Showing papers in "Journal of Neural Transmission in 1977"

Naloxone-induced reversal of schizophrenic hallucinations.

Abstract: In a single-blind pilot study 0.4 mg naloxone i.v. was found temporarily to reduce or abolish auditory hallucinations in four cases of chronic schizophrenia whereas saline was without effect. In one of these patients there was a similar reversal also of her visual hallucinations. Two additional cases who denied hearing voices before the injections, reported no subjective effects.

Brain tyrosine level controls striatal dopamine synthesis in haloperidol-treated rats.

Abstract: Animals received either haloperidol (2 mg/kg) or probenecid (200 mg/kg) in conjunction with tyrosine (100 mg/kg) or its diluent. Striatal homovanillic acid levels increased in probenecid-treated animals to the same range whether they were given tyrosine or not. In haloperidol-treated animals the levels of homovanillic acid were significantly elevated in animals receiving tyrosine. Tyrosine and homovanillic acid levels were highly correlated as determined by linear regression analysis.

On the presence of different populations of pinealocytes in the mammalian pineal gland.

Abstract: The different categories of cells described by many authors in the pineal gland of mammals have been critically considered. In some mammalian species, two different populations of pinealocytes have been observed. To each of these populations a specific secretory process can be attributed. One is characterized by the formation of granular vesicles originating from the Golgi apparatus, the other by the formation of material directly from the cisterns of the granular endoplasmic reticulum. Both of these secretory processes appear to be also present in the pineal of the mole, the hedgehog, and the rat, mammals in which generally only one population of pinealocytes has been described. The physiological consequences of these findings have been discussed.

Effect of apomorphine on schizophrenic symptoms.

Abstract: The effects of apomorphine on psychotic symptoms were evaluated in chronic schizophrenic patients using double-blind placebo controlled procedures. Although on the basis of dopamine theory of schizophrenia, apomorphine was expected to increase schizophrenic symptoms, in this study apomorphine substantially reduced psychotic symptoms in some chronic schizophrenic patients. No patient showed the substantial increase in psychotic symptoms previously demonstrated after the administration of IV methylphenidate. These clinical effects of apomorphine in schizophrenia may be relevant to recent pharmacological research which has indicated that apomorphine also has potent effect on presynaptic dopamine neurons, in addition to its previously described postsynaptic receptor stimulation.

The effect of 4-aminopyridine on acetylcholine release.

Abstract: The effect of 2-, and 4-aminopyridine (4-APYR) on the release mechanism of acetylcholine (ACh) from the nerve terminals of the Auerbach plexus-longitudinal muscle preparation of the guinea-pig ileum, suspended in eserinized Krebs' solution, was investigated. 2- and 4-APYR increased the release of ACh from the nerve terminals at rest and at both low and high frequency stimulation. The enhanced ACh release was found to be due to increased volley output. At lower frequency of stimulation, the potentiation of ACh release was much higher than at higher rate of stimulation. 4-APYR was able to increase ACh release in the absence of [Ca2+]0. However, when a Ca-chelating agent, EDTA, was also added to the Ca-free Krebs' solution, 4-APYR was entirely ineffective. The depression of ACh release induced by Mg-excess was completely antagonized by 4-APYR. Tetrodotoxin (TTX) prevented augmentation of ACh release by 4-APYR. It is suggested that 4-APYR lowers the demand of nerve terminals for [Ca2+]0 required for the excitation-secretion coupling process. The presence of a low concentration [Ca2+]0, however, is essential for the action of 4-APYR.

Diurnal and seasonal variations in human platelet serotonin in man

Abstract: Platelet serotonin (5-HT) was found to be an individually constant parameter correlating with the uptake of exogenous 5-HT. A pronounced diurnal pattern of 5-HT, with a minimum in the afternoon and higher values in the morning and evening, was similar to the diurnal variations in plasma free tryptophan. Platelet 5-HT was significantly higher at 8 a.m. than 4 p.m. in spring but no longer in autumn, and was similar in both men and women. It appeared that peripheral diurnal variations in 5-HT were opposite in phase to the central 5-HT rhythm.

