A role for histamine in cardiovascular regulation in late stage embryos of the red-footed tortoise, Chelonoidis carbonaria Spix, 1824

A chorioallantoic membrane artery in embryos of the red-footed tortoise, Chelonoidis carbonaria was occlusively cannulated for measurement of blood pressure and injection of drugs. Two age groups of embryos in the final 10 % of incubation were categorized by the ratio of embryonic body to yolk mass. All embryos first received cholinergic and β-adrenergic blockade. This revealed that β-adrenergic control was established in both groups whereas cholinergic control was only established in the older group immediately prior to hatching. The study then progressed as two series. Series one was conducted in a subset of embryos treated with histamine before or after injection of ranitidine, the antagonist of H2 receptors. Injection of histamine caused an initial phasic hypertension which recovered, followed by a longer lasting hypertensive response accompanied by a tachycardia. Injection of the H2 receptor antagonist ranitidine itself caused a hypotensive tachycardia with subsequent recovery of heart rate. Ranitidine also abolished the cardiac effects of histamine injection while leaving the initial hypertensive response intact. In series, two embryos were injected with histamine after injection of diphenhydramine, the antagonist to H1 receptors. This abolished the whole of the pressor response to histamine injection but left the tachycardic response intact. These data indicate that histamine acts as a non-adrenergic, non-cholinergic factor, regulating the cardiovascular system of developing reptilian embryos and that its overall effects are mediated via both H1 and H2 receptor types. © 2013 Springer-Verlag Berlin Heidelberg.

Investigação da toxicidade reprodutiva do fungicida Procloraz, com ênfase sobre aspectos morfofuncionais do epidídimo de ratos adultos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Interleucina-9 estimula a expressão de CCL17/TARC em células epiteliais de pulmão murino

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Possible involvement of A1 receptors in the inhibition of gonadotropin secretion induced by adenosine in rat hemipituitaries in vitro

We investigated the participation of A₁ or A₂ receptors in the gonadotrope and their role in the regulation of LH and FSH secretion in adult rat hemipituitary preparations, using adenosine analogues. A dose-dependent inhibition of LH and FSH secretion was observed after the administration of graded doses of the R-isomer of phenylisopropyladenosine (R-PIA; 1 nM, 10 nM, 100 nM, 1 µM and 10 µM). The effect of R-PIA (10 nM) was blocked by the addition of 8-cyclopentyltheophylline (CPT), a selective A₁ adenosine receptor antagonist, at the dose of 1 µM. The addition of an A₂ receptor-specific agonist, 5-N-methylcarboxamidoadenosine (MECA), at the doses of 1 nM to 1 µM had no significant effect on LH or FSH secretion, suggesting the absence of this receptor subtype in the gonadotrope. However, a sharp inhibition of the basal secretion of these gonadotropins was observed after the administration of 10 µM MECA. This effect mimicked the inhibition induced by R-PIA, supporting the hypothesis of the presence of A₁ receptors in the gonadotrope. R-PIA (1 nM to 1 µM) also inhibited the secretion of LH and FSH induced by phospholipase C (0.5 IU/ml) in a dose-dependent manner. These results suggest the presence of A₁ receptors and the absence of A₂ receptors in the gonadotrope. It is possible that the inhibition of LH and FSH secretion resulting from the activation of A₁ receptors may have occurred independently of the increase in membrane phosphoinositide synthesis.

