neurons. Lergotrile mesylate (20 mg/kg) also increased brain levels of 5-hydroxyindoleacetic acid and of 3-methoxy-4-hydroxyphenylethylene glycol sulfate, metabolites of serotonin and norepinephrine, respectively, and these increases were not antagonized by spiperone, a dopamine receptor antagonist.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Effect of uptake inhibitors on the depletion of brain norepinephrine and serotonin after alpha-methyl-m-tyrosine administration to rats.

The depletion of brain norepinephrine after alpha-methyl-m-tyrosine injection into rats was antagonized by pretreatment with an uptake inhibitor (protriptyline or chlorimipramine) but was not completely prevented. Administration of protriptyline after alpha-methyl-m-tyrosine injection, at a time when norepinephrine had been depleted, partially reversed the depletion. Serotonin depletion after alpha-methyl-m-tyrosine was not altered by pretreatment with fluoxetine, an inhibitor of uptake into serotonin neurons. Apparently part of the norepinephrine (but not serotonin) depletion occurring after alpha-methyl-m-tyrosine injection is due to the action of amine products that enter the norepinephrine neuron via the membrane uptake pump and whose presence within the nerve terminals is maintained by the uptake pump.

Animals↗
PubMed1978

Effect of prazosin on norepinephrine concentration and turnover in rat brain and heart.

Prazosin hydrochloride injected i.p. into rats markedly increased MOPEG sulfate (3-methoxy-4-hydroxy-phenylethylene glycol sulfate) concentration in brain and the rate of MOPEG sulfate accumulation after probenecid. The increase in MOPEG sulfate was dose-related over a 5-40 mg/kg dose range. After a 20 mg/kg dose of prazosin, the increase in MOPEG sulfate was greater than after the same dose of phenoxybenzamine and persisted for up to 24 hr. The rate of metaraminol disappearance from rat brain after alpha-methyl-m-tyrosine injection and the decline in brain norepinephrine after inhibition of its synthesis by alpha-methyltyrosine injection were increased in rats pretreated with prazosin. These findings indicate that prazosin increased brain norepinephrine turnover, probably via compensation to central alpha adrenoceptor blockade. Prazosin increased sertonin and 5-hydroxy-indoleacetic acid concentration and slightly decreased 3,4-dihydroxy-phenylacetic acid in rat brain. Although prazosin had little effect on brain norepinephrine concentration, heart norepinephrine was depleted for up to 16 hr after a 20 mg/kg dose of prazosin, and the depletion at 4 hr was dose-related down to 2 mg/kg of prazosin. These biochemical changes may all result from prazosin's block of alpha adrenergic receptors.

3,4-Dihydroxyphenylacetic Acid↗