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L Jennes

Publications and source records attributed to L Jennes.

At least 37 records · Page 2Linked to original sources
PubMed1998

Identification of kainate-preferring glutamate receptor subunit GluR7 mRNA and protein in the rat median eminence.

In situ hybridization and immunohistochemistry were used to determine the presence of kainate-preferring glutamate receptor subunits GluR6 and GluR7 mRNA and protein in the median eminence of the rat. The results show that most tanycytes lining the ventral third ventricle and many astrocytes within the median eminence contain the GluR7 receptor subunit mRNA but not the GluR5 and GluR6 receptor subunit mRNA. Immunohistochemical stainings show that the GluR6/7 receptor protein was localized to tanycytic cell bodies, their basal processes and to many other astrocytes in different layers of the median eminence. The results suggest that glutamate can act directly on the glial cells in the median eminence by binding to the GluR7 subunit which may be important for the control of the secretion of releasing and inhibiting hormones from axon terminals in the external layer. In order to determine if these receptor subunits are functional, kainic acid was injected and c-fos expression monitored. Results show that kainic acid induced c-fos synthesis in most of these glial cells.

Animals↗
PubMed1998

Identification of alpha1B adrenergic receptor protein in gonadotropin releasing hormone neurones of the female rat.

Noradrenaline is an important neurotransmitter which regulates GnRH release from the median eminence in the female rat during both basal GnRH secretion and the preovulatory or steroid hormone-induced GnRH-mediated LH surge. However, it is not clear at which sites in the brain this predominantly stimulatory influence is exerted nor is it known which adrenergic receptor subtype(s) mediate(s) the effects of noradrenaline. In order to determine if the GnRH neurones in the septum-diagonal band-preoptic area and/or their axon terminals in the median eminence are direct targets for noradrenaline, immunohistochemical triple-labelling studies were conducted to localize simultaneously GnRH peptide, dopamine-beta-hydroxylase and alpha1B adrenergic receptor protein. The results show that about 80% of all GnRH neurones examined contained patches of immunoreactive alpha1B adrenergic receptor protein at or near the plasma membrane and that some of these alpha1B adrenergic receptors were adjacent to dopamine-beta-hydroxylase containing axons. The GnRH neurones which did not contain alpha1B adrenergic receptors were preferentially located in the rostral portion of the septum and diagonal band while all GnRH neurones in the caudal septum, diagonal band and in the preoptic area expressed alpha1B adrenergic receptors. In the median eminence, a few alpha1B adrenergic receptor patches were seen in the external layer and these receptors were only rarely observed to be associated with GnRH containing axon terminals. The results suggest that the effects of noradrenaline on GnRH release are, at least in part, mediated by the activation of alpha1B adrenergic receptors which are located on most GnRH perikarya while the median eminence is not a likely site at which GnRH release is regulated by alpha1B adrenergic receptors.

Animals↗
PubMed1998

Identification of gap junctional connexin-32 mRNA and protein in gonadotropin-releasing hormone neurons of the female rat.

Pulsatile gonadotropin-releasing hormone (GnRH) release from the median eminence is critical for the appropriate function of the pituitary gonadotropes and for the generation of a preovulatory gonadotropin surge. The mechanisms by which many GnRH axon terminals are synchronized to release GnRH in a coordinated fashion into the capillaries of the primary plexus are unknown as are the anatomical sites at which the regulation of GnRH neurons takes place. While many neurotransmitters have been shown to influence GnRH release, it is not clear if such neurotransmitters regulate GnRH neurons directly through synaptic interactions or through intermediate neurons. An alternative mechanism of interneuronal communication is provided by gap junctions which allow a rapid, bidirectional exchange of signals. In order to explore if GnRH neurons synthesize the appropriate proteins to form gap junctions with adjacent cells we used double immunohistochemistry for GnRH and connexins-26, -32 or -43 as well as dual in situ hybridization to identify GnRH mRNA and connexin-32 mRNA. The results show that all GnRH neurons contain connexin-32 immunoreactive puncta at their perikarya and, occasionally, at their axon terminals in the median eminence while connexin-26 and -43 immunoreactivity was absent in GnRH neurons. In addition, connexin-32 mRNA was detected in GnRH mRNA containing neurons. However, gap junctional connections between adjacent GnRH neurons were not observed. The data suggest that gap junctional coupling of GnRH neurons with neighboring non-GnRH containing cells may occur and may represent a mechanism by which GnRH neurons can be synchronized or by which hormonal or neurotransmitter signals can be conveyed to the GnRH neurons.

