Somatostatin inhibition of GnRH neuronal activity and the morphological relationship between GnRH and somatostatin neurons in rats.

In rodents, GnRH neurons are diffusely distributed from the medial septum through to the medial preoptic area and control gonadal functions through the pituitary. The activity of GnRH neurons is regulated by a variety of bioactive substances, including the inhibitory peptide somatostatin. In the present study, we focused on somatostatin because intracerebroventricular injection of somatostatin inhibits the LH surge in rats and reduces LH secretion in ewes.

Prevalence of equine herpesvirus type 1 strains of neuropathogenic genotype in a major breeding area of Japan.

A single non-synonymous nucleotide substitution of guanine (G) for adenine (A) at position 2254 in the viral DNA polymerase gene (encoded by open reading frame [ORF] 30) of equine herpesvirus type 1 (EHV-1) has been significantly associated with neuropathogenic potential in strains of this virus. To estimate the prevalence of EHV-1 strains with the neuropathogenic genotype (ORF30 G(2254)) in the Hidaka district--a major horse breeding area in Japan--we analyzed the ORF30 genomic region in cases of EHV-1 infection in this area during the years 2001-2010. Of the 113 cases analyzed, 3 (2.

Voltage-gated Ca2+ channel mRNAs and T-type Ca2+ currents in rat gonadotropin-releasing hormone neurons.

Gonadotropin-releasing hormone (GnRH) neurons play a pivotal role in the neuroendocrine regulation of reproduction. We have previously reported that rat GnRH neurons exhibit voltage-gated Ca(2+) currents. In this study, oligo-cell RT-PCR was carried out to identify subtypes of the alpha(1) subunit of voltage-gated Ca(2+) channels in adult rat GnRH neurons.

Cetrorelix, a gonadotropin-releasing hormone antagonist, induces the expression of melatonin receptor 1a in the gonadotropin-releasing hormone neuronal cell line GT1-7.

Melatonin has been implicated in the control of the reproductive system, and the modulatory actions of melatonin on gonadotropin-releasing hormone (GnRH) neurons have been assumed to be indirectly mediated through afferent neurons. However, our previous studies demonstrate sexually dimorphic modulation of A-type gamma-aminobutyric acid (GABA) receptor (GABA(A)R) currents by melatonin in adult rat GnRH neurons and a preferential expression of melatonin 1a receptor (MT1) in male GnRH neurons. Using immortalized GnRH neurons (GT1-7 cells), the present study investigated the mechanism by which the expression of melatonin receptors is regulated in GnRH neurons.

GABAA receptors mediate excitation in adult rat GnRH neurons.

Gonadotropin-releasing hormone (GnRH) neurons form the final common pathway for the central regulation of reproduction. Gamma-amino butyric acid (GABA), the main inhibitory neurotransmitter in the adult brain, has long been implicated in playing key roles in the regulation of GnRH neurons. Two groups reported recently that GABA depolarizes GnRH neurons, although one group reported a hyperpolarizing action of GABA.

Gene structures, biochemical characterization and distribution of rat melatonin receptors.

G-protein coupled receptors for the pineal hormone melatonin have been partially cloned from rats. However, insufficient information about their cDNA sequences has hindered studies of their distribution and physiological responses to melatonin using rats as an animal model. We have cloned cDNAs of two rat membrane melatonin receptor subtypes, melatonin receptor 1a (MT1) and melatonin receptor 1b (MT2), using a rapid amplification of cDNA end (RACE) method.

Sexually dimorphic modulation of GABA(A) receptor currents by melatonin in rat gonadotropin-releasing hormone neurons.

Gonadotropin-releasing hormone (GnRH) neurons represent the final output neurons in the central control of reproduction. gamma-Amino butyric acid (GABA), one of the major regulators of GnRH neurons, depolarizes GnRH neurons isolated from adult rats via GABA(A) receptors. The presence of GABA(A) receptors in GnRH neurons has also been demonstrated morphologically.

Rat GnRH neurons exhibit large conductance voltage- and Ca2+-Activated K+ (BK) currents and express BK channel mRNAs.