Brain-noradrenaline and 3-methoxy-4-hydroxyphenylglycol in Parkinson's syndrome

Abstract: 1. Significantly reduced values of noradrenaline in Parkinson's disease were observable in all brain areas which were studied. 2. A topographic distribution of free 3-methoxy-4-hydroxyphenylglycol (MHPG) can be demonstrated in the human brain. As MHPG in the various brain areas shows a different pattern of concentration it seems that this metabolite of noradrenaline is of physiological significance and is able to reflect noradrenaline turnover. The highest values of free MHPG were found in the hypothalamus, n. accumbens, thalamus and n. ruber. 3. In a limited series of patients with Parkinson's disease post mortem analysis indicated lower values of MHPG in caudate n., putamen, s. nigra, red nucleus and n. accumbens. All other brain areas did not show significant alterations. 4. Parkinsonian patients who died during Madopar® therapy demonstrated a significant increase of MHPG in caudate n., putamen, s. nigra, n. ruber, n. amygdalae and n. accumbens when compared to the untreated group, indicating an enhanced turnover of noradrenaline in these areas. 5. Bound MHPG has been estimated in various brain areas as to be in the range of 13–38 percent of free MHPG.

The adrenal medulla may mediate the increase in pineal melatonin synthesis induced by stress, but not that caused by exposure to darkness.

Abstract: As previously shown (Lynch et al.: Proc. Nat. Acad. Sci. [U.S.A.]70, 1704–1707 [1973]), the activity of the enzyme serotonin-N-acetyltransferase (NAT) in the rat pineal increases when the animal is placed in darkness or is subjected to the stress of physical immobilization; partial sympathetic denervation (i.e., pretreatment of the animal with intravenous 6-hydroxydopamine [6-OHDA]) does not block either response. The present studies explored the roles of the pineal sympathetic nerves and the adrenal medullas in mediating these responses. The stress-induced increase in pineal NAT activity was blocked by bilateral adrenalectomy, but not by bilateral superior cervical ganglionectomy or by treatment with 6-OHDA (both of which potentiate the NAT response in normal rats and restore it in adrenalectomized ones). The increase in pineal melatonin content caused by immobilization was also blocked by adrenalectomy, but potentiated by pineal sympathetic denervation. In contrast, bilateral adrenalectomy did not affect the darkness-induced rise in pineal NAT activity, although pineal sympathetic denervation (by bilateral superior cervical ganglionectomy) did block this response. 6-OHDA pretreatment neither blocked the response to darkness nor restored it in ganglionectomized animals; thus, this treatment apparently fails to produce a complete pineal denervation. The pineal response to stress has previously been shown to be blocked byβ-adrenergic blocking agents. The present studies demonstrate thatα-adrenergic blockade (with phenoxybenzamine) potentiates this response in intact animals and restores it in adrenalectomized rats (possibly by acting presynaptically on receptors on pineal sympathetic terminals and thereby augmenting norepinephrine release). These observations show that the rat pineal organ normally receives information from two “channels”,i.e., trans-synaptically (from pineal sympathetic nerves) and via the circulation (from the adrenal medullas and, perhaps, from distant sympathetic nerves).

Antagonism by haloperidol of locomotor depression induced by small doses of apomorphine

Abstract: Administration of 0.025–0.1 mg/kg of apomorphine i.p. to mice produced a dose-dependent locomotor depression. Haloperidol, 0.025 mg/kg, produced locomotor stimulation, whereas 0.1 mg/kg caused locomotor depression. Pretreatment with haloperidol also reversed the depression caused by apomorphine. The functional antagonism is discussed in terms of a possible agonist-antagonist interaction on dopaminergic autoreceptors.