Animals↗
PubMed1997

Presence of mu and kappa opioid receptor mRNAs in galanin but not in GnRH neurons in the female rat.

Using a combination of radioactive and non-radioactive in situ hybridizations, the expression of mu and kappa opioid receptor mRNA was investigated in neurons in the female rat preoptic nucleus expressing galanin and gonadotropin-releasing hormone (GnRH) mRNA. Numerous cells expressing both mu or kappa and galanin were found in the intermediate and rostral regions of the preoptic area whereas little co-localization was observed at the rostral level. The number of kappa/galanin expressing cells was greater than that of mu/galanin cells. mu/galanin co-localization was observed essentially in the anteroventral preoptic nucleus while neurons expressing kappa/galanin were present in both the anteroventral preoptic nucleus and in the periventricular hypothalamic nucleus. Co-localization of GnRH with mu or kappa could not be detected in the preoptic area. These observations showed that galaninergic neurons but not GnRH neurons of the preoptic area might be directly regulated by endogenous opioid peptides.

Animals↗
PubMed1997

The inhibition of growth and down-regulation of gonadotropin releasing hormone (GnRH) receptor in alphaT3-1 cells by GnRH agonist.

Gonadotropin releasing hormone (GnRH) and its analogs inhibit the growth of hormone-dependent tumors in vivo and in vitro. The inhibition of growth and proliferation of tumor cells in vitro by GnRH and its analogs indicates that the tumor suppressing effect of the hormone is only partially due to suppression of pituitary gonadotropin release which reduces circulating steroid levels that are required for proliferation. Demonstration of GnRH-binding sites on some tumors suggests a direct inhibitory effect of GnRH and its analogs. However, the mechanism by which GnRH and its analogs inhibit tumor cell growth is not known. Our hypothesis is that the inhibition of growth and proliferation of tumor cells by GnRH and its analogs are mediated through down-regulation of its receptor expression. To test this hypothesis, mouse pituitary gonadotrope cell line (alphaT3-1) was selected as a model since this is the only cell line which expresses a sufficiently high level of GnRH receptors for precise measurements of the mRNA for the receptor. Addition of GnRH agonist (D-Lys6)GnRH to the cell cultures caused a time-dependent decrease in both cell growth, as measured by cell number, and cell proliferation, as measured by [3H]thymidine incorporation into DNA. After 1 h of treatment of alphaT3-1 cells with 1 microM of (D-Lys6)GnRH, the cell number was reduced to 83.0 +/- 13.4 compared to control, decreased to 75.1 +/- 3.2 at 2 h, 63.2 +/- 0.66 at 4 h and 52.2 +/- 0.87 at 24 h. This decrease in cell number was accompanied by a parallel decrease in [3H]thymidine incorporation into DNA. The inhibition of cell growth and [3H]thymidine incorporation by treatment with 1 microM of (D-Lys6)GnRH was sustained for at least 72 h. Inhibition of alphaT3-1 cell growth and [3H]thymidine incorporation was dose-dependent; thus 10(-9) M (D-Lys6)GnRH resulted in about 30% inhibition within 4h which was comparable to 10(-6) M (D-Lys6)GnRH, whereas 10(-12) M (D-Lys6)GnRH was ineffective. Measurement of mRNA for the GnRH receptor by Northern blot analysis showed a decrease in levels of mRNA by 5% within 2 h of treatment of alphaT3-1 cells with 1 microM (D-Lys6)GnRH, by 30% at 4 h and by 50% at 24 h. In conclusion these data demonstrate that treatment of alphaT3-1 cells with (D-Lys6)GnRH causes an inhibition of cell growth and proliferation, and down-regulates the GnRH receptor mRNA levels.

