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D H Versteeg

Publications and source records attributed to D H Versteeg.

At least 91 records · Page 5Linked to original sources

Effect of des-Tyr1-gamma-endorphin and des-Tyr1-alpha-endorphin on alpha-MPT-induced catecholamine disappearance in rat brain nuclei: a dose--response study.

The effect of des-Tyr1-gamma-endorphin (beta-LPH62-77, DT gamma E) and des-Tyr1-alpha-endorphin (beta-LPH62-76, DT alpha E), administered intracerebroventricularly (icv) in doses of 0.01, 0.1, 1 and 10 micrograms, was studied on the alpha-methyl-p-tyrosine-(alpha-MPT) induced disappearance of catecholamines in a number of microdissected rat brain regions, which were selected on the basis of the neuroanatomy of the dopamine systems in the brain and of previous observations. A dose-dependent increase in the disappearance of dopamine in alpha-MPT-pretreated rats was observed following icv administration of DT gamma E in the nucleus interstitialis striae terminalis, the paraventricular nucleus, the anterior hypothalamic nucleus and the zona incerta. In these same brain regions a decrease in the alpha-MPT-induced disappearance of dopamine was found following the administration of DT alpha E, but only after doses of 0.01, 0.1 and 1 microgram. In none of these regions were effects observed after 10 micrograms of DT alpha E. No effects were seen on dopamine utilization in the nucleus accumbens, caudate nucleus and median eminence after any of the doses of DT gamma E or DT alpha E. The alpha-MPT-induced disappearance of noradrenaline was significantly enhanced in the anterior hypothalamic nucleus of rats treated with DT gamma E. It is concluded that DT gamma E and DT alpha E induce opposite changes in the utilization of dopamine selectively in brain regions which are predominantly innervated by neurons belonging to the intradiencephalic dopamine systems.

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Involvement of catecholamines in Haemophilus influenzae induced decrease of beta-adrenoceptor function.

The deeper airways of patients with asthmatic bronchitis are often infected with Haemophilus influenzae. Vaccination of guinea pigs with H. influenzae resulted in a significant impairment of the isoproterenol induced relaxation of isolated tracheal spirals by approximately 50% 4 days following vaccination. In the present study we further investigated the effects of some drugs affecting catecholamine release on the H. influenzae induced functional desensitization of tracheal spirals. Benserazide, an inhibitor of dopa-decarboxylase, completely prevented the reduction in isoproterenol-induced relaxation after H. influenzae vaccination, while no effect on relaxation of tracheal spirals from control animals was detected. On the other hand, inhibiting the re-uptake of catecholamines with desipramine did not influence the relaxation in the H. influenzae vaccinated tracheal spirals. Treatment of control animals with desipramine however resulted in a decreased relaxation of the isolated spirals by 40%. One day following vaccination with H. influenzae the level of norepinephrine in lung tissue was significantly elevated by 71%, and in plasma by 77%, while after 4 days no significant effects were observed. The spontaneous release of norepinephrine, epinephrine and dopamine of tracheal incubates was increased at days 1 and 4 following vaccination. The release of catecholamines from minced lung incubates of H. influenzae pretreated guinea pigs did not differ from that of controls. On the basis of these results it may be suggested that catecholamine metabolism is changed in lungs from H. influenzae vaccinated animals. Catecholamines, accordingly may play a role in the desensitization of beta-adrenoceptors by H. influenzae.

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Effect of depletion of spinal noradrenaline by 6-hydroxydopamine on the development of renal hypertension in rats.

1. A single injection in rats of 250 microgram of 6-hydroxydopamine HCl (6-OHDA) into the subarachnoidal space of the spinal cord of rats resulted in a lasting, selective depletion of spinal noradrenaline. Dopamine levels in the spinal cord and catecholamine levels in various brain regions were not markedly affected. 2. When ether anesthesia was used spinal noradrenaline was found to be almost completely depleted by the administration of 6-OHDA. Only partial depletion was achieved when pentobarbitone anaesthesia or neuroleptic analgesia was used. 3. The blood pressure rise caused by electrical stimulation of the posterior hypothalamus was not affected by 6-OHDA treatment 7 days previously. 4. 6-OHDA administration did not influence the development of two-kidney Goldblatt hypertension. When 6-OHDA was administered 7 days before clipping, a slight delay of the development was observed, but this did not occur when 6-OHDA treatment was given 3--4 h before clipping. 5. It is concluded that intact spinal noradrenergic neurotransmission is neither a prerequisite for the development of two-kidney Goldblatt hypertension, nor for the pressor response to hypothalamic stimulation.

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Hypothalamic catecholamine levels in dogs with spontaneous hyperadrenocorticism.

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic-depletion as the cause of PDH.

Adrenal Gland Neoplasms↗

Noradrenaline concentration and turnover in nuclei of the hyothalamus and the medulla oblongata at two stages in the development of renal hypertension in the rat.