Agonist--antagonist interaction on dopamine receptors in brain, as reflected in the rates of tyrosine and tryptophan hydroxylation.

Abstract: The effect of haloperidol and apomorphine, and both drugs in combination, on the first steps in the synthesis of catecholamines and 5-hydroxytryptamine (5-HT) has been studied in three rat brain regions. The rate of formation of dopa and 5-hydroxytryptophan (5-HTP) was studied by measuring the accumulation of these amino acids during 30 min after administration of the inhibitor of the aromatic L-amino acid decarboxylase, NSD 1015 (3-hydroxybenzylhydrazine HCl). Haloperidol caused an increase in dopa and no change in 5-HTP formation. The threshold dose was severalfold higher in the noradrenaline-predominated hemisphere portion than in the dopamine-rich striatal and limbic regions, suggesting a higher affinity of haloperidol for dopamine than for noradrenaline receptors. Apomorphine caused a decrease in dopa formation in all three brain regions studied, although the effect was much more pronounced in the regions dominated by dopamine. The threshold dose was about 30 microng/kg, i.e. an order of magnitude lower than the threshold dose for apparent postsynaptic dopaminergic receptor activation. This discrepancy is suggested to be due to preferential activation of inhibitory dopaminergic autoreceptors by low apomorphine doses. This phenomenon may also contribute to explain the complex dose-response curves of apomorphine. Low doses of apomorphine caused a decrease and high doses an increase in 5-HTP formation. These effects, like those on noradrenaline synthesis, are suggested to be secondary to activation of dopaminergic pre- and post-synaptic receptors. The interaction between apomorphine and haloperidol with respect to dopa formation appears to be largely explicable on the assumption of a competition between an agonist and an antagonist for dopaminergic receptors. However, very large doses of apomorphine cause a haloperidol-resistant inhibition of tyrosine, and probably also tryptophan, hydroxylation, which may be due to a direct inhibition of the aromatic amino acid hydroxylase involved.

Suppression by GABAergic drugs of the locomotor stimulation induced by morphine, amphetamine, and apomorphine: evidence for both pre- and post-synaptic inhibition of catecholamine systems.

Abstract: Locomotor stimulation induced in mice by morphine and amphetamine was antagonized by pretreatment withγ-butyrolactone (GBL) and aminooxyacetic acid (AOAA) at doses which had little effect on saline treated animals. The effects of morphine and AOAA on the turnover of brain catecholamines (CA) were determined by measuring both the accumulation of dopa after inhibition of central aromatic L-amino acid decarboxylase and by measuring the depletion of noradrenaline (NA) after inhibition of tyrosine hydroxylase byα-methyltyrosine (α-MT). Morphine and AOAA were found to have opposite effects on CA turnover,i.e. morphine caused an increase and AOAA, a decrease. AOAA also antagonized the morphine-induced increase in CA turnover. These data might suggest that the well documented ability of GABAergic drugs to inhibit the firing of DA-containing neurons may be of importance in explaining the present findings. However, the locomotor stimulation induced by the directly-acting CA agonists, apomorphine and clonidine after pretreatment with reserpine andα-MT was also inhibited by the GABAergic drugs. It is therefore concluded that the suppressant effects of the GABAergic agents on hypermotility are not solely mediated by their effects on presynaptic CA mechanisms, but also by a postsynaptic inhibition at some point beyond the CA neurons.