Animals↗
PubMed1997

Expression of glutamate receptor subunit mRNAs in gonadotropin-releasing hormone neurons during the sexual maturation of the female rat.

Excitatory amino acids, particularly glutamate, are thought to be important for the maturation of the brain-pituitary-gonadal axis and the induction of puberty in the rat. We have previously shown that, in the female rat, GnRH neurons preferentially express the KA2 and NMDAR2A receptor subunit mRNAs, but not AMPA or NMDAR1 mRNA. The aim of the present study was to determine whether the onset or rate of KA2 and NMDAR2A receptor expression in GnRH neurons is correlated with the onset of puberty. Dual in situ hybridization using digoxigenin-labeled GnRH cRNA probes and 35S-labeled glutamate receptor subunit probes, followed by autoradiography and image analysis were used to measure the KA2 or NMDAR2A mRNA content in GnRH neurons in 20- to 50-day-old female rats which were sacrificed at 08.00 or 17.00 h. The results show that: (a) the KA2 mRNA content of GnRH neurons and the number of GnRH neurons expressing KA2 mRNA increase progressively in the morning hours between postnatal days 20 and 40; (b) the diurnal pattern of KA2 mRNA levels in GnRH neurons changes between days 40 and 50 from high KA2 levels in the morning hours before day 40 to high KA2 mRNA levels in the afternoon in 45- and 50-day-old animals; (c) while the high levels of KA2 mRNA in GnRH neurons in the morning hours of 20- to 40-day-old animals are paralleled by an overall increase in KA2 expression in the preoptic area, the rise in KA2 mRNA in GnRH neurons in the afternoon of 45- and 50-day-old animals appears to be specific for the GnRH neurons, and (d) no significant differences were detected for the NMDAR2A mRNA content in GnRH neurons among the different age groups and the morning and afternoon values. Since the gradual increase in the KA2 mRNA content in GnRH neurons of animals reaching puberty as well as the reversal of diurnal rhythmicity in KA2 receptor mRNA content of GnRH neurons coincide with the times of vaginal opening and first ovulation, it is suggested that glutamate, acting through KA2 receptors directly on GnRH neurons is, at least in part, an important factor in the excitatory regulation of the postnatal sexual development of the female rat. In contrast, expression of the NMDA-preferring receptor, NMDAR2A, in GnRH neurons appeared to be unchanged during this development.

Animals↗
PubMed1997

Brain gonadotropin releasing hormone receptors: localization and regulation.

In this review, the current information about the location of GnRH receptor protein and GnRH receptor mRNA in the rat central nervous system is summarized as well as the changes that occur in the GnRH receptor mRNA levels during different endocrine conditions of the animals. The results of these studies show that GnRH receptor protein and mRNA levels change in parallel in the hippocampus, suggesting that pretranscriptional factors control the synthesis of the receptor. In the arcuate and ventromedial nuclei of the hypothalamus, GnRH receptor mRNA levels are highest during the early morning of proestrus and during the morning of an estrogen-progesterone-induced LH surge. The timing of the changes in GnRH receptor mRNA levels indicates that increasing levels of estradiol are responsible for the increase in GnRH receptor synthesis. Binding of GnRH agonist to the brain GnRH receptor causes a dose-dependent increase in inositol phosphates as well as changes in intracellular Ca++ levels of the target neurons. Together, it is suggested that GnRH functions in the brain as a neurotransmitter and/or modulator linking the peripheral endocrine effects of GnRH to actions of the peptide inside the central nervous system where it can facilitate, for example, reproductive behaviors.

