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K Modigh

Publications and source records attributed to K Modigh.

At least 37 records · Page 2Linked to original sources
PubMed1982

Up- and down- regulation of central postsynaptic alpha 2 receptors reflected in the growth hormone response to clonidine in reserpine-pretreated rats.

The alpha-adrenergic mechanisms exert a stimulatory influence on the secretion of growth hormone (GH) in the rat. In the present study the alpha receptors involved in GH regulation were characterized with respect to subtype. It was also investigated whether the GH response to alpha receptor agonists can be utilized to assess change in the responsiveness of central alpha receptors. The experiments were performed on rats with implanted intra-aortic cannulae allowing frequent blood sampling from freely moving animals. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg) caused a suppression of the normal pulsatile secretory pattern of GH. The alpha receptor agonist clonidine (CLON) given to reserpine-pretreated animals induced a dose-dependent increase in plasma GH. The effect of CLON (0.2 mg/kg) was prevented by pretreatment with the alpha 2 receptor antagonist yohimbine (3 mg/kg), but not by the alpha 1 receptor antagonist phenoxybenzamine (10 mg/kg). Chronic pretreatment with CLON or imipramine, either of which can be expected to produce a reduced sensitivity of central alpha 2 receptors, resulted in reduced GH responses to CLON. On the other hand, chronic treatment with yohimbine, which should cause denervation supersensitivity of alpha 2 receptors, led to enhanced GH responses to CLON. The results indicate that GH release in the rat is stimulated by postsynaptic alpha 2 receptors. They also suggest that the GH response to CLON can be used as a valid in vivo model reflecting decreased, as well as increased responsiveness of this type of receptor.

Animals↗
PubMed1982

Neuroendocrine evidence for increased responsiveness of dopamine receptors in humans following electroconvulsive therapy.

The previous finding that electroconvulsive therapy (ECT) enhances effects of dopamine (DA) agonists was further investigated in the present clinical experiment using neuroendocrine techniques. Apomorphine chloride (AP) (0.18-0.24 mg IV) induced stimulation of growth hormone (GH) and suppression of prolactin (PRL), as shown 2-3 days before and after ECT in mentally depressed patients (N = 12) and therapy-resistant parkinsonian patients with on-off phenomena (N = 9). AP-stimulated GH secretion was not significantly affected by ECT, whereas AP-induced suppression of PRL, expressed as percentage of baseline PRL levels, was significantly enhanced after ECT. Changes in clinical and hormonal parameters were not significantly correlated. Control patients not receiving ECT showed no significant changes in AP-induced GH secretion or PRL suppression in repeated investigations. The results support the view that ECT increases responsiveness of DA receptors and indicates that AP-induced suppression of PRL is a useful model to reflect these changes in humans.

Adult↗
PubMed1982

Effects of gonadectomy and testosterone replacement on growth hormone response to alpha 2 adrenergic stimulation in the male rat.

The growth hormone (GH) response to clonidine in reserpine-pretreated rats is a putative in vivo model to reflect activation of central postsynaptic alpha 2 receptors. In the present study the influence of testosterone on the responsiveness of central alpha 2 receptors was investigated using this method. One week after operation the GH response to clonidine was drastically reduced in gonadectomized adult male rats compared to sham-operated controls. Testosterone replacement completely antagonized the effect. The results suggest an influence of testosterone on central postsynaptic alpha 2 receptors or on structures connected to these receptors.

Animals↗
PubMed1981

Predictors for improvement after electroconvulsive therapy in parkinsonian patients with on-off symptoms.