Effects of estrogen on prolactin and tuberoinfundibular dopaminergic neurons

Abstract: Serum prolactin concentrations and dopamine turnover in the striatum and median eminence were studied in male rats after the administration of estradiol benzoate. Theα-methyltyrosine-induced reduction of dopamine concentrations in these brain regions was used to evaluate relative rates of turnover. Steady state dopamine concentrations in the median eminence and striatum were not altered by 1, 3 or 5 days of estradiol treatment. However, 3 or 5 days of estradiol administration enhanced dopamine turnover in the median eminence but not in the striatum. Estradiol treatment failed to alter dopamine turnover in the median eminence of hypophysectomized rats. Estradiol increased serum prolactin concentrations at all of the times examined. Althoughα-methyltyrosine also increased serum prolactin, this increase was further enhanced in estradiol-treated rats. The increased prolactin response toα-methyltyrosine and increased dopamine turnover in the median eminence of estradiol-treated rats suggests that tuberoinfundibular dopaminergic neurons may be part of a hormonalneuronal negative feedback loop which functions to regulate prolactin secretion.

Correlation of anxiety and related symptoms with cerebrospinal fluid 5-hydroxyindoleacetic acid in depressed women.

Abstract: Cerebrospinal fluid 5-hydroxyindoleacetic acid levels were determined in 31 women with unipolar involutional depression using the probenecid technique. Values were found to be lower in depression as compared to controls, but they did not correlate with the severity of the clinical picture. Anxiety, insomnia and drug response however showed significant correlation with pretreatment 5-HIAA level. Some possible interpretations are discussed.

Alterations in forebrain catecholamine metabolism produced by cerebellar lesions in the rat

Abstract: Projections from the midline cerebellar nuclei to norepinephrine (NE) and dopamine (DA) cell groups in the brain stem have been demonstrated histologically. To determine if these connections are significant biochemically, unilateral electrolytic lesions were placed in either vermis or paravermis and levels of DA, NE and gamma-aminobutyric acid (GABA) were measured in each half of the forebrain at 1 1/2, 3 or 6 weeks.

The interactions of bromocriptine and lergotrile with dopamine and α-adrenergic receptors

Abstract: Bromocriptine and lergotrile, which are clinically used as antiparkinsonian (AP) agents, compete for the binding of H3-dopamine, H3-apomorphine, and H3-haloperidol to striatal membrane sites. Lergotrile has a higher affinity for the H3-dopamine binding to bovine striatal membranes than bromocriptine. Lergotrile and bromocriptine are almost equipotent in competing for the binding of H3-apomorphine to rat striatal membranes, but bromocriptine is more potent in competing for the binding of H3-haloperidol than lergotrile. These results indicate that lergotrile and bromocriptine are mixed putative agonist-antagonist with respect to the postsynaptic dopamine receptors. Lergotrile and bromcriptine at higher concentrations inhibit synaptosomal tyrosine hydroxylase activity, and reverse the apomorphine elicited enzyme inhibition. Thus, these ergot alkaloids behave as mixed agonist-antagonist also with respect to the presynaptic dopamine receptors. Bromocriptine and lergotrile, as well as other tested DH-ergot alkaloids and neuroleptics, compete for the binding of theα-antagonist H3-WB-4101 to rat cerebral cortical membranes. The displacing potencies of the tested DH-ergot alkaloids and of the neuroleptics indicate that they have a high affinity for theα-adrenoreceptors in the CNS.

The pineal gland of nocturnal mammals. I. The pinealocytes of the bat (Nyctalus noctula, Schreber).

Abstract: The ultrastructure of the pinealocytes of noctule bats, mammals which live most of the time in darkness or very low light intensities, was examined and compared with the pinealocytes of other mammals. Two different populations of pinealocytes (I and II) were observed. They differ in general aspect, in location and especially in their content of cell organelles involved in synthetic processes. Mitochondria, ribosomes, lysosomes and lipid inclusions were present in the perikaryon of pinealocytes of both populations. In the pinealocytes of population I some granular vesicles, of presumed Golgi origin, and some other structures were observed. Pinealocytes of population II are characterized by many glycogen granules, more or less associated with a large vacuolar system. Moreover, some small vacuoles originating from cisterns of the granular endoplasmic reticulum and containing flocculent material of a moderate electron density are described. The possibility is discussed that these small vacuoles are involved in one of the secretory processes of the pineal gland while the granular vesicles of the pinealocyte of the population I are the products of another.