The noradrenaline concentration and the alpha-methyl-para-tyrosine (alpha-MPT)-induced disappearance of noradrenaline were determined in several nuclei of the hypothalamus and the medulla oblongata of renal hypertensive rats (two-kidney Goldblatt hypertension). A decreased alpha-MPT-induced disappearance of noradrenaline was found in the nucleus interstitialis striae terminalis and the nucleus paraventricularis 3 days after renal artery constriction, when blood pressure was slightly, but significantly higher than that of sham operated rats. At this stage the alpha-MPT-induced disappearance of noradrenaline was enhanced in the nucleus commissuralis and the A1-region of hypertensive rats while the noradrenaline concentration in the A1-region was significantly elevated. No significant differences were found in both parameters in hypothalamic and medullary nuclei 3.5 weeks after the operation, when hypertension had fully developed. These findings are indicative of the occurrence of transient changes in the activity of noradrenergic neurons located in the medulla oblongata and projecting to the hypothalamus during the initiation of the development of two-kidney Goldblatt hypertension.

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Adrenergic innervation of the rat hypothalamus.

The adrenergic innervation of the hypothalamus was studied by measuring hypothalamic adrenaline levels following surgical transection of the lower brain stem or electrolytic lesion of the medullary adrenaline-containing cell groups. The adrenaline levels in some hypothalamic nuclei and in the median eminence showed a slight decrease after partial transection of the medulla oblongata, whilst there was a pronounced decrease (by 59-78%) 7-10 days following total hemisection or unilateral lesion of the C1-catecholaminergic cell group in the medulla oblongata.

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Effect of oxytocin and vasopressin on memory consolidation: sites of action and catecholaminergic correlates after local microinjection into limbic-midbrain structures.

The effects of local postlearning microinjections of arginine-vasopressin (AVP) and oxytocin (OXT) on one-trial learning passive avoidance behavior and the influence of AVP on alpha-MPT-induced disappearance of norepinephrine (NE) and dopamine (DA) in discrete brain regions have been studied in the rat. OXT injected bilaterally in the hippocampal dentate gyrus (25-25 pg) or in the midbrain dorsal raphe nucleus (50 pg) significantly attenuated passive avoidance behavior. Facilitation of passive avoidance behavior was observed when the peptide was injected into the dorsal septal nucleus. AVP facilitated passive avoidance behavior when administered into the hippocampal dentate gyrus, dorsal raphe nucleus or dorsal septal nucleus. Injection of either neuropeptides into the central amygdaloid nucleus appeared to be ineffective. One week after the behavioral experiments a repeated injection of AVP into the hippocampal dentate gyrus increased the disappearance of NE in the dentate gyrus and in the nucleus ruber. An injection into the dorsal septal nuclei decreased the NE disappearance in the dorsal septal nucleus itself and increased it in the nucleus ruber. Injection in the dorsal raphe nucleus led to an increase in the disappearance of DA in the locus coeruleus and in the nucleus ruber. It is concluded that memory consolidation can be oppositely influenced by local application of minute amounts of either OXT or AVP into certain limbic-midbrain structures, suggesting an involvement of these brain regions in the memory effects of these peptides. Modulation of catecholamine turnover in specific brain areas after AVP administration may be related to this behavioral effect.

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Facilitation of memory consolidation by vasopressin: mediation by terminals of the dorsal noradrenergic bundle?

Administration of arginine-vasopressin (AVP, 5 micrograms, s.c.) immediately after the learning trial results in a long-term facilitation of a one-trial learning passive avoidance response. This effect of AVP is absent in animals with prior destruction of the ascending dorsal noradrenergic bundle by bilateral microinjection of 6-hydroxydopamine (6-OHDA). Postlearning local microinjection of a minute amount of AVP via chronically implanted cannulae into the locus coeruleus did not influence passive avoidance behavior. Upon injection into the midbrain dorsal raphe nucleus, however AVP facilitated passive avoidance behavior. This effect, however, was absent in rats receiving previous microinjection of 5,6-dihydroxytryptamine (5,6-DHT) or of 6-OHDA into the dorsal raphe nucleus. Bilateral 6-OHDA-induced lesions of the nucleus accumbens or 5,6-DHT-induced destruction of the dorsal raphe nucleus did not prevent the effect of AVP administered subcutaneously. The data suggest that vasopressin facilitates memory consolidation processes by modulating noradrenergic neurotransmission in terminals of the dorsal noradrenergic bundle. The serotoninergic neuronal network originating from the dorsal raphe nucleus has a secondary--norepinephrine-mediated--influence upon these processes.

5,6-Dihydroxytryptamine↗

Vasopressin modulates the activity of catecholamine containing neurons in specific brain regions.

Following the i.c.v. administration of antivasopressin serum the alpha-MPT-induced disappearance of noradrenaline was decreased in the dorsal septal nucleus, parafascicular nucleus and the rostral part of the nucleus tractus solitarii, whereas that of dopamine was lowered in the caudate nucleus and in the A2 region of the medulla oblongata. In general the effects are opposite to those previously found following the i.c.v. administration of vasopressin. The results support the hypothesis that vasopressin modulates catecholamine neurotransmission in specific brain regions of the rat.

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