The antiparkinsonian effect of electroconvulsive therapy (ECT) was investigated in nine parkinsonian patients with "on-off" phenomena. The patients were maintained on previously adjusted doses of antiparkinsonian drugs during and after ECT. Parkinsonian as well as mental symptoms were rated before and after treatment. Basal serum levels of prolactin (PRL) and growth hormone (GH) as well as apomorphine induced changes (0.24 mg i.v.) in these levels were investigated three days before start of treatment. Marked improvement of parkinsonian symptoms was seen in five patients. Two further patients showed slight improvements. The improvement persisted for 2-41 weeks. Improvement after ECT was found to correlate with age at the time of treatment and with duration of L-dopa therapy as well as the estimated life-dose of L-dopa. No correlation was found between depression before treatment, basal serum levels of GH and PRL or apomorphine induced changes in these hormone levels. The investigation indicates that ECT is a valuable adjuvant in the treatment of a selected group of parkinsonian patients with "on-off" phenomena. Furthermore, the results support our earlier proposal that ECT increases the responsiveness in postsynaptic dopamine sensitive structures.

Aged↗
PubMed1981

Evidence for a growth hormone releasing factor mediating alpha-adrenergic influence on growth hormone secretion in the rat.

The effects of adrenergic receptor agonists on GH secretion were studied in adult, male rats pretreated with reserpine and somatostatin antiserum. Frequent blood samples were obtained from intra-aortic cannulae. Plasma GH was determined by radioimmunoassay. Reserpine (10 mg/kg i.p.) caused a complete suppression of the normal, pulsatile secretion of GH in all animals. Administration of somatostatin antiserum resulted in rapid elevations of plasma GH in reserpine-pretreated rats with peak levels at 30 min. GH levels then fell but remained slightly elevated for the duration of the sampling period (8 h). Apomorphine (0.5 mg/kg i.p.) had no effect on plasma GH levels, whereas clonidine (0.5 mg/kg i.p.) induced release of GH in both antiserum treated and control rats. The results indicate that the alpha-adrenergic influence on the secretion of GH is mediated not by inhibition of somatostatin release but rather by effects on the release of a GHRF.

Animals↗
PubMed1981

Importance of norepinephrine alpha 2-receptor activation for morphine-induced rat growth hormone secretion.

The normal pulsatile secretion of rat growth hormone (rGH) requires intact function in monoaminergic neurons. The importance of norepinephrine (NE) for the secretion is well documented, while the roles of dopamine (DA) and 5-hydroxytryptamine (5-HT) are still a matter of controversy. Morphine, as well as endogenous opioid peptides, are known to stimulate the secretion of GH. Whether the opiate-induced GH release is dependent on monoamines was investigated in the present study. Administration of morphine (10 mg/kg) resulted within 30 min in elevations of plasma rGH exceeding 40 ng/ml. This effect was almost completely antagonized by reserpine (10 mg/kg), given 5 h before morphine and partially antagonized by reserpine (2 mg/kg) administered 25 h before morphine. Administration of tetrabenazine (75 mg/kg) protects monoamine granules from irreversible destruction and counteracted the morphine antagonistic effects of reserpine (2 mg/dg) on rGH secretion indicating that the latter effect is due to blockade of monoaminergic neurotransmission. Pretreatment with either haloperidol (1 mg/kg), p-chlorophenylalanine (PCPA) (300 mg/kg x III) or phenoxybenzamine (10 mg/kg) did not reduce the effect of morphine on rGH release whereas yohimbine (3 mg/kg) effectively prevented it. In reserpine-pretreated animals administration of clonidine (0.5 mg/kg) potentiated the GH releasing effect of morphine. These results indicate that morphine-induced GH release is dependent on activation of postsynaptic NE receptors of the alpha 2-subtype.

Animals↗
PubMed1980

Ultradian rhythm in rat hypothalamic dopamine levels.

Rats housed under identical conditions were sacrificed with 15-min intervals between 9.30 a.m. and 2.15 p.m. for determinations of DA and NA concentrations in whole hypothalami. The NA levels showed no obvious fluctuation with time, whereas the DAS levels showed an apparent periodicity with a cycle length of approximately 2 hours and with peaks around 11.30 a.m. and 1.45 p.m. A possible relation between this DA rhythm and the secretion of pituitary hormones is discussed.

Animals↗
PubMed1980

Enhanced growth hormone response to clonidine in the spontaneously hypertensive rat.

Plasma concentrations of growth hormone (GH) were measured after administration of clonidine (0.5 mg/kg) to spontaneously hypertensive (SH) rats and normotensive Wistar Kyoto controls. All rats were pretreated with reserpine (10 mg/kg). The GH response to clonidine was significantly higher in SH rats than in controls, indicating that in SH rats the responsiveness of post-synaptic alpha-adrenergic structures in the hypothalamus may be increased.

Animals↗
PubMed1979

Monoaminergic control of episodic growth hormone secretion in the rat: effects of reserpine, alpha-methyl-p-tyrosine, p-chlorophenylalanine, and haloperidol.

The effects on GH secretion of reserpine, alpha-methyl-p-tyrosine (alpha-MT), p-chlorophenylalanine (PCPA), and haloperidol were studied in undisturbed, unanesthetized male rats with implanted intraaortic cannulae. The effects of the various drug treatments on motor activity and brain levels of catecholamines (CAs) and 5-hydroxytryptamine (5-HT) as well as the synthesis of the biogenic amines were also studied. Reserpine (10 mg/kg, ip) completely inhibited GH secretion for at least 15 h. Repeated injections of reserpine prolonged this inhibition. Episodic GH secretion reappeared 36 h after the last administration of reserpine, at which time the behavioral inhibition and blepharospasm induced by the drug was less pronounced than after 24 h, but brain levels of CAs and 5-HT were still markedly reduced. Administration of alpha-MT (150 mg/kg; 12, 4, and 2 h before experiments) inhibited episodic GH secretion and caused marked inhibition of motor activity and brain levels of CAs but not 5-HT. The inhibition of episodic GH secretion was more pronounced with haloperidol (0.5 mg/kg; 30 min before experiments) than with alpha-MT but was not as complete as that found 12 h after administration of reserpine. Administration of p-chlorophenylalanine (300 mg/kg; 72, 48, and 24 h before experiments) had no effect on episodic GH secretion, whereas brain levels of 5-HT and 5-HT synthesis were markedly reduced.

Animals↗
PubMed1975

Electroconvulsive shock and postsynaptic catecholamine effects: increased psychomotor stimulant action of apomorphine and clonidine in reserpine pretreated mice by repeated ECS.

Male mice were administered electric convulsive shocks (ECS) once daily for one (ECS X I), three (ECS X III) or seven days (ECS X VII). One (day 1), three (day 3) or six days (day 6) later they received reserpine 10 mg/kg, followed 2 hours later by clonidine, 1.5 mg/kg, and/or apomorphine, 1.5 mg/kg. Control animals received the same drug treatments but no ECS. The motor activity was recorded for 1 hour, starting immediately after the last drug injection. The behavioral depression induced by reserpine was equally pronounced in ECS-pretreated animals as in the control animals. The psychomotor stimulant effects of clonidine and/or apomorphine, given after reserpine was, however, enhanced by pretreatment with ECS X VII, DAY 1. Pretreatment wit- ECS X VII increased the motor activity also in animals given reserpine, apomorphine and clonidine at day 3 or day 6. ECS X III was also effective in this respect at day 1, whereas ECS X I, day 1, was ineffective. Mice given ECS X VII but no drug treatment showed at day 1 an increased motor activity during the initial 10 min and a decreased activity during the last 10 of the 1 hour recording period. At day 3 and day 6 after ECS X VII the motor activity was increased in comparison to that in untreated control animals during the whole 1 hour period. Animals given repeated ECS furthermore showed increased irritability and reduced body weight. The results indicate that repeated ECS increase the sensitivity of postsynaptic catecholamine receptors in the brain or alter neuronal structures which are connected to these receptors.

Animals↗