Animals↗
PubMed1996

Dynamic changes in gonadotropin releasing hormone receptor mRNA content in the mediobasal hypothalamus during the rat estrous cycle.

The purpose of the present study was to determine if GnRH receptor mRNA levels in the rat brain undergo changes during the estrous cycle. We focused on the arcuate and ventromedial nuclei of the hypothalamus and on the hippocampus which are sites in the rat central nervous system that have been shown to contain measurable amounts of GnRH receptor mRNA. Groups of regularly cycling female rats were decapitated at 08.00 and 17.00 h of each day of the estrous cycle, trunk blood was collected for radioimmunoassay analysis of circulating LH levels, and the brains were processed for 'in situ' hybridization. A cDNA probe encoding the rat pituitary GnRH receptor was transcribed 'in vitro' in the presence of (33)P-alpha UTP and used under saturating conditions to label GnRH receptor mRNA. The results show that in the arcuate and ventromedial nuclei GnRH receptor mRNA levels are relatively high during diestrus 1, they decline slightly during diestrus 2 before they rise to the highest levels at 08.00 h of proestrus. By 17.00 h of proestrus, GnRH receptor mRNA levels had declined to the lowest levels of the estrous cycle where they remain through the morning of estrus. The GnRH receptor mRNA levels rise again sharply during the afternoon of estrus. The changes in the hippocampus follow a similar pattern in that a decline in GnRH receptor mRNA levels to its lowest levels occurs between 08.00 and 17.00 h of proestrus. However, the changes in the hippocampus did not reach statistical significance. It is concluded that GnRH receptor mRNA levels in the arcuate and ventromedial nuclei are upregulated in the morning of proestrus, probably by rising estradiol levels, in preparation for the GnRH-LH preovulatory surge while this effect of estradiol is not apparent in the hippocampus.

Animals↗
PubMed1995

Expression of gonadotropin-releasing hormone and gonadotropin-releasing hormone receptor mRNAs in various non-reproductive human tissues.

Recently, cloning of the gonadotropin-releasing hormone (GnRH) receptor from the human breast tumor cell line (MCF-7) and from an ovarian tumor, and its expression in various other human tumors, tumor cell lines and reproductive organs have been reported (Kakar et al., Mol. Cell. Endocrinol., 106 (1994) 145-149). In the present studies, we investigated the expression of GnRH and GnRH receptor mRNAs in normal human non-reproductive tissues. Using reverse transcriptase-polymerase chain reaction (RT-PCR) techniques and specific oligonucleotide primers derived from the placental GnRH cDNA sequence, PCR products of the expected size were obtained from human liver, heart, skeletal muscle, kidney, placenta, and pituitary. The authenticity of the PCR products was confirmed by Southern blot analysis with an internal oligonucleotide primer as probe. Similarly, using specific oligonucleotide primers for the GnRH receptor selected from the human pituitary GnRH receptor cDNA sequence, PCR products of the expected size were amplified from human liver, heart, skeletal muscle, kidney, placenta, and pituitary, and these strongly hybridized with the human GnRH receptor cDNA on Southern blot. Cloning and nucleotide sequencing of the PCR products for the GnRH and GnRH receptor from heart revealed identical sequences when compared to the human placental GnRH and pituitary GnRH receptor cDNAs, respectively. These data demonstrate for the first time the existence of GnRH and GnRH receptor mRNAs in normal human non-reproductive tissues and suggest that GnRH and its receptor may play an important role in the regulation of cellular functions in an autocrine or paracrine manner, in addition to regulating the secretion of gonadotropins from the anterior pituitary.

Base Sequence↗
PubMed1995

Comparative localization of serotonin1A, 1C, and 2 receptor subtype mRNAs in rat brain.

