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Biomedical subjects

L Lima

Publications and source records attributed to L Lima.

At least 91 records · Page 5Linked to original sources
PubMed1990

Cerebral serotonin in viral encephalitis.

In order to evaluate central serotonergic function during viral encephalitis biochemical, behavioural and immunohistofluorescence studies were carried out. Mice were inoculated with the moderate virulent strain of venezuelan equine encephalomyelitis virus, Pixuna. Signs of encephalitis were observed in 50-60% of infected animals. Levels of serotonin and 5-hydroxyindolacetic acid, and the ratio of the indolamine and its metabolite in raphe and cortex did not change with respect to sham-inoculated mice. A differential decrease in turnover rate by pharmacological methods, such as pargyline, p-chlorophenylalanine and probenecid administration, was observed in raphe and cortex. The ratio serotonin turnover rate/steady state concentration of serotonin was only decreased in the raphe of sick animals. The response to 5-methoxy-N,N-dimethyltryptamine was greater in infected animals. The duration of immobility in the swim test was shorter in the infected group. A greater number of viral antigen particles was localized in raphe and periraphe areas than in cortex, brain stem or striatum. The results suggest a serotonin presynaptic deficit, a postsynaptic hyperreactivity of serotonin system, and a region-selective distribution of the virus.

Animals↗
PubMed1990

[3H]ketanserin binds to non-5-HT2 sites in rabbit cerebral cortex and neostriatum.

A characterization of [3H]ketanserin ([3H]KTS) binding in the frontal cortex (fCTX) and neostriatum (caudate-putamen, CPU) of rabbit was carried out to determine whether this ligand labels a non-serotoninergic receptor. The association and dissociation kinetics in fCTX were rapid, and could be fitted to two-site models, suggesting [3H]KTS is labeling two cortical sites. Using the serotonin-2 (5-HT2) antagonist mianserin to determine nonspecific binding, the saturation curves revealed a single high-affinity binding site. In contrast, when unlabeled ketanserin was used for nonspecific counts, the Scatchard plots were best fitted to a two-site model but the binding parameters of the high-affinity site were similar to that obtained in the presence of mianserin. The 5-HT2 antagonists mianserin, methysergide and ritanserin inhibited [3H]KTS binding in fCTX at nanomolar concentrations, however, the curves were best fitted to two-site models. In contrast, [3H]KTS binding to membrane preparations from the CPU could only be inhibited by high (micromolar) concentrations of these antagonists. Low micromolar concentrations of the monoamine uptake blockers GBR12909, desipramine, nomifensine, cocaine and fluoxetine competed with [3H]KTS in both fCTX and CPU. This study demonstrates that [3H]KTS labels a non-serotoninergic recognition site in the rabbit fCTX and CPU similar to that found in the rat neostriatum, i.e.: probably a monoamine transport site.

Animals↗
PubMed1990

Alpha 2-adrenergic agonism enhances the growth hormone (GH) response to GH-releasing hormone through an inhibition of hypothalamic somatostatin release in normal men.

The purpose of this study was to investigate the precise mechanism by which central alpha 2-adrenergic pathways modulate GH secretion in humans. In 10 normal subjects we compared the pattern of clonidine-induced GH release to that elicited by GH-releasing hormone (GHRH) given at a time of presumably similar responsiveness of the somatotrope. We also evaluated the effect of stimulation by GHRH (either endogenous, by administration of clonidine, or exogenous) on the GH response to a further exogenous GHRH stimulation. In 2 experiments the administration of clonidine (0.150 mg, orally) at 0 or 60 min was followed by a GHRH [GRF-(1-29); 1 micrograms/kg, iv] challenge at 180 min. In other experiments subjects received on separate occasions placebo or clonidine at 0 min, followed by GHRH at 60 min and again at 180 min. In a further experiment the administration of clonidine at 0 min was followed by 2 GHRH challenges (60 and 180 min later). The administration of clonidine 60 or 120 min, but not 180 min, before the GHRH bolus significantly (P less than 0.01) increased the GH responses to this challenge compared to those elicited by GHRH when given after placebo in a period of a similar somatotrope responsiveness. These, in turn, were significantly (P less than 0.05) higher than those elicited by clonidine alone. The close relationship between pre-GHRH plasma GH values and GHRH-elicited GH peaks, not observed for clonidine, was lost after pretreatment with this drug. These data indicate that clonidine was able to disrupt the intrinsic hypothalamic-somatotroph rhythm, suggesting that alpha 2-adrenergic pathways have a major inhibitory effect on somatostatin release. Our data also indicate that GH responses to a GHRH bolus administered 120 min after a prior GHRH challenge are dependent on two parameters: the intrinsic hypothalamic-somatotroph rhythm at the time of the second GHRH bolus, and the magnitude of GH secretion elicited by the previous somatotroph stimulation. In summary, alpha 2-adrenergic agonism appears to act primarily in GH control by inhibiting the hypothalamic release of somatostatin, rather than by stimulating GHRH secretion.