Influence of the dopaminergic system, CREB, and transcription factor-B on cocaine neurotoxicity

Cocaine is a widely used drug and its abuse is associated with physical, psychiatric and social problems. Abnormalities in newborns have been demonstrated to be due to the toxic effects of cocaine during fetal development. The mechanism by which cocaine causes neurological damage is complex and involves interactions of the drug with several neurotransmitter systems, such as the increase of extracellular levels of dopamine and free radicals, and modulation of transcription factors. The aim of this review was to evaluate the importance of the dopaminergic system and the participation of inflammatory signaling in cocaine neurotoxicity. Our study showed that cocaine activates the transcription factors NF-κB and CREB, which regulate genes involved in cellular death. GBR 12909 (an inhibitor of dopamine reuptake), lidocaine (a local anesthetic), and dopamine did not activate NF-κB in the same way as cocaine. However, the attenuation of NF-κB activity after the pretreatment of the cells with SCH 23390, a D1 receptor antagonist, suggests that the activation of NF-κB by cocaine is, at least partially, due to activation of D1 receptors. NF-κB seems to have a protective role in these cells because its inhibition increased cellular death caused by cocaine. The increase in BDNF (brain-derived neurotrophic factor) mRNA can also be related to the protective role of both CREB and NF-κB transcription factors. An understanding of the mechanisms by which cocaine induces cell death in the brain will contribute to the development of new therapies for drug abusers, which can help to slow down the progress of degenerative processes.

LESION OF THE COMMISSURAL NUCLEUS OF THE SOLITARY TRACT/A2 NORADRENERGIC NEURONS FACILITATES THE ACTIVATION OF ANGIOTENSINERGIC MECHANISMS IN RESPONSE TO HEMORRHAGE

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Expression of receptors for BMP15 is differentially regulated in dominant and subordinate follicles during follicle deviation in cattle

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Pancreatic Alpha-Cell Dysfunction Contributes to the Disruption of Glucose Homeostasis and Compensatory Insulin Hypersecretion in Glucocorticoid-Treated Rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Healing Process of Autogenous Bone Graft in Spontaneously Hypertensive Rats Treated With Losartan: An Immunohistochemical and Histomorphometric Study

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Hyperalgesic and edematogenic effects of Secapin-2, a peptide isolated from Africanized honeybee (Apis mellifera) venom

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cimetidine Reduces Alveolar Bone Loss in Induced Periodontitis in Rat Molars

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Avaliação do estado emocional associado à catalepsia causada pela administração intraperitoneal de haloperidol

Haloperidol is a dopamine receptor antagonist used to treat schizophrenia. When systemically administered in rodents, haloperidol induces catalepsy, a state of immobility very similar to that seen in Parkinson's disease. It is known that many of Parkinson's disease symptoms are dependent on the emotional state since patients are still able to respond to external triggers such as loud noise or visual signaling. Recent data highlighted the importance of glutamatergic neurotransmission in the inferior colliculus (IC) on the cataleptic state induced by haloperidol in rats. Given the importance of IC in the brain aversion system and its connections to motor pathways, and based on the clinical reports of the emotional influence on the motor aspect of Parkinson's disease, the objective of the present study was to evaluate the emotional aspect related to catalepsy induced by intraperitoneal administration of haloperidol. To this end, we analysed ultrasonic vocalizations (UVs) of 22 kHz (indicative of aversion) in rats during the tests of catalepsy, open field and contextual conditioned fear. Systemic administration of haloperidol affected the motor activity, inducing catalepsy and decreasing exploratory activity in the open field. There were no UVs of 22 kHz resulting from treatment with haloperidol in catalepsy or open field tests. In the contextual conditioned fear test, haloperidol increased freezing when administered before the test, but decreased freezing on test day when administered before training. In this same test, haloperidol decreased the UVs on the day it was administered (training or test). The catalepsy induced by systemic administration of haloperidol seems to have also affected the motor aspect of UVs. In this way, it was not possible to clarify the existence of an aversive emotional state associated haloperidol induced catalepsy

Interação entre estradiol e receptores 5 - H T 1A no Núcleo Mediano da Rafe em ratas ovariectomizadas: na aquisição da informação aversiva e associação ao contexto

Pós-graduação em Biociências - FCLAS

Activation of μ opioid receptors in the LPBN facilitates sodium intake in rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Gabaergic and opioid receptors mediate the facilitation of NaCl intake induced by α₂-adrenergic activation in the lateral parabrachial nucleus

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)