Serotonin (5-HT) mediates its effects on neurons in the central nervous system through a number of different receptor types. To gain better insight as to the localization of 5-HT responsive cells, the distribution of cells expressing mRNAs encoding the three 5-HT receptor subtypes 1A, 1C, and 2 was examined in rat brain with in situ hybridization using cRNA probes. 5-HT1A receptor mRNA labeling was most pronounced in the olfactory bulb, anterior hippocampal rudiment, septum, hippocampus (dentate gyrus and layers CA1-3), entorhinal cortex, interpeduncular nucleus, and medullary raphe nuclei. 5-HT1C receptor mRNA labeling was the most abundant and widespread of the three 5-HT receptor subtypes examined. Hybridization signal was densest in the choroid plexus, anterior olfactory nucleus, olfactory tubercle, piriform cortex, septum, subiculum, entorhinal cortex, claustrum, accumbens nucleus, striatum, lateral amygdala, paratenial and paracentral thalamic nuclei, subthalamic nucleus, substantia nigra, and reticular cell groups. 5-HT2 receptor mRNA was localized to the olfactory bulb, anterior hippocampal rudiment, frontal cortex, piriform cortex, entorhinal cortex, claustrum, pontine nuclei, and cranial nerve motor nuclei including the oculomotor, trigeminal motor, facial, dorsal motor nucleus of the vagus, and hypoglossal nuclei. The distributions of mRNAs for the three different 5-HT receptor subtypes overlap with regions that bind various 5-HT receptor-selective ligands and are present in nearly all areas known to receive serotonergic innervation. The results of this study demonstrate that neurons which express these 5-HT receptor subtypes are very widespread in the central nervous system, yet possess unique distributions within the rat brain. Moreover, previously unreported regions of 5-HT receptor subtype expression were observed, particularly with the 5-HT2 receptor riboprobe in the brainstem. Finally, several brain areas contain multiple 5-HT receptor subtype mRNAs, which leads to the possibility that individual cells may express more than one 5-HT receptor subtype.

Animals↗
PubMed1995

Regulation of hippocampal gonadotropin releasing hormone (GnRH) receptor mRNA and GnRH-stimulated inositol phosphate production by gonadal steroid hormones.

The purpose of the present study was to determine if gonadal steroids can alter the amounts of GnRH receptor mRNA in the pyramidal and granule neurons of the hippocampus of female and male rats and if GnRH causes a change in the production of inositol phosphates in hippocampal slices in vitro. The results show that in the ovariectomized rat the amount of GnRH receptor mRNA is increased to 137% in area CA1 and to 147% in area CA3 and in the dentate gyrus when compared to the ovariectomized, estradiol-progesterone treated animal. Similarly, in the orchidectomized male rat the amount of GnRH receptor mRNA is increased to 155% in area CA1, to 146% in area CA3 and to 145% in the dentate gyrus when compared to the intact male rat. There was no significant difference in the relative amounts of GnRH receptor mRNA when gonadectomized male and female rats were compared. Addition of GnRH (100 pM-1 microM) to hippocampal slices in vitro caused a dose-dependent increase in the production of [3H]inositol phosphate which was abolished by co-administration of a GnRH antagonist. The increase in inositol phosphate production was significantly higher at low doses of GnRH (100 pM-1 nM) in estradiol-progesterone treated female and in intact male rats when compared to gonadectomized rats. The results suggest that the amount of GnRH receptor mRNA in the hippocampus is at least in part regulated by gonadal steroids and that the steroid hormones can sensitize the GnRH target neurons to respond more robustly to a GnRH stimulus.

Animals↗
PubMed1995

GH3 cells transfected with gonadotropin-releasing hormone (GnRH) receptor complementary deoxyribonucleic acid release secretogranin-II through a constitutive pathway after GnRH analog-regulated synthesis: evidence that secretory proteins do not contain a sequence that obligates processing through a secretory granule or by regulated secretion.

GGH3 cells (lactotropic GH3 cells transfected with rat GnRH receptor complementary DNA) respond to GnRH agonists with time- and dose-dependent release of secretogranin-II (SII), a molecule believed to be a marker of the regulated pathway of release and a component of secretory granules. Release requires both protein and RNA synthesis and is also stimulated by analogs of the cyclic nucleotides. Release, as such, appears to be determined by the availability of SII, because this process is constitutive once the molecule is synthesized, and intracellular levels are at the same steady state whether the receptor is occupied by an agonist or an antagonist or is unoccupied. This synthetic requirement is consistent with the lag in time from stimulation to release and the inhibitory actions of either cycloheximide or actinomycin-D on secretion as well as the morphologic observation that storage granules (i.e. secretory granules) are absent in these cells. SII, accordingly, can be released constitutively and does not require processing through the so-called regulated secretory pathway. These observations suggest, in addition, that proteins associated with release through regulated pathways do not have "sorting" domains that preclude release via constitutive routes or require processing through secretory granules.

Animals↗
PubMed1994

Gonadotropin-releasing hormone and its receptors in rat brain.

Since the chemical identification of gonadotropin-releasing hormone (GnRH) in 1971, significant progress has been made in understanding the mechanisms by which GnRH action is mediated in the anterior pituitary. In contrast, relatively little information is available which identifies the intracerebral sites and mechanisms of action of GnRH in the brain. Early immunohistochemical studies of GnRH distribution in the central nervous system, together with behavioral and electrophysiological experiments, suggested that GnRH functioned as a neurotransmitter and was, possibly, involved in the expression of reproductive behaviors. The subsequent identification and characterization of GnRH receptors in the brain further strengthened the view that GnRH caused specific effects in select regions of the brain known to be involved in the neuroendocrine regulation of the anterior pituitary and in the generation of reproductive behaviors. After the mouse pituitary GnRH receptor was cloned it became possible to identify brain neurons which contained the GnRH receptor mRNA. Comparison of the locations of the GnRH peptide, the GnRH receptor protein, and the neurons which contain the GnRH receptor mRNA suggests that the GnRH neuronal system itself can potentially provide a direct link between the neuroendocrine regulation of anterior pituitary function and the intracerebral regulation of reproductive behaviors; furthermore, it is possible that the GnRH neuronal system takes an active part in intracerebral feedback loop systems between the mediobasal hypothalamus and the septum-diagonal band which regulate GnRH release from the median eminence.

Amino Acid Sequence↗
PubMed1994

Neuropeptide-Y neurons projectioning to the medial septum-diagonal band do not have access to fenestrated capillaries in the rat brain.

The aims of this study were to (1) determine the localization of neuropeptide-Y (NPY)-containing perikarya which project to the medial septum-diagonal band (MSDB), a brain region rich in gonadotropin-releasing hormone (GnRH) producing perikarya, and (2) determine if NPY neurons have access to fenestrated capillaries as well. Fluorescent retrograde tracing after microinjection of fluororuby (FR) into the MSDB, and peripheral injection of fluorogold (FG), was used in combination with immunofluorescence for NPY. Injection of FR into the MSDB resulted in retrograde labeling of neurons in the hypothalamic arcuate nucleus (ARC) and brainstem noradrenergic cell groups A1 and A2, as well as other regions. The largest populations of NPY neurons were located in the ventromedial ARC and several of these perikarya contained FR indicating that they project to the MSDB. Defined cell groups in the areas A1 and A2 of the brainstem also contained large numbers of NPY neuron perikarya, and several of these contained FR. In addition, we observed isolated incidences of FR-labeled NPY perikarya in the amygdala and hippocampus. A small population of NPY neurons in the ARC contained FG, indicating that they are in contact with fenestrated capillaries and hence are neuroendocrine cells; however, none of these neurons contained FR. We suggest that NPY neurons in the ARC modulate GnRH function via innervation of the MSDB and LH release via release into fenestrated capillaries of the hypophysial-portal system.