Acetylcholine releasing effect of laser irradiation on Auerbach's plexus in guinea-pig ileum

Abstract: An increased acetylcholine release could be produced by ruby laser from the Auerbach plexus of the guinea-pig ileum.

Fluvoxamine-a new serotonin re-uptake inhibitor: first clinical and psychometric experiences in depressed patients.

Abstract: The clinical efficacy of fluvoxamine (DU 23000)--the first selective serotonin re-uptake inhibitor of the new class of 2-aminoethyloximethers of aralkylketones was investigated in endormorphous depressed patients during 5 weeks treatment with mean daily dosages of approximately 150 mg DU 23000. A marked and statistically significant improvement of the overall and detailed psychopathology was noted by means of the Global Clinical Impression and Hamilton Rating Scale as early as in the first week of drug administration. Bipolar patients tended to improve more than unipolar ones, retarded depressions more than agitated ones. An additional anxiolytic medication was occasionally required. The drug was well tolerated. Psychometric and laboratory findings did not show any significant changes. The findings are discussed in the light of the indolamine hypothesis of depression.

Hyperthyroidism: Specifically increased response to central NA-(α-)receptor stimulation and generally increased monoamine turnover in brain

Abstract: Repeated treatment with thyroxine (T4) caused in mice enhanced response,i.e. locomotor stimulation, to central noradrenaline (NA)-receptor activation by clonidine but not to central dopamine (DA)-receptor activation by apomorphine or ET 495 after previous depletion of endogenous catecholamines (CA) by reserpine and inhibition of the CA-synthesis byα-methyl-p-tyrosine. Increasing the dosese of the receptor agonists in control animals did not increase the locomotor stimulation but merely prolonged the effect. In chronically T4-treated rats with a significantly elevated plasma level of T4 and T3 the apomorphine-induced stereotypies were not increased and the response to small amounts of DA locally applied in N. accumbens was not significantly affected by the T4-pretreatment. The synthesis rates of NA and DA, reflected in the amount of L-Dopa accumulated in predominantly NA- and DA-rich brain parts, respectively, during 30 min after administration of the centrally active, aromatic L-amino acid decarboxylase inhibitor NSD 1015, were both increased by T4-pretreatment. Also the brain serotonin (5-hydroxytryptamine, 5-HT)-synthesis was increased, measured in an analogous way. In contrast, utilization of brain CA or 5-HT seemed not affected by the T4-pretreatment, as disclosed by unchanged disappearance rates of NA, DA or 5-HT after inhibition of tyrosine hydroxylase and tryptophan hydroxylase, respectively. Release of brain CA, as reflected in the amount of O-methylated metabolites after monoamine oxidase inhibition, was not affected by the hormone pretreatment. We conclude that moderate hyperthyroidism is associated with a specific, increased sensitivity at or beyond central NA-(α-)receptors. This effect may be implicated in: 1. The potentiation by thyroid hormone of tricyclic antidepressive drugs; 2. the affective symptoms in hyperthyroidism,e.g. anxiety and increased susceptibility to emotional stress; 3. the cardiovascular symptoms in hyperthyroidism.

Brain monoamines in metabolic (endotoxic) coma a preliminary biochemical study in human postmortem material

Abstract: Spectrofluorometric assays of DA, 5-HT and 5-HIAA were performed in different areas of postmortem brains of humans who died in hepatic and uremic coma. Brain DA showed a mild general decrease, the average reduction being 20 to 30 percent of the controls. By contrast, 5-HT and 5-HIAA were markedly increased in most brain areas, most significantly in the reticular and raphe nuclei of the brainstem and in some parts of the limbic system. Despite individual and regional differences, the monoamine changes had similar patterns in both hepatic and uremic coma. These data in human brain which confirm previous clinical and experimental studies in hepatic encephalopathy suggest some common disorders of central monoamine metabolism in endotoxic coma of different origin. Brain edema, a constant feature in toxic coma, is probably due to increased 5-HT content in the brain, the pathophysiologic effect of 5-HT on the blood-brain barrier being well established. The prominent changes of indoleamine metabolism in the reticular brainstem and limbic systems may be related to disorders of consciousness.

Dl-phenylalanine in depressed patients: an open study.

Abstract: In an open study dl-phenylalanine in doses from 75-200 mg/day was administered to 20 depressed patients for 20 days. Patients were classified according to the International Classification of Diseases (ICD). The AMP system, the Hamilton depression scale and the von Zerssen self rating questionnaire were used for documentation of psychopathological, neurologic and somatic changes. In addition a global clinical impression was agreed upon by experienced psychiatrists. At the end of the trial 12 patients (8 with complete, 4 with good response) could be discharged without any further treatment. 4 patients with partially untypical depressions experienced mild to moderate responses, whereas 4 patients did not respond at all to the phenylalanine administration. Depressive "core symptoms" as depressed mood, retardation and/or agitation were preferentially, anxiety and sleep disturbances moderately and hypochondriasis and compulsiveness were not influenced. It is concluded that dl-phenylalanine might have substantial antidepressant properties and that further more controlled investigations are warranted.

Interaction of haloperidol and gamma-butyrolactone with (+)-amphetamine-induced changes in monoamine synthesis and metabolism in rat brain.

Abstract: The interaction of (+)-amphetamine with haloperidol andγ-butyrolactone on synthesis of monoamines in rat brain regions was investigated using anin vivo method, in which the accumulation of dopa and 5-hydroxytryptophan (5-HTP) was measured after inhibition of the aromatic amino acid decarboxylase by means of 3-hydroxybenzylhydrazine. The accumulation of 3-methoxytyramine (3-MT) after inhibition of the monoamine oxidase with pargyline was taken as an indicator of thein vivo release of dopamine (DA) into the extraneuronal space.

The demonstration of a change in responsiveness of mice to physostigmine and atropine after withdrawal from long-term haloperidol pretreatment.

Abstract: Mice, administered haloperidol 3 mg/kg/day, in their drinking water for 21 days, were tested for their responsiveness to cholinergic and anticholinergic drugs 4 days after withdrawal from haloperidol (or vehicle). Haloperidol-treated animals administered methylhyoscine (1 mg/kg i.p.) and various doses of physostigmine (5 to 1215μg/kg) displayed significantly less depression of locomotor activity than vehicle-treated animals. Atropine, 5 mg/kg, whilst ineffective in producing locomotor stimulation in vehicle-treated animals, produced marked stimulation in haloperidol-treated animals. Methylatropine (5 mg/kg) did not produce significant stimulation in either group. Dopamine receptor supersensitivity was present in these animals as haloperidol-treated mice, pretreated withα-methyl-tyrosine and reserpine, displayed a significantly greater locomotor response to apomorphine than did vehicle-treated animals. The data support the hypothesis that long-term administration of haloperidol produces an apparent hyposensitivity of central muscarinic receptors.

Regional distribution of acid phosphatase-positive axonal systems in the rat spinal cord and medulla, representing central terminals of cutaneous and visceral nociceptive neurons.

Abstract: In addition to the substantia gelatinosa Rolandi, acid phosphatase active axonal systems are described (1) in the viscerosensory nucleus of the vagus nerve, (2) in Lissauer's band, (3) in the fasciculus cornus posterions (Cajal), and (4) in the nucleus basilaris externus (Cajal). Electron microscopically, acid phosphatase is located in between synaptic vesicles of axon terminals; the vesicle population of such terminals in the Rolando substance, however, markedly differs from that in systems 1–4, characterized by the presence of large dense-core vesicles. While acid phosphatase-active axon terminals in the Rolando substance appear to subserve cutaneous nociception, circumstantial evidence suggests participation of systems 1–4 in processing visceral nociception.

Antagonism by locally applied dopamine into the nucleus accumbens or the corpus striatum of alpha-methyltyrosine-induced disruption of conditioned avoidance behaviour.

Abstract: Male Sprague-Dawley rats were trained to avoid an electric shock in a two-way shuttle-box. The local application of dopamine into the nucleus accumbens or the corpus striatum was found to antagonize the suppression of conditioned avoidance behaviour induced by systemically administeredα-methyltyrosine, emphasizing the importance of these dopamine-rich brain structures in mediating conditioned avoidance behaviour.

Separation of pineal extracts by gelfiltration

Abstract: After separation of aqueous extracts of sheep pineal bodies and sheep cerebral cortex on Sephadex G-25, a high fluorescence peak showing an excitation maximum at 305→310 nm and a fluorescence maximum at 350→355 nm was observed in pineal extracts, which could not be detected in cerebral cortex extracts. Separation of this pineal fluorescence peak on Sephadex G-10 with water elution, followed by gradient elution of water and NaOH, gave rise to several highly fluorescent peaks. From one of these it was possible to isolate a substance with Rf-values, using thinlayer chromatographic, fluorescence and mass spectra studies, identical with synthetic 5-hydroxyindole-3-acetic acid. From another peak a substance, identical with synthetic 5-methoxyindole-3-acetic acid, could be isolated. The results are compared with those obtained in previous studies.

Influence de la photopériode sur l'ultrastructure de l'épiphyse avant et pendant la phase génitale saisonniére chez la femelle du lérot (Eliomys quercinus)

Abstract: Le pinealocyte de la femelle du Lerot, presente des caracteristiques ultrastructurales correlatives a un etat genital donne

6-Hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats

Abstract: The role of brain catecholaminergic neurones in the pathogenesis of DOCA-salt hypertension in the rat was investigated by selective depletion of central catecholamines using intraventricular or intracisternal administration of 6-hydroxydopamine (6-OHDA). Only the intraventricular injections prevented the development of hypertension. In addition, intraventricular 6-OHDA reversed the hypertension produced by two weeks but not six weeks of DOCA-salt treatment. The ability of intraventricular injections of 6-OHDA to prevent or reverse DOCA-salt hypertension while intracisternal injections do not, appears to be related to the greater depletion of brain catecholamines produced by the intraventricular injections. Only in the spinal cord and in the locus coeruleus were the norepinephrine contents depleted equally by either injection route. These findings suggest that central catecholaminergic neurones other than those originating in the locus coeruleus or descending in the spinal cord are important in the initiation, but not in the long term maintenance, of DOCA-salt hypertension. The influence of the central catecholamine neurons involved in the development of DOCA-salt hypertension might be mediated neurally via nonadrenergic pathways or hormonally via the brain-pituitary-endocrine system.

Effect of injecting 5-methoxy indoles, pineal compounds, on testicular weight of white leghorn cockerels (Gallus domesticus L.)

Abstract: White leghorn cockerels of the same age with combs of about equal size and raised under identical conditions were injected with melatonin, 5-methoxytryptophol, or with 5-methoxytryptophol in combination with melatonin. Melatonin, injected in animals with small comb sizes, has no effect on testicular growth, whereas an inhibiting effect is noticed in animals with larger comb sizes. The 5-methoxytryptophol treated animals demonstrated stimulated testicular growth, which can be interpreted as an acceleration of the rhythm of growth. The stimulatory effect on testicular growth is more distinct if 5-methoxytryptophol is injected in combination with melatonin.

The influence of bromocriptine on serotonin neurons.

Abstract: Bromocriptine (CB-154) is regarded as a dopamine agonist, hence is used in the treatment of Parkinson's disease. In the paper presented a possibility of the influence of bromocriptine on central serotonin neurons has been studied.