Adolescent↗
PubMed1989

Spatial distribution of glutamate, taurine and GABA in teleosts and mammals retina: in vivo and in vitro study.

Teleost and amphibian retina grows throughout life at the circumferential margin distal to the center. Retinas of two teleosts, goldfish and Eugerres plumieri; and two mammals, rat and rabbit were dissected into concentric regions; center and periphery; or center, intermediate and periphery. The concentration of glutamic acid, taurine, and gamma-aminobutyric acid was determined in these areas. A non-significant difference was found between the center and periphery of retinas dissected into two regions. By dissecting the teleost retina in three concentric regions a progressive increase of gamma-aminobutyric acid and taurine for center to periphery was observed, which was statistically significant for taurine. Rat and rabbit retina did not present this difference. The concentration of these amino acids was also determined in two concentric regions of goldfish retina 24 hr after crush of the optic nerve. Taurine content significantly increased in the center of the regenerating retina, but not in the periphery. Outgrowth was measured in explants prepared from central and peripheral retina in the presence of exogenous taurine. The amino acid produced an increase of the nerve growth index of central explants, but inhibited the growth from peripheral explants. This report presents a correlation between taurine concentration in a region of the retina that could be considered as embryonic tissue, suggesting that this amino acid plays a role in the formation of new cells. Moreover, the results from post-crush and cultured retina, with respect to taurine concentration or regenerating effect, suggest a saturation of the taurine-enriched zone.

Animals↗
PubMed1989

The interaction of substrate and taurine modulates the outgrowth from regenerating goldfish retinal explants.

Retinal growth from explants attached to different substrates was evaluated in the absence and the presence of various concentrations of taurine. Fiber thickness was higher in poly-L-lysine, collagen and laminin than in the other substrates tested. Explants on wheatgerm, soybean, and red kidney bean lectins did not show emission of neurites at 5 days in culture; growth on laminin was very poor at this period of time. By day 10 nerve growth index was possible to evaluate on soybean and laminin. Outgrowth from retinal explants on wheatgerm lectin was only observed in the presence of taurine. The percentage of growing explants on laminin was increased by the amino acid. Emission of neurites from explants on concanavalin A and lentil lectin was constant from 5 to 10 days in culture and was not accelerated or increased by taurine. Growth on poly-L-lysine and collagen was stimulated by the addition of taurine in a concentration-dependent manner. The amino acid stimulates outgrowth from explants attached to peanut lectin in a bell-shaped concentration dependency similar to that observed on poly-L-lysine. The effect of taurine on retinal explants is substrate-dependent, as an indication of the interaction of soluble molecular components plus charge and structure of the extracellular matrix in order to modulate the outgrowth from regenerating tissue.

Animals↗
PubMed1989

Reasons for the variability in growth hormone (GH) responses to GHRH challenge: the endogenous hypothalamic-somatotroph rhythm (HSR).

The aims of this study were: (1) to test the possibility that pre-GHRH plasma GH values could reflect the functional status of the hypothalamic-somatotroph rhythm (HSR) at testing, and thus explain if it is responsible for the marked variability in GH responsiveness to GHRH challenge and (2) to see if exogenous somatostatin (SS) could disrupt this endogenous HSR and thus make the GH responses homogeneous. (1) Two to 14 GHRH acute tests (GRF-29, 1 micrograms/kg, i.v. bolus) were performed in 12 normal men and 10 normal women at the same time (0830 h) at random intervals (2 to 60 days). Blood samples to measure plasma GH were drawn at 15 min intervals before and after GHRH challenge. Given that the increments in pre-GHRH plasma GH values (I = value at 0 min minus value at -15 min) were highly correlated with either GHRH-elicited peaks of GH (men, r = 0.81; women; r = 0.69; P less than 0.0001) or the rise in GH after the challenge (r = 0.685; P less than 0.0001, in the total of tests performed), three theoretical HSR phases were proposed: (A) I greater than or equal to 0.4 microgram/l Secretory Phase; (B) I less than or equal to 0, (from GH at -15 min greater than or equal to 1.5 microgram/l), Secretion Plateau; (C) I less than or equal to 0, (from GH at -15 min less than or equal to 1.5 microgram/l), Refractory Phase. Individually, 91% of the men and 86% of the women showed a constant HSR phase when tested at the same time of day independently of the intervals between tests. GH responses (peaks, mean +/- SEM, g/l) in Phase A (women, 51.5 +/- 4.1; men, 31.4 +/- 3.2) were significantly higher (P less than 0.01) than those in Phase B (women, 22.6 +/- 1.8; men, 19.7 +/- 1.5), and these than those in Phase C (women, 9.2 +/- 1.5; men, 6.2 +/- 0.5). The great dispersion observed when GH peaks were analysed as a whole disappeared (except in Phase A in women) when they were evaluated according to the HSR Phase at testing. (2) In seven men and eight women 7 min after stopping an infusion of SS (250 micrograms/h for 3 h) a new GHRH test was performed. Plasma GH variations prior to SS infusion expressed the previous HSR Phase, while the GHRH-elicited peak of GH established the Phase at the moment of testing.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1989

Growth hormone (GH) responsiveness to GHRH in normal adults is not affected by short-term gonadal blockade.

The effects of changes in circulating gonadal steroids on GH secretion elicited by GHRH challenge (1 microgram/kg) in normal adults volunteers (aged 18-24 years), were evaluated in 10 women and 10 men before and after gonadal blockade was achieved by a GnRH agonist (1500 micrograms/day by nasal spray for 40 days). To see if the effect of testosterone on GH secretion was dependent on its aromatization to estradiol (E2), GHRH tests were performed in 7 normal men prior to administration of testosterone enanthate (250 mg im), 8 days after this treatment had began, and again after E2 receptor blockade with tamoxifen (30 mg for 2 days plus 10 mg on the third day 2 h before the GHRH test, po) administered 8 days after testosterone enanthate. The study of the functional status of the somatotropes at the time of GHRH testing was made according to our previous postulate. Short-term gonadal blockade did not affect the parameters of GH response to GHRH in neither women nor men. Thus, the functional blockade of the gonads may be advisable as an adjunct therapy in the treatment of hypothalamic GH-deficiency during the peripubertal stage. In the other group of men, administration of testosterone enanthate significantly increased GHRH-elicited GH release, but this was reverted after E2 receptor blockade. Since the hypothalamic-somatotrope rhythm was altered by both these pharmacological manipulations, it appears that testosterone acts on GH release mainly at the suprapituitary level, and that this action is secondary to its aromatization to E2.

Adolescent↗
PubMed1988

Inhibitory effect of cabergoline on the development of estrogen-induced prolactin-secreting adenomas of the pituitary.

Cabergoline 1-[(6-allylergolin-8 beta-yl)carbonyl]-1-[3-(dimethylamino) propyl]-3-ethylurea is a recently developed ergot derivative with a long-lasting dopamine agonist action. We now studied the ability of cabergoline to counteract the development of a prolactin-secreting tumor (prolactinoma) induced in female rats by long-term administration of high doses of estrogens. The effect of cabergoline was compared to that of bromocriptine. Cabergoline (0.6 mg/kg p.o.) had a marked and sustained prolactin-lowering effect in freely moving female rats, its effect still being present 3 days after a single dose. Bromocriptine, at a dose 5-fold higher (3 mg/kg s.c.), induced a strong and short-lasting prolactin inhibitory effect which, however, had completely disappeared 24 h post-injection. Intermittent administration of cabergoline (0.6 mg/kg p.o. every 3 days), starting from the first day of estrogen treatment, completely counteracted the development of the prolactinoma, as judged by the weight of the pituitary and the stimulating effect of estrogens on plasma prolactin and mitotic rate and DNA synthesis of pituitary cells. These effects of cabergoline were shared by a 5-fold higher dose of bromocriptine (3 mg/kg s.c.) given daily. The potent anti-tumorigenic effect of cabergoline, coupled to a sustained prolactin-lowering effect, the most prolonged ever seen with an ergot derivative, makes cabergoline a most suitable drug for the treatment of human macroprolactinomas.

Adenoma↗
PubMed1988

Behavioural effects produced in mice infected with venezuelan equine encephalomyelitis virus.

Pixuna, a strain of intermediate virulence of venezuelan equine encephalomyelitis virus, was inoculated intracranially to 24-day-old mice. Signs of encephalitis were present in 60% of the animals between 6 and 9 days with a maximum at 7 days postinoculation. The rest of the infected mice did not show clinical signs of encephalitis. In order to study the functional state of serotonergic systems a series of tests susceptible to modifications by serotonin activity were carried out. Locomotor activity was measured in an open field test. Virus-inoculated animals presented a variety of changes in their locomotor behavior at various days postinoculation with respect to the sham-inoculated group, however, they were not significant. Central serotonergic function was examined by the production of the serotonergic syndrome with the receptor agonist, 5-methoxy-N,N-dimethyltryptamine and the precursor, 5-hydroxytryptophan, both administered 4 days after the inoculation. The dose of the agonists was established by a prior drug-response analysis. Intensity of the syndrome was significantly higher in infected mice than in the sham-inoculated group only in 5-methoxy-N,N-dimethyltryptamine-treated animals. The behaviour in the swim test was also measured. Duration of immobility was much shorter in infected than in control mice. The decrease in central serotonin turnover previously reported might be responsible for the modification in locomotor behaviour and for the supersensitivity of serotonin receptors observed in infected mice.

Animals↗
PubMed1988

Taurine effect on neuritic growth from goldfish retinal explants.

Explants from retinas from which the optic nerve was previously crushed exhibited neuritic outgrowth after 4-5 days in culture, and up to 10 days in the presence of the same nutrient medium. Intact retinas did not exhibit vigorous outgrowth. Taurine added in the medium to post-crush explants accelerated the emission of neurites in 1-2 days, and increased the nerve growth index in a concentration-dependent manner up to 4 mM. Greater concentration did not produce any effect on the nerve growth index. The effect of taurine was produced between 0 and 5 days in culture; from day 5 to day 10 explants did not exhibit further growth in the presence of the amino acid. However, post-crush control explants exhibited growth between 5 and 10 days. Taurine effect is blocked in the absence of fetal calf serum, and is reduced in the presence of dialysed serum. Providing new medium on days 1 and 2, but not later, elevated the nerve growth index with respect to explants regenerating in the same medium since day 0. In addition, taurine supplied at various days after plating produced the same pattern of growth as that observed by adding fresh medium, but the nerve growth index was statistically greater in the presence of the amino acid. The mechanisms for these observations remain to be elucidated.

Animals↗
PubMed1988

Adrenal androgen secretion and dopaminergic activity in anorexia nervosa.

The aim of the present study was to investigate if the postulated deficient adrenal androgen secretion in Anorexia Nervosa (AN), could be associated with a status of sustained dopaminergic hyperactivity. The adrenal responses to ACTH and PRL response to dopaminergic receptor blockade were studied in seven patients with Anorexia Nervosa and seven regularly menstruating women. AN patients showed lower baseline DHEA-sulphate (DHEA-S), androstenedione (Adione) and prolactin (PRL) levels than controls. The response to ACTH revealed evidences of significantly decreased 17-20 desmolase activity in AN, with apparent predominance of glucocorticoid over androgenic pathways relative to controls. Because dopaminergic receptor blockade with Domperidone (DOM) showed intense dopaminergic hyperactivity in AN, we postulate that the adrenal regression seen in the disease is the consequence of a reduced zona reticularis as a consequence of the lack of trophic support by PRL and/or intermediate lobe proopiomelanocortin (IL-POMC). This is consistent with our previous results in pre-adrenarchal dogs and rabbits.

Adolescent↗
PubMed1988

Depending on the time of administration, dexamethasone potentiates or blocks growth hormone-releasing hormone-induced growth hormone release in man.

In humans, corticoids suppress growth hormone (GH) secretion elicited by a variety of stimuli, while in vitro they potentiate GH release. To further study this problem, the effect of two doses of dexamethasone on GH secretion elicited by GH-releasing hormone (GHRH) in 6 normal volunteers was studied. Each subject underwent three tests, on 3 separate days with GHRH 1-29 (1 microgram/kg i.v. at 12.00 h). On the control day, only GHRH was given, on the second day dexamethasone 4 mg i.v. was administered at 09.00 h (3 h before GHRH) and on the third day dexamethasone 8 mg p.o. was given 12 h before GHRH (at 00.00 h). The GHRH-induced GH peak was 9.9 +/- 2.0 ng/ml, while 4 mg dexamethasone significantly (p less than 0.05) potentiated GH secretion elicited by GHRH (29.2 +/- 5.7 ng/ml). When dexamethasone 8 mg was given 12 h before, GHRH-induced GH secretion was completely blocked (3.0 +/- 1.1 ng/ml) (p less than 0.05). These results indicate that corticoids have two different actions: an acute potentiating activity on GHRH, and a delayed blocking action on GHRH-induced GH secretion.

Adult↗
PubMed1987

Serotonin turnover rate in raphe and cortex of mice infected with Venezuelan equine encephalomyelitis virus.

The turnover of serotonin (5HT) was determined in the raphe area and cortex of mice infected with Pixuna, a strain of intermediate virulence of Venezuelan equine encephalomyelitis virus (VEEV). NMRI-mice, 24 days old, were inoculated intracerebrally (ic) with 300 LD50 of the virus. The animals were sacrificed 4, 7, 15, 21, 30, and 60 days postinoculation. 5HT and 5-hydroxyindoleacetic acid (5HIAA) in raphe and cortex were determined by high performance liquid chromatography (HPLC) with electrochemical detection. Turnover rate of 5HT was determined by the administration of pargyline, p-chlorophenylalanine, and probenecid. The content of 5HT or 5HIAA and 5HT/5HIAA ratios were not significantly different in infected compared with control mice. However, a decrease of 5HT turnover rate, determined after pargyline treatment, was observed in the raphe and not in the cortex of infected mice at 4 and 7 days after the inoculation. The turnover rate/(5HT)0 in raphe is decreased in infected mice with signs of illness, suggesting a lower density of 5HT innervation in this brain area. The administration of p-chlorophenylalanine and probenecid showed that the cortex is also affected, but the synthesis is less modified than metabolism or elimination. Cell bodies of 5HT neurons seem to be more susceptible than projections to infection by Pixuna strain of VEEV.

Animals↗
PubMed1987

Morphological and functional stimulation of adrenal reticularis zone by dopaminergic blockade in dogs.

In order to investigate factors affecting adrenal maturation leading to adrenarche, the effect of dopaminergic blockade on the morphology and function of the adrenal reticularis zone was studied in fourteen preadrenarchal dogs. Seven animals of 7 weeks of age (adrenarche at 11 weeks) were treated with domperidone (DOM) 3 times/day p.o. (3 mg/kg) at 09.00 h, 14.00 h, and 21.00 h, plus an additional injection of DOM s.c. (0.6 mg/kg) at 21.00 h for 15 days. Seven control animals received diluent. Twelve hours after the last injection, dogs received 0.25 mg ACTH i.m. and were sacrificed 60 min later. Blood was collected and adrenals removed. After histological evaluation, the percent of the reticularis, fasciculata, and glomerulosa zones with respect to the total cortex was calculated. Plasma androstenedione (A), dehydroepiandrosterone (DHA), 17-OH-progesterone (17P), and cortisol (F) levels in response to ACTH were also assessed. DOM-treated dogs show a significant development of the zona reticularis compared to control animals (19.2 +/- 0.6% vs 8.8 +/- 2.09% respectively, X +/- SE, P less than 0.01). In the same animals, the DHA response to ACTH (9.0 +/- 1.6 ng/dl) was significantly higher than in placebo-treated dogs (3.8 +/- 1.1 ng/dl, P less than 0.05) while no significant differences were found in F, A, and 17P levels between the two groups. Finally the post-ACTH A/DHA ratio of DOM-treated dogs (1.33 +/- 0.28) was significantly decreased in respect to the placebo-treated animals (5.49 +/- 2.54, P less than 0.01). These data demonstrate that the morphological and functional development of zona reticularis may be subject to dopaminergic control and this could represent an important step in the initiation of adrenarche. However, the cellular mechanism responsible remains to be clarified.

17-alpha-Hydroxyprogesterone↗
PubMed1987

Growth hormone and prolactin secretion after growth hormone-releasing hormone administration, in anorexia nervosa patients, normal controls and tamoxifen-pretreated volunteers.

Anorexia nervosa is associated with several abnormalities in GH secretion elicited by different stimuli. To investigate the precise mechanism of this alteration, GHRH was administered to 14 women: a group of eight anorexia nervosa patients in the acute phase of their illness and a control group of six age-matched volunteers. As patients with anorexia nervosa have chronic low oestrogen values, the volunteer women of the control group underwent a second GHRH test after pretreatment with the oestrogen receptor blocker tamoxifen. GHRH 1-29 (1 microgram/kg i.v.) induced a GH peak (mean +/- SEM) of 28.2 +/- 5.1 ng/ml (GH ng/ml x 2 = mU/l) at 30 min in the anorectic patients. This value was no different from the GHRH-stimulated GH peak in the control women (28.1 +/- 10.0 ng/ml). Tamoxifen pretreated women had a GH peak after GHRH of 35.6 +/- 9.7 ng/ml, not significant versus control test. Compared with the control group, oestrogen levels were significantly lower in anorectic patients and higher in tamoxifen-treated women. GHRH administration induced a small PRL peak at 15 min that was similar in the three groups tested. After this 15 min peak, PRL in both anorexic and tamoxifen-treated women returned toward basal values steadily. However, in untreated control women a second PRL peak was evident at 60 min. In conclusion, GHRH-induced GH secretion in anorexia nervosa patients was similar to that in control subjects and in controls under oestrogen receptor blockade.

Acute Disease↗
PubMed1987

Adrenal cortex and type II polycystic ovary syndrome.

The aim of this study was to investigate whether the adrenal gland participates in the pathogenesis of type II polycystic ovary syndrome (PCO), and, if so, to see if an altered pattern of ACTH secretion might be responsible. Circadian secretion and pulsatility (morning and evening) of ACTH, and adrenal and pituitary responsiveness to exogenous ACTH and GnRH, respectively, were evaluated in 10 women with type II PCO and 10 normally menstruating women. After the patients had been administered oral dexamethasone (0.5 mg each night) for 3 months, studies were repeated. Mean plasma values of PRL, testosterone, DHA-S and 17-OH progesterone (17-P) measured by RIA were significantly higher (p less than 0.05) in patients than in controls. FSH and sex hormone binding globulin (SHBG) were significantly lower (p less than 0.05). Cortisol and 17-P responses to ACTH, and the LH/FSH ratio (both in basal conditions and after GnRH stimulation) were significantly higher (p less than 0.05) in patients. ACTH circadian secretion and pulsatility were similar in both groups. Treatment with dexamethasone significantly reduced plasma values of testosterone, DHA-S, androstenedione (adione), cortisol and the LH/FSH ratio (basal and after GnRH), but adrenal hyperresponsiveness to ACTH was maintained. ACTH pulsatility and secretion were significantly (p less than 0.05) reduced in the morning. Our results suggest that there are abnormalities at the adrenal level in type II PCO. Given that ACTH secretion appears to be normal and that adrenal hyperresponsiveness is still observed after treatment with dexamethasone, it is tempting to speculate that excessive trophic stimulation of the gland by a factor other than ACTH could exist in such patients.

17-alpha-Hydroxyprogesterone↗
PubMed1986

Pharmacological analysis of the neurotransmitter mechanisms regulating phenylethanolamine N-methyltransferase in the adrenal gland.

The i.p. administration of reserpine daily for 4 days to rats brought about an increase of adrenal phenylethanolamine N-methyltransferase (PNMT) activity. However, the combination of the systemic administration of p-chlorophenylalanine (PCPA) and reserpine for 3 days produced an earlier increase in this adrenal enzyme. The effect was reduced significantly in the denervated gland. Prior administration of 5,7-dihydroxytryptamine (DHT) i.c.v. to rats greatly potentiated the inducing effect of reserpine. On the other hand, the depletion of catecholamines by giving rats alpha-methyl-p-tyrosine (AMPT) i.p. or 6-hydroxydopamine (6-OHDA) i.c.v. did not alter the action of reserpine on adrenal PNMT. PCPA, DHT, AMPT and 6-OHDA did not have any effect by themselves on adrenal PNMT, but the combination of PCPA and AMPT, each given i.p., caused increased adrenal PNMT activity. The administration of dopamine agonists, a treatment that increases adrenal TH, did not modify adrenal PNMT. We conclude that the induction of PNMT by reserpine involves depletion of catecholamines and serotonin, the depletion of serotonin having the more powerful effect. A monoaminergic (serotonergic) inhibitory pathway is involved in the central regulation of adrenal PNMT activity.

Adrenal Glands↗