Animals↗
PubMed1994

Functional and morphological characterization of four cell lines derived from GH3 cells stably transfected with gonadotropin-releasing hormone receptor complementary deoxyribonucleic acid.

Four cell lines, stably transfected with rat GnRH receptor complementary DNA, have been prepared from the lactotropic GH3 cell line. All four lines (as well as the parent line and a line transfected with the vector DNA) show extensive rosettes of circular polyribosomes, characteristic of high protein synthetic activity, although secretory granules are virtually absent; the rough endoplasmic reticulum (rER) cisternae were short and straight. Instances were observed in which the ER reaches to the plasma membrane, suggesting a possible nongranular secretory route. All four lines (but not the parent or a control transfected line) expressed GnRH receptors that were down-regulated (1-5 h, depending on the cell line) after exposure to 10 nM GnRH; receptors then recovered (2-7 h). This pattern is reminiscent of the GnRH receptor in the primary gonadotrope cell cultures. All cell lines released PRL (4-96 h) in response to a GnRH agonist (D-tBuSer6-des-Gly10-Pro9-ethylamide-GnRH), an event that was inhibited by all three major classes of Ca+2 ion channel antagonists (methoxyverapamil, 1,4-dihydropyridines, and diltiazem); in contrast, GnRH-stimulated LH release from pituitary-derived primary cultures is only inhibited by methoxyverapamil. One line became refractory to GnRH analog stimulation after 24 h, although the other three released PRL vigorously up to the longest time point examined (96 h). All four lines responded substantially more robustly to 1 microgram/ml Buserelin than to 1 microgram/ml TRH. All four lines produced inositol phosphate metabolites and released immunoassayable cAMP (24 h) in response to treatment with Buserelin. These cell lines are good models for understanding the mechanisms by which the GnRH receptor is coupled to second messenger systems and for comparing these mechanisms with TRH-receptor coupling in the same cell.

Animals↗
PubMed1993

Lack of expression of serotonin receptor subtype -1a, 1c, and -2 mRNAs in gonadotropin-releasing hormone producing neurons of the rat.

Serotonin is one of the neurotransmitters which participates in the regulation of gonadotropin-releasing hormone (GnRH) release from the hypothalamus. In order to test the hypothesis that serotonin acts directly on the GnRH neurons, dual in situ hybridization with 35S-labeled cRNA probes encoding for the serotonin receptor subtypes-1a, -1c, or -2 together with digoxigenin-labeled GnRH cRNA probes was applied to histological sections of the septum-diagonal band and preoptic area. The results of these studies show that many neurons in these brain regions contain the various serotonin receptor mRNAs, however, no cells were detected that contain both GnRH mRNA and serotonin receptor mRNAs. It is therefore suggested that the effects of serotonin on GnRH release are not mediated by direct actions of the neurotransmitter through serotonin-1a, -1c or -2 receptors on GnRH neurons but instead through other, yet unidentified serotonin receptor subtypes or through non-serotoninergic intermediary neurons.

Animals↗
PubMed1993

Gonadotropin-releasing hormone agonist binding in tiger salamander nasal cavity.

Binding of the iodinated gonadotropin-releasing hormone (GnRH) agonist, buserelin, was examined in the nasal cavities of tiger salamanders using in vitro autoradiography. Binding of [125I]buserelin was seen within the chemosensory epithelium of the main nasal cavity and Jacobson's (vomeronasal) organ. Highest levels of binding were observed over the chemosensory neuron dendrites. Given the apparent lack of GnRH-immunoreactive fibers within the chemosensory epithelium as we have observed in a previous study, these observations suggest that GnRH may diffuse from fibers in the lamina propria of the chemosensory mucosa into the sensory epithelium to modulate chemosensory reception.

Ambystoma↗