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Biomedical subjects

H Rigter

Publications and source records attributed to H Rigter.

At least 91 records · Page 5Linked to original sources
PubMed1976

Reversal of amnesia by an orally active ACTH 4-9 analog (Org 2766).

The ACTH 4-9 analog, H-Met((O2)-Glu-His-Ph-D-Lys-Phe-OH (Or 2766), attenuates in rats CO2-induced amnesia for a one-trial passive avoidance step-through response when administered prior to the retrieval test but not when given prior to acquisition. Even a dose of 0.001 mug/rat Org 2766 yields an anti-amnesic effect. In this respect Org 2766 is more active than the ACTH fragment ACTH 4-10. An anti-amnesic effect was also obtained when Org 2766 was administered orally. ACTH 4-10 (100 mug/rat) has to be given SC within 8 hr of the retrieval test in order to be effective. A similar time span of effectiveness was observed when Org 2766 was SC injected in a dose of 0.1 mug/rat. The anti-amnesic effect of ACTH 4-10 remains when the time interval between acquisition and retrieval is extended beyond the usual 24 hr. The same appeared to be true for SC ADMINISTERED Org 2766. It is suggested that ACTH-like peptides, and particularly the orally active Org 2766, may be helpful in the treatment of deficient mental performance.

Administration, Oral↗
PubMed1976

The action of psychotropic drugs on DOPA induced behavioural responses in mice.

The "DOPA potentiation" test in mice was investigated for its usefulness in the detection of compounds with antidepressant properties. It was found that the anti-depressant drugs imipramine, amitriptyline, 5-methylamino-acetyl-6-methyl-5,6-dihydro-phenanthridine-HCl (Org OI77) and 1,2,3,4,10,14b-hexahydro-2-methyl-dibenzo[c,f]pyrazino[1,2-a]azepine-HCl (mianserin, Org GB 94) potentiated the behavioural effect of DOPA in groups of mice which had been treated 17 h previously with the monoamine oxidase inhibitor (MAOI) iproniazid. However, the DOPA response was also potentiated by a variety of centrally acting drugs which do not have antidepressant properties (atropine, methysergide, chlordiazepoxide, apomorphine). The peptide hormones ACTH4-10 and desglycinamide lysine vasopressin had equivocal effects while melanocyte stimulating hormone release-inhibiting factor (MIF) had no effect on the DOPA response. The DOPA response was inhibited by the neuroleptics chlorpromazine and haloperidol. There appeared to be no correlation between the effects of the drugs on the behavioural responses elicited by DOPA and the changes found in the brain concentration of noradrenaline, dopamine, serotonin, gamma-aminobutyric acid, tryptophan and tyrosine. It is concluded that the "DOPA potentiation" test cannot be considered as a reliable test in the detection of anti-depressant compounds.

Animals↗
PubMedDate not supplied

Apomorphine: facilitation of sexual behaviour in female rats.

Sexual receptivity of spayed female rats was studied by recording lordosis responses to a mounting male. Administration of apomorphine (0.25 mg/kg) to oestrogen+progesterone-primed females produced an increase in lordosis behaviour 2--48 hr after injection. An increase was also found when apomorphine was substituted for progesterone. These results suggest a role for dopamine in controlling sexual receptivity.

Adrenal Glands↗
PubMedDate not supplied

Changes in brain monoamine metabolism and carbon dioxide induced amnesia in the rat.

The effect of treatment with carbon dioxide (CO2) on the performance of rats 24 hr after receiving a foot shock in a passive avoidance task was studied. Foot shock induced avoidance. Carbon dioxide produced retrograde amnesia for the foot shock induced avoidance response. Changes in brain monoamine metabolism were studied in groups of rats which had been treated with CO2, foot shock or foot shock +CO2. The rats were killed 24 hr after treatment. Changes mainly occurred in the brain stem and hippocampus. In the rats which had received foot shock alone, brain stem and hippocampal serotonin concentration were raised. This rise was not observed when the foot shock was followed by CO2 treatment. Furthermore, it was found that there was an increased release of noradrenaline in those rats subjected to foot shock alone but a decreased release of this amine in the group which received foot shock followed by CO2. It is suggested that the amnesic effect of CO2 parallels changes in brain serotonin and noradrenaline metabolism.

