Disease relevance of Neurokinin beta

• Excessive placental secretion of neurokinin B during the third trimester causes pre-eclampsia [1].
• Hypertrophy and increased gene expression of neurons containing neurokinin-B and substance-P messenger ribonucleic acids in the hypothalami of postmenopausal women [2].
• Somatostatin-, neuropeptide Y-, neurokinin B- and cholecystokinin-containing neurons were investigated in the rat hippocampus in two chronic models of temporal lobe epilepsy, i.e. 30 days after rapid kindling or electrically induced status epilepticus (post-status epilepticus) [3].
• These results suggest that activation of spinal NK1R and NK2R, presumably by their endogenous ligands (substance P and neurokinin A), maintain visceral hyperalgesia and support the notion that activation of NK3R (presumably by neurokinin B) is pronociceptive [4].
• Finally, the ID co-injection of the NK, receptor antagonist SR 142801 significantly inhibited (53%, 76%, 53%, and 100%, respectively) the edema formation caused by NKB and NKA or by SP and senktide [5].

Psychiatry related information on Neurokinin beta

• Substance P, neurokinin A, neuropeptide K, and neurokinin B were measured in both control (neurologically normal) and Huntington's disease brains obtained post mortem [6].
• We investigated and compared the effects of two amphibian tachykinins, the NK1 receptor agonist PG-SPI and the NK3 receptor agonist PG-KII, and the mammalian tachykinins substance P, neurokinin A and neurokinin B on the reaction time to a painful radiant heat stimulus (tail-flick test in rats) after intracerebroventricular injection [7].
• Neurokinin B (NKB), a decapeptide of mammalian origin exhibits a variety of biological activities such as regulatory functions in reproduction, pre-eclampsia and neuroprotection in Alzheimer's disease [8].
• Effects of water deprivation on neurokinin B production by the arginine-vasopressin neurons of hypothalamic paraventricular and supraoptic nuclei [9].

High impact information on Neurokinin beta

• Here we have cloned a complementary DNA from human placental messenger RNA encoding a precursor protein of 121 amino acids which gives rise to a mature peptide identical to the neuropeptide neurokinin B (NKB) of other mammalian species [1].
• Here we identify epitopes on the NK1 receptor responsible for the specific binding of CP 96345 by systematic exchange of corresponding segments between the NK1 receptor and the homologous NK3 (neurokinin B) receptor, which does not bind the non-peptide ligand [10].
• Close intraarterial infusions of NKA, neurokinin B, SP, NPK, eledoisin, and physalaemin at doses of 0.1-100 pmol/min induced dose-dependent contractions of the proximal and distal colon (P less than 0.001) and vasodilatation (P less than 0.001), NKA being the most potent [11].
• Tachykinin 4 gene expression was detected primarily in adrenal gland and in the placenta, where, like neurokinin B, significant amounts of EKB-like immunoreactivity were detected [12].
• This cell line also bound [125I-MePhe7]neurokinin B; however, neurokinin B was an effective competitor [13].

Chemical compound and disease context of Neurokinin beta

• We have observed alterations in hypothalamic morphology and gene expression in older women, including hypertrophy and increased gene expression of neurokinin B (NKB) neurones, elevated levels of gonadotropin releasing-hormone (GnRH) mRNA and decreased numbers of neurones expressing pro-opiomelanocortin (POMC) mRNA [14].
• Marked changes in the expression of the tachykinin peptide neurokinin B (NKB) have been recently observed in animal models of epilepsy [15].

Biological context of Neurokinin beta

• Climacteric flushes may be caused by hyperactivity of the neurokinin-B or LHRH neurons in this nucleus [16].
• Scatchard analysis showed the presence of high-affinity binding sites, and binding competition assays using SP, neurokinin A, or neurokinin B indicated that the high-affinity 125I-SP binding sites on these neurons were type NK1 tachykinin receptors, or SP receptors (SPRs) [17].
• Neurokinin B is a paracrine vasodilator in the human fetal placental circulation [18].
• Menopause is associated with increased neurokinin B (NKB) gene expression and decreased proopiomelanocortin (POMC) gene expression in the human hypothalamus [19].
• This amino acid sequence is the same as that of mammalian neurokinin B [20].

Anatomical context of Neurokinin beta

• Interestingly, in contrast to neurokinin B, [Cys3,6]SP is a weak agonist of the neurokinin 2 receptor subtype, as evidenced by its binding potency in inhibiting 3H-labeled neurokinin A-specific binding on rat duodenum and in inducing the contractions of the rabbit pulmonary artery, a neurokinin 2-type bioassay [21].
• Moreover, [Cys3,6]SP is as potent as neurokinin B in inhibiting 125I-labeled Bolton and Hunter eledoisin-specific binding on rat cortical synaptosomes as well as in stimulating rat portal vein, two tests specific for the neurokinin 3 receptor [21].
• In addition, interactions between SP and other growth factors and neuropeptides including insulin, platelet factors, neurokinin A, neurokinin B, and calcitonin gene-related peptide (CGRP) were studied on endothelial cell growth and compared [22].
• The tachykinin NKB has antinociceptive effects in the spinal cord and is contained in intrinsic spinal neurons; thus, NKB may also contribute to the processing of sensory information [23].
• Neurokinin-B transcription in erythroid cells: direct activation by the hematopoietic transcription factor GATA-1 [24].

Associations of Neurokinin beta with other chemical compounds

• These results provide strong support for the hypothesis that the increased NKB gene expression in the hypothalamus of postmenopausal women is secondary to estrogen withdrawal [19].
• 2. Perfusion of tracheal mucosa with neurokinin A (NKA) or substance P (SP) dose dependently increased PD in the presence of amiloride, with the potency being NKA > SP, but neurokinin B (NKB) had no effect [25].
• The biologically active tachykinins, which, in addition to SP, consist of physalaemin, eledoisin, kassinin, neurokinin-A, and neurokinin-B, could inhibit the binding in a concentration-dependent manner [26].
• 1H nuclear magnetic resonance determination of the membrane-bound conformation of senktide, a highly selective neurokinin B agonist [27].
• Ranakinin: a novel NK1 tachykinin receptor agonist isolated with neurokinin B from the brain of the frog Rana ridibunda [20].

Gene context of Neurokinin beta

• Neurokinin B induces oedema formation in mouse lung via tachykinin receptor-independent mechanisms [28].
• Estrogen regulation of neurokinin B gene expression in the mouse arcuate nucleus is mediated by estrogen receptor alpha [29].
• The data show that the mRNAs of tachykinins (particularly NKB and HK-1), tachykinin receptors, and NEP are locally expressed in the mouse uterus, and their expression changes during the estrous cycle and during pregnancy [30].
• A reverse transcription-polymerase chain reaction (RT-PCR) assay was used to analyse the expression of TAC1 and TAC3, the genes that encode substance P/neurokinin A and neurokinin B, respectively, and the genes encoding the tachykinin NK(1), NK(2) and NK(3) receptors in different human tissues [31].
• The tachykinin neurokinin B (NKB) has been implicated in the hypertension that characterises pre-eclampsia, a condition where tissue oedema is also observed [28].

Analytical, diagnostic and therapeutic context of Neurokinin beta

• Because the antiserum K-12 recognizes various tachykinins, such as neurokinin A (100%), kassinin (103%), eledoisin (51%), neurokinin B (18%), physalaemin (0.7%), and substance P (0.7%), the immunoreactivity detected in this enzyme immunoassay has been termed TK-LI [32].
• Using an antiserum raised against a 30-residue peptide fragment (Peptide 2) of the protein precursor to neurokinin B, we have mapped the distribution of Peptide 2 by immunocytochemistry [33].
• