Role of the bed nucleus of the stria terminalis in cardiovascular changes following chronic treatment with cocaine and testosterone: A role beyond drug seeking in addiction?

Neural plasticity has been observed in the bed nucleus of the stria terminalis (BNST) following exposure to both cocaine and androgenic-anabolic steroids. Here we investigated the involvement of the BNST on changes in cardiovascular function and baroreflex activity following either single or combined administration of cocaine and testosterone for 10 consecutive days in rats. Single administration of testosterone increased values of arterial pressure, evoked rest bradycardia and reduced baroreflex-mediated bradycardia. These effects of testosterone were not affected by BNST inactivation caused by local bilateral microinjections of the nonselective synaptic blocker CoCl2. The single administration of cocaine as well as the combined treatment with testosterone and cocaine increased both bradycardiac and tachycardiac responses of the baroreflex. Cocaine-evoked baroreflex changes were totally reversed after BNST inactivation. However, BNST inhibition in animals subjected to combined treatment with cocaine and testosterone reversed only the increase in reflex tachycardia, whereas facilitation of reflex bradycardia was not affected by local BNST treatment with CoCl2. In conclusion, the present study provides the first direct evidence that the BNST play a role in cardiovascular changes associated with drug abuse. Our findings suggest that alterations in cardiovascular function following subchronic exposure to cocaine are mediated by neural plasticity in the BNST. The single treatment with cocaine and the combined administration of testosterone and cocaine had similar effects on baroreflex activity, however the association with testosterone inhibited cocaine-induced changes in the BNST control of reflex bradycardia. Testosterone-induced cardiovascular changes seem to be independent of the BNST. © 2013 IBRO.

Supressor eletromagnético de componentes harmônicas de sequência zero

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Influência do diltiazem sobre o tecido gengival: estudo histológico e histométrico em ratos

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

GABA and glutamate transporters: new events and function in the vertebrate retina

The neural retina is a highly complex tissue composed of excitatory and inhibitory neurons and glial cells. Glutamate, the main excitatory neurotransmitter, mediates information transfer from photoreceptors, bipolar cells, and ganglion cells, whereas interneurons, mainly amacrine and horizontal cells, use γ-aminobutyric acid (GABA), the main inhibitory neurotransmitter. In this review we place an emphasis on glutamate and GABA transporters as highly regulated molecules that play fundamental roles in neurotransmitter clearance, neurotransmitter release, and oxidative stress. We pharmacologically characterized glutamate transporters in chicken retina cells and identified two glutamate transporters: one Na+-dependent transporter and one Na+-independent transporter. The Na+-dependent uptake system presented characteristics related to the high-affinity xAG- system (EAAT1), and the Na+-independent uptake system presented characteristics related to the xCG- system, which highly contributes to glutamate transport in the retina. Glutamate shares the xCG- system with another amino acid, L-cysteine, suggesting the possible involvement of glutathione. Both transporter proteins are present mainly in Müller glial cells. GABA transporters (GATs) mediate high-affinity GABA uptake from the extracellular space and terminate the synaptic action of GABA in the central nervous system. GABA transporters can be modulated by molecules that act on specific sites to promote transporter phosphorylation and dephosphorylation. In addition to a role in the clearance of GABA, GATs may also release GABA through a reverse transport mechanism. In the chicken retina, a GAT-1 blocker, but not GAT2/3 blocker, was shown to inhibit GABA uptake, suggesting that GABA release from retina cells is mainly mediated by a GAT-1-like transporter.

Efeitos da bupropiona sobre o comportamento sexual, parâmetros espermáticos e fertilidade de ratos machos e sobre a contratilidade do ducto epididimático in vitro

Pós-graduação em Biologia Geral e Aplicada - IBB

Ultrastructural Morphology and Nuclear Maturation Rates of Immature Equine Oocytes Vitrified with Different Solutions and Exposure Times

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Cardiorespiratory effects of gap junction blockade in the locus coeruleus in unanesthetized adult rats

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

Evaluation of Antimalarial Activity and Toxicity of a New Primaquine Prodrug

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

Endothelial AT(1) and AT(2) pathways in aortic responses to angiotensin II after stress and ethanol consumption in rats

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Vias de sinalização endotelial α2, AT1, e AT2 sobre a reatividade da aorta de ratos após consumo de etanol e exposição ao estresse, isoladamente e em associação

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeitos da administração subaracnoidea em punção única, de cetamina S(+) a 5%, sem conservantes, sobre a medula espinal e as meninges de coelhos

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Hydrogen peroxide attenuates the dipsogenic, renal and pressor responses induced by cholinergic activation of the medial septal area

Cholinergic activation of the medial septal area (MSA) with carbachol produces thirst, natriuresis, antidiuresis and pressor response. In the brain, hydrogen peroxide (H2O2) modulates autonomic and behavioral responses. In the present study, we investigated the effects of the combination of carbachol and H2O2 injected into the MSA on water intake, renal excretion, cardiovascular responses and the activity of vasopressinergic and oxytocinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. Furthermore, the possible modulation of carbachol responses by H2O2 acting through K+ATP channels was also investigated. Male Holtzman rats (280–320 g) with stainless steel cannulas implanted in the MSA were used. The pre-treatment with H2O2 in the MSA reduced carbachol-induced thirst (7.9 ± 1.0, vs. carbachol: 13.2 ± 2.0 ml/60 min), antidiuresis (9.6 ± 0.5, vs. carbachol: 7.0 ± 0.8 ml/120 min,), natriuresis (385 ± 36, vs. carbachol: 528 ± 46 μEq/120 min) and pressor response (33 ± 5, vs. carbachol: 47 ± 3 mmHg). Combining H2O2 and carbachol into the MSA also reduced the number of vasopressinergic neurons expressing c-Fos in the PVN (46.4 ± 11.2, vs. carbachol: 98.5 ± 5.9 c-Fos/AVP cells) and oxytocinergic neurons expressing c-Fos in the PVN (38.5 ± 16.1, vs. carbachol: 75.1 ± 8.5 c-Fos/OT cells) and in the SON (57.8 ± 10.2, vs. carbachol: 102.7 ± 7.4 c-Fos/OT cells). Glibenclamide (K+ATP channel blocker) into the MSA partially reversed H2O2 inhibitory responses. These results suggest that H2O2 acting through K+ATP channels in the MSA attenuates responses induced by cholinergic activation in the same area.

Combined measurement of the Higgs Boson Mass in pp collisions at root s=7 and 8 TeV with the ATLAS and CMS experiments

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effect of the gadolinium ion on body fluid regulation

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Cardiovascular effects of the microinjection of L-proline into the third ventricle or the paraventricular nucleus of the hypothalamus in unanesthetized rats

We investigated the cardiovascular effects of the microinjection of L-proline (L-Pro) into the third ventricle (3V) and its peripheral mechanisms. Different doses of L-Pro into the 3V caused dose-related pressor and bradycardiac responses. The pressor response to L-Pro injected into the 3V was potentiated by intravenous pretreatment with the ganglion blocker pentolinium (5 mg/kg), thus excluding any significant involvement of the sympathetic nervous system. Because the response to the microinjection of L-Pro into the 3V was blocked by intravenous pretreatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP (50 mu g/kg), it is suggested that these cardiovascular responses are mediated by a vasopressin release. The pressor response to the microinjection of L-Pro into the 3V was found to be mediated by circulating vasopressin, so, given that the paraventricular nucleus of the hypothalamus (PVN) is readily accessible from the 3V, we investigated whether the PVN could be a site of action for the L-Pro microinjected in the 3V. The microinjection of L-Pro (0.033 mu moles/0.1 mu l) into the PVN caused cardiovascular responses similar to those of injection of the 3V and were also shown to be mediated by vasopressin release. In conclusion, these results show that the microinjection of L-Pro into the 3V causes pressor and bradycardiac responses that could involve stimulation of the magnocellular cells of the PVN and release of vasopressin into the systemic circulation. Also, because the microinjection of L-Pro into the PVN caused a pressor response, this is the first evidence of cardiovascular effects caused by its injection in a supramedullary structure. (c) 2012 Wiley Periodicals, Inc.