Localization and function of NK3 subtype tachykinin receptors of layer V pyramidal neurons of the guinea-pig medial prefrontal cortex

Simmons, Mark A.; Sobotka-Briner, Cynthia D.; Medd, Amy

doi:10.1016/j.neuroscience.2008.08.037

Cited by 6 publications

(2 citation statements)

References 21 publications

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“…In the first experiments, we determined whether these antagonists at concentrations known to inhibit NKR3 (37,38) blocked the stimulatory actions of the NK3R agonist Senktide on kisspeptin neurons. Both SR142801 (1 M; n ϭ 5; 5 mice) and SB222200 (3 M; n ϭ 7; 6 mice) completely blocked the effects of Senktide on kisspeptin neurons as evidenced by an A2/A1 ratio of 0.03 Ϯ 0.01 and 0.09 Ϯ 0.05, respectively (Figure 3, E-G; P Ͻ .001; Kruskal-Wallis test).…”

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confidence: 99%

Neurokinin B Activates Arcuate Kisspeptin Neurons Through Multiple Tachykinin Receptors in the Male Mouse

2013

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Kisspeptin neurons located in the arcuate nucleus (ARN) coexpress dynorphin and neurokinin B (NKB) and may interact to influence gonadotropin secretion. Using a kisspeptin-green fluorescent protein mouse model, the present study examined whether the neuropeptides kisspeptin, dynorphin, and NKB modulate the electrical activity of ARN kisspeptin neurons in the adult male mouse. Cell-attached recordings showed that kisspeptin itself had no effect on kisspeptin neuron firing. Dynorphin and the -opioid receptor agonist U50-488 evoked a potent suppression of all ARN kisspeptin neuron firing that was blocked completely by the -opioid receptor antagonist norBinaltorphimine. Both NKB and Senktide, a neurokinin 3 receptor agonist, exerted a potent stimulatory action on ϳ95% of ARN kisspeptin neurons. Although the selective neurokinin 3 receptor antagonists SB222200 and SR142801 blocked the effects of Senktide on kisspeptin neurons, they surprisingly had no effect on NKB activation of firing. Studies with selective neurokinin 1 receptor (SDZ-NKT343) and neurokinin 2 receptor (GR94800) antagonists revealed that the activation of kisspeptin neurons by NKB was only blocked completely by a cocktail of antagonists against all 3 tachykinin receptors. Whole-cell recordings revealed that individual kisspeptin neurons were activated directly by all 3 tachykinins substance, P, neurokinin A, and NKB. These experiments show that dynorphin and NKB have opposing actions on the electrical activity of kisspeptin neurons supporting the existence of an interconnected network of kisspeptin neurons in the ARN. However, the effects of NKB result from an unexpected activation of multiple tachykinin receptors. (Endocrinology 154: 2750 -2760, 2013)

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Neurokinin B Activates Arcuate Kisspeptin Neurons Through Multiple Tachykinin Receptors in the Male Mouse

2013

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“…Neurokinin B (NKB) is a member of the tachykinin family which includes substance P, neurokinin A, and neuropeptide K. It has been shown to have modulatory functions in several regions of the brain, including excitatory roles in synaptic transmission in pyramidal neurons of the medial prefrontal cortex (Simmons et al, 2008). NKB binds to its G protein-coupled receptor, NK3R, and activates various signaling cascades including IP and PKC signaling pathways (Khawaja and Rogers, 1996).…”

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confidence: 99%

G protein-coupled receptors involved in GnRH regulation: Molecular insights from human disease

Noel

Kaiser

2011

Molecular and Cellular Endocrinology

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In the past two decades, an increasing body of evidence has demonstrated that several G protein-coupled receptor (GPCR)-ligand pairs are critical for normal human reproductive development and function. Patients harboring genetic insults in either the receptors or their cognate ligands have presented with reproductive disorders characterized by varying degrees of GnRH deficiency. These disorders include idiopathic hypogonadotropic hypogonadism (IHH) and Kallmann Syndrome (KS). Conversely, mutations in some of these ligand-receptor pairs have been associated with accelerated reproductive maturation, manifested as central precocious puberty (CPP). To date, a series of elegant studies have characterized four GPCRs that play important roles in the neuroendocrine control of human reproductive development and function: GnRHR, KISS1R, PROKR2 and NK3R. Furthermore, these studies provide insights into the mechanisms by which mutations in these receptors give rise to reproductive disease phenotypes. This report will review mutations identified in GPCRs involved in the neuroendocrine control of the human reproductive axis with the aims of elucidating structure-function relationships of these GPCRs and identifying correlations between these structure-function relationships and the genotypic-phenotypic characterization of the patients.

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Will Modulation of Neuropeptide Receptors Produce the Next Generation of Antipsychotic Drugs? A Focus on the Neurokinin and Neurotensin Systems

Dawson

Smith

Watson

2012

Targets and Emerging Therapies for Schizophrenia

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Localization and function of NK3 subtype tachykinin receptors of layer V pyramidal neurons of the guinea-pig medial prefrontal cortex

Cited by 6 publications

References 21 publications

Neurokinin B Activates Arcuate Kisspeptin Neurons Through Multiple Tachykinin Receptors in the Male Mouse

Neurokinin B Activates Arcuate Kisspeptin Neurons Through Multiple Tachykinin Receptors in the Male Mouse

G protein-coupled receptors involved in GnRH regulation: Molecular insights from human disease

Will Modulation of Neuropeptide Receptors Produce the Next Generation of Antipsychotic Drugs? A Focus on the Neurokinin and Neurotensin Systems

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