Amnesia↗
PubMedDate not supplied

Hippocampal monoamine metabolism and the CO2 induced retrograde amnesia gradient in rats.

It was found that in rats a gradient of retrograde amnesia for a passive avoidance response could be established when carbon dioxide (CO2) was used as the amnesic agent. The extent of passive avoidance increased as the period between application of a mild foot shock and CO2 treatment was increased. The amnesia gradient was found to cover a period of at least 60 min. Changes in hippocampal serotonin metabolism parallelled the amnesia gradient. Thus, the concent increased. The changes in hippocampal noradrenaline and dopamine did not correlate with the amnesia gradient.

Amnesia↗
PubMedDate not supplied

Time-dependent aspects of CO2 induced amnesia and hippocampal monoamine metabolism in rats.

The time course of amnesia for a one-trial passive avoidance response after treatment with carbon dioxide (CO2) was studied. Amnesia developed gradually over the first 4 hr following the amnesic treatment. Once established, amnesia remained during a 4 week test period. Previously, we reported that acquisition of the passive avoidance response was attended with a rise in the hippocampal concentration of serotonin 24 hr later and that this rise was not observed when acquisition was followed by amnesic treatment. In the present study, it was found that a rise in hippocampal serotonin parallelled the transient retention of the avoidance response 2 hr after amnesic treatment. However, 2 weeks after acquisition and amnesic treatment no changes in hippocampal monomine metabolism could be detected. Hippocampal noradrenaline did not correlate with avoidance and amnesia.

Amnesia↗
PubMedDate not supplied

Vasopressin and ethanol preference. I. Effects of vasopressin and the fragment DGAVP on altered ethanol preference in Brattleboro diabetes insipidus rats.

Preference for concentrations of ethanol between 2.2 and 10 percent versus tap water was studied in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Administration of lysine vasopressin or the vasopressin fragment des-9-Glycinamide-[Arginine8] vasopressin (DGAVP) using osmotic minipumps enhanced ethanol preference scores, reduced ethanol (g/day) intake, and restored total daily fluid intake in di/di rats. When di/di and di/+ rats were first allowed to develop stable ethanol preference before treatment with DGAVP, the peptide had no effect on preference scores. Thus, no treatment was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.

Alcohol Drinking↗
PubMedDate not supplied

Vasopressin and ethanol preference. II. Altered preference in two strains of diabetes insipidus rats and nephrogenic diabetes insipidus mice.

In the first paper of this series, the influence of a single gene (di) for vasopressin deficiency on ethanol intake in rats was demonstrated. We studied preference for concentrations of ethanol between 2.2 and 10 percent versus tap water in Brattleboro rats homozygous for diabetes insipidus (di/di), heterozygous (di/+) or normal (+/+). The di/di rats, totally lacking in vasopressin, had greatly reduced preference scores for all concentrations of ethanol. Their intake of ethanol (g/day) was higher than heterozygotes or normals, but only when 2.2 percent ethanol was offered as a choice. Treatment with vasopressin or related peptides restored ethanol drinking to normal but also corrected water balance. In the experiments reported here, Roman High Avoidance (RHA) rats of three genotypes (+/+, di/+, and di/di) were also tested for ethanol intake and preference with similar but not identical results. Thus, the effects of the di gene are independent of the genetic background on which it is placed to at least some extent. Chlorothiazide, a drug unrelated to vasopressin, also normalized ethanol drinking and corrected water balance in di/di rats. In nephrogenic diabetes insipidus mice, there was a strong negative correlation between severity of polydipsia and preference for ethanol. Thus, no paradigm tested was effective in dissociating polydipsia from reduced ethanol preference and increased ethanol intake. While these results cannot exclude a possible regulatory role for endogenous vasopressin in ethanol preference drinking, they more strongly suggest that reduced preference for ethanol and increased ethanol intake are epiphenomena secondary to a polydipsic state.

Alcohol Drinking↗