CULTURA POLÍTICA NO PAMPA

Este estudo foi desenvolvido a partir do projeto de pesquisa CulturaPolítica em São Borja, financiado pelo Programa de Bolsas deDesenvolvimento Acadêmico (PBDA) da Universidade Federal doPampa, em 2013. A pesquisa tem por principal objetivo obter ummapa da participação e da cultura política da cidade de São Borja,a partir de uma coleta de dados por questionário conforme a típicaanálise survey, buscando oferecer um quadro pormenorizado dostipos e níveis de participação e cultura política. A duração média deaplicação de cada questionário foi de 15 minutos, com a contagemtotal de 274 questionários. Entre as várias ferramentas de análise,foi criado um índice que intitulamos de «civicness», representandouma atitude cívica, em termos de participação cidadã por partedos entrevistados. Destacando que: 43,8% dos são-borjensesentrevistados abririam mão do voto se este não fosse obrigatório;somente 19,8 % são filiados a algum partido; no voto para vereador,77,8% escolhe seu candidato pela pessoa, independentemente dopartido ao qual está filiado; entre outros. O estudo da cultura políticalocal se torna muito importante para compreender o funcionamentodas instituições e da democracia, assim, pelo caso da região doPampa, mais especificadamente São Borja.Palavras-chave: Cultura política. Participação política. Surve

Gonadotropin-Releasing Hormone (GnRH) Activates the M-Current in GnRH Neurons: An Autoregulatory Negative Feedback Mechanism?

GnRH autoregulates GnRH neurons through an ultrashort feedback loop. One potential mechanism is the regulation of K+ channel activity through the GnRH receptor. Whereas GnRH inhibits the activity of the M-current in peripheral neurons, there is no direct evidence that the M-current is involved in the autoregulatory pathway of GnRH or if the M-current is expressed in GnRH neurons. The M-current is a noninactivating, subthreshold K+ current that inhibits cell excitability and is ubiquitously expressed in the central nervous system. We found that GnRH neurons expressed the neuronal M-current subunits, KCNQ2, -3, and -5 in addition to GnRH receptor (GnRH R1). Therefore, using whole-cell patch clamp recording and single-cell RT-PCR, we explored the effects of mammalian GnRH peptide on enhanced green fluorescent protein-tagged GnRH neurons acutely dispersed as well as in slice preparations. GnRH (100nm) inhibited GnRH neuronal excitability by hyperpolarizing the membrane. In the presence of CdCl2, BaCl2, and tetrodotoxin, GnRH activated an outward current in a dose-dependent manner (EC50 11 nm) in 30% of GnRH neurons. In voltage clamp, the selective M-channel blocker, XE-991, inhibited a K+ current in GnRH neurons. XE-991 also antagonized the outward K+ current induced by GnRH. Moreover, the GnRH effects on the M-current were blocked by the GnRH R1 antagonist antide. Therefore, these findings indicate that GnRH activates the M-current in a subpopulation of GnRH neurons via GnRH R1. This ultrashort circuit is one potential mechanism by which GnRH could modulate its own neuronal excitability through an autoreceptor

Adipokine Profile and Urinary Albumin Excretion in Isolated Growth Hormone Deficiency

Background: GH deficiency (GHD) is often associated with cardiovascular risk factors, including abdominal fat accumulation, hypercholesterolemia, and increased C-reactive protein. Despite the presence of these risk factors, adults with congenital lifetime isolated GHD (IGHD) due to an inactivating mutation in the GHRH receptor gene do not have premature atherosclerosis

The Neurobiology of Preovulatory and Estradiol-Induced Gonadotropin-Releasing Hormone Surges

Ovarian steroids normally exert homeostatic negative feedback on GnRH release. During sustained exposure to elevated estradiol in the late follicular phase of the reproductive cycle, however, the feedback action of estradiol switches to positive, inducing a surge of GnRH release from the brain, which signals the pituitary LH surge that triggers ovulation. In rodents, this switch appears dependent on a circadian signal that times the surge to a specific time of day (e.g., late afternoon in nocturnal species). Although the precise nature of this daily signal and the mechanism of the switch from negative to positive feedback have remained elusive, work in the past decade has provided much insight into the role of circadian/diurnal and estradiol-dependent signals in GnRH/LH surge regulation and timing. Here we review the current knowledge of the neurobiology of the GnRH surge, in particular the actions of estradiol on GnRH neurons and their synaptic afferents, the regulation of GnRH neurons by fast synaptic transmission mediated by the neurotransmitters γ-aminobutyric acid and glutamate, and the host of excitatory and inhibitory neuromodulators including kisspeptin, vasoactive intestinal polypeptide, catecholamines, neurokinin B, and RFamide-related peptides, that appear essential for GnRH surge regulation, and ultimately ovulation and fertility