[3H]haloperidol binding to more than one site in rat brain striatum.
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Animals↗
Biomedical subjects
D M Helmeste
Publications and source records attributed to D M Helmeste.
Spontaneous and apomorphine-induced locomotor changes parallel dopamine receptor differences in two rat strains.
Two inbred strains of rats (F344 and Buffalo) were tested for differences in spontaneous and apomorphine-induced inhibition of locomotor activity. F344 rats showed greater percentage decreases in locomotion after apomorphine (0.25, 1.0 and 2.5 mg/kg) compared to the Buffalo strain. F344 rats also showed higher levels and slower habituation of spontaneous locomotor activity. F344 rats had previously been shown to have significantly higher densities of D2-dopamine receptors in the striatum and olfactory tubercle and also more apomorphine-induced stereotypy when compared to Buffalo rats. These results confirm and extend previous studies suggesting that genetic differences in brain D2-dopamine receptors can predict behavioral differences in locomotor activity.
Animals↗
Genetic differences in brain dopamine receptors and amphetamine response: possible model for hyperkinetic children.
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Amphetamine↗
Amphetamine-induced hypolocomotion in mice with more brain D2 dopamine receptors.
The relationship between brain D2 dopamine receptors and locomotor response to amphetamine was investigated in eight strains of mice. The D2 receptor is defined as that dopaminergic site with high affinity (nanomolar) for neuroleptics and low affinity (micromolar) for agonists. D2 receptors were measured in the striatum and olfactory tubercle using [3H]spiperone and 10 microM sulpiride to define specific binding. Four inbred strains of mice (CBA/J; C57BL/6J; DBA/2J; SEC/1ReJ) had low receptor densities of about 380 and 160 fmoles/mg protein in the striatum and olfactory tubercle, respectively; all these mice were essentially nonresponsive (i.e., locomotion) to low doses of amphetamine (0.5 and 1.0 mg/kg i.p.) or showed hyperlocomotion to high doses (5 mg/kg). Three other mouse strains (BALB/cJ; A/J; C3H/HeJ) had higher densities of about 600 and 230 fmoles/mg protein in the striatum and olfactory tubercle, respectively, and these mice all responded with hypolocomotion to the low doses and hyperlocomotion to the high dose of amphetamine. The two genetically different populations, one of which responded to amphetamine with hypolocomotion while the other did not, are analogous to hyperactive children, only 70% of whom respond to amphetamine-like drugs. Thus, the mice with high receptor density may serve as a model for studying the hyperactivity syndrome which may be associated with dopaminergic dysfunction.
Animals↗
Relation between brain catecholamine receptors and dopaminergic stereotypy in rat strains.
In order to examine the potential relation between behaviour elicited by apomorphine and the density of catecholamine receptors, we studied stereotypy and the binding of [3H]spiperone to D2-(or neuroleptic/dopamine) receptors, of [3H]WB-4101 to alpha1-adrenoceptors, and [3H]clonidine to alpha2-adrenoceptors in two strains of rats. The F344 rats exhibited significantly more stereotypy to apomorphine than the Buffalo strain of rats. Other F344 rats which did not receive apomorphine and 34% more D2-receptors in the striatum and 50% more D2-receptors in the olfactory tubercle. Alpha2-Receptors in the frontal cortex were 20% higher in F344 rats when compared to the Buffalo strain, while alpha 1-receptors were the same across both strains. These results suggest a relation between D2-dopamine/neuroleptic receptor density and behavioural responsiveness to the direct-acting and specific dopamine agonist, apomorphine.
Analysis of Variance↗
The contribution of CNS MHPG to plasma MHPG in the rat.
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Animals↗
The effect of clonidine withdrawal on total 3-methoxy-4-hydroxyphenylglycol in the rat brain.
The effect of clonidine withdrawal on the brain norepinephrine system was studied in the rat. Clonidine suppresses brain total 3-methoxy-4-hydroxyphenylglycol (MHPG) significantly and no tolerance to this effect was observed up to 21 days. Cessation of clonidine treatment resulted in an elevation in the level of brain total MHPG. The suitability of the clonidine withdrawal syndrome as a model of bipolar depression is discussed.
Animals↗
Interaction of antidepressants with clonidine on rat brain total 3-methoxy-4-hydroxyphenylglycol.
The effects of some antidepressants on brain total 3-methoxy-4-hydroxyphenylglycol (MHPG) were studied in the rat. Desipramine decreased and mianserine increased the brain total MHPG concentration while the other antidepressants had no effect. They were also the only antidepressants that attenuated the lowering action of clonidine on brain total MHPG, but possibly through different mechanisms. Two tertiary amine tricyclic antidepressants, amitriptyline and imipramine, appeared to enhance the lowering action of clonidine on brain total MHPG. The results suggest that antidepressants are heterogeneous in their action on brain noradrenergic mechanisms in the rat.
Animals↗
The effect of acute and chronic desipramine and amitriptyline treatment on rat brain total 3methoxy-4-hydroxyphenylglycol.
The effect of acute (single dose), short-term (4 days), and chronic treatment (21 days) with two tricyclic antidepressants desipramine and amitriptyline on brain 3-methoxy-4-hydroxyphenylglycol (MHPG) was examined in the rat. Amitriptyline had no effect on brain total MHPG irrespective of the duration of the treatment and did not interfere with the lowering effect of clonidine on brain total MHPG. Acute and short-term desipramine treatment decreased brain total MHPG in rats, while chronic desipramine treatment increased it. The differential effect of acute and chronic treatment of desipramine on the brain total MHPG was further demonstrated by the lack of interference with the lowering effect of clonidine on brain total MHPG by one single dose of desipramine; partial interference after 4 days and complete interference after 21 days of desipramine treatment.
Amitriptyline↗