Gonadotropin-releasing hormone (GnRH) neurons form the final common pathway for the central regulation of reproduction. As in other neurons, the discharge pattern of action potentials is important for these neurons to function properly. Therefore it is important to elucidate the expression patterns of various types of ion channels in these neurons because they determine cell excitability.

17beta-estradiol at physiological concentrations augments Ca(2+) -activated K+ currents via estrogen receptor beta in the gonadotropin-releasing hormone neuronal cell line GT1-7.

Estrogens play essential roles in the neuroendocrine control of reproduction. In the present study, we focused on the effects of 17beta-estradiol (E2) on the K(+) currents that regulate neuronal cell excitability and carried out perforated patch-clamp experiments with the GnRH-secreting neuronal cell line GT1-7. We revealed that a 3-d incubation with E2 at physiological concentrations (100 pm to 1 nm) augmented Ca(2+)-activated K(+) [K(Ca)] currents without influencing Ca(2+)-insensitive voltage-gated K(+) currents in GT1-7 cells.

Neural interaction between galanin-like peptide (GALP)- and luteinizing hormone-releasing hormone (LHRH)-containing neurons.

Galanin-like peptide (GALP), commonly known as an appetite-regulating peptide, has been shown to increase plasma luteinizing hormone (LH) through luteinizing hormone-releasing hormone (LHRH). This led us to investigate, using both light and electron microscopy, whether GALP-containing neurons in the rat brain make direct inputs to LHRH-containing neurons. As LHRH-containing neurons are very difficult to demonstrate immunohistochemically with LHRH antiserum without colchicine treatment, we used a transgenic rat in which LHRH tagged with enhanced green fluorescence protein facilitated the precise detection of LHRH-producing neuronal cell bodies and processes.

The SK channel blocker apamin inhibits slow afterhyperpolarization currents in rat gonadotropin-releasing hormone neurones.

Gonadotropin-releasing hormone (GnRH) neurones play an essential role in the hypothalamo-pituitary-gonadal axis. As for other neurones, the discharge pattern of action potentials is important for GnRH neurones to properly function. In the case of a luteinizing hormone (LH) surge, for example, GnRH neurones are likely to continuously fire for more than an hour.

Generation of transgenic rats expressing enhanced green fluorescent protein in gonadotropin-releasing hormone neurons.

Hypothalamic gonadotropin-releasing hormone (GnRH) neurons govern reproductive function by controlling the release of gonadotropins from the pituitary. To facilitate identification of living GnRH neurons, here we attempted to generate transgenic rats that express enhanced green fluorescent protein (EGFP) in GnRH neurons. About 3 kb of rat GnRH promoter region was inserted into the EGFP reporter cassette, and the expression of EGFP fluorescence was confirmed in several cell lines following transient transfection.

High expression of the R-type voltage-gated Ca2+ channel and its involvement in Ca2+-dependent gonadotropin-releasing hormone release in GT1-7 cells.

The GT1 cell has been widely used as a model cell to study cellular functions of GnRH neurons. Despite the importance of Ca(2+) channels, little is known except for L- and T-type Ca(2+) channels in GT1 cells. Therefore, we studied the diversity of voltage-gated Ca(2+) channels in GT1-7 cells with perforated-patch clamp and RT-PCR.

Characterization of voltage-gated calcium currents in gonadotropin-releasing hormone neurons tagged with green fluorescent protein in rats.

Functional analysis of GnRH neurons is limited, although these neurons play an important role in neuroendocrine regulation. Therefore, we decided to conduct cell physiological analysis of GnRH neurons. To identify GnRH neurons, we tagged the neurons with green fluorescence protein by a transgenic technique.

3',5'-cyclic adenosine monophosphate augments intracellular Ca2+ concentration and gonadotropin-releasing hormone (GnRH) release in immortalized GnRH neurons in an Na+ -dependent manner.

In GT1-7 cells, cAMP increases the intracellular Ca2+ concentration ([Ca2+](i)) through activation of the voltage-gated Ca2+ channels, thereby facilitating GnRH release. To activate these channels, the membrane potential must be depolarized. In the present study we hypothesize that cAMP depolarizes the cells by increasing the membrane Na+ permeability, as in the case of somatotrophs and pancreatic beta-cells.