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Thyrotropin-releasing hormone (TRH) is released from the median eminence upon neural stimulation such as cold or suckling exposure. Concomitant with the cold- or suckling-induced release of TRH is a rapid and transient increase in the expression of proTRH mRNA in the paraventricular nucleus (PVN) of the hypothalamus. We employed two strategies to determine(More)
Nitric oxide (NO) is an unstable gas that is produced in brain tissues involved in the control of the activity of the hypothalamus-pituitary-adrenal (HPA) axis. Transcripts for constitutive neuronal NO synthase (NOS I), one of the enzymes responsible for NO formation in the brain, is up-regulated by systemic endotoxin [lipopolysaccharide (LPS)] injection.(More)
Levels of thyrotropin-releasing hormone (TRH), TRH mRNA and pyroglutamyl peptidase II were analyzed in the hypothalamus-adenohypophyseal axis during lactation and estrous cycle. Mediobasal hypothalamic levels of TRH dropped 41% (p less than 0.01) from pregnancy levels (taken as 100%) on the first day of lactation, recovering until day 15 to the values(More)
Subthreshold electrical stimulation of the amygdala (kindling) activates neuronal pathways increasing the expression of several neuropeptides including thyrotropin releasing-hormone (TRH). Partial kindling enhances TRH expression and the activity or its inactivating ectoenzyme; once kindling is established (stage V), TRH and its mRNA levels are further(More)
1. Thyrotropin releasing hormone (TRH), synthesized in the paraventricular nucleus of the hypothalamus (PVN), is released in response to physiological stimuli through medianeminence nerve terminals to control thyrotropin or prolactin secretion from the pituitary. 2. Several events participate in the metabolism of this neuropeptide: regulation of TRH(More)
Fasting down-regulates the hypothalamus-pituitary-thyroid (HPT) axis activity through a reduction of TRH synthesis in neurons of the parvocellular paraventricular nucleus of the hypothalamus (PVN). These TRH neurons project to the median eminence (ME), where TRH terminals are close to the cytoplasmic extensions of β2 tanycytes. Tanycytes express(More)
Thyrotropin releasing hormone (TRH) is released from the median eminence in response to neural stimuli evoked by different physiologic conditions (i.e. cold stress or suckling). The paraventricular nucleus (PVN) synthesizes pro-TRH and responds to negative thyroid hormone feedback. With the aim of determining if TRH biosynthesis is regulated in coordination(More)
Brain derived neurotrophic factor (BDNF) increases the levels of pre-pro-thyrotropin releasing hormone (TRH) mRNA in fetal rodent hypothalamic neurons that express TrkB receptors. The present studies aimed at better understanding the role of BDNF in establishing and maintaining the TRH phenotype in hypothalamic neurons during early development. To determine(More)
TRH (pGlu-His-ProNH2) inactivation in the brain and pituitary extracellular fluid is reviewed. While TRH could be eliminated by alternative mechanisms, i.e. uptake or internalization, modification, hydrolysis by broad specificity peptidases such as pyroglutamyl peptidase I and prolyl endopeptidase, evidence accumulates to support a specific(More)
Thyrotropin releasing hormone (TRH) biosynthesis is subject to a multifactorial control. TRH mRNA levels are negatively regulated by thyroid hormones in the paraventricular hypothalamic nucleus, and positively in cold exposure or suckling. Effect of second messenger pathways stimulation, a known response to membrane receptors, was studied in vitro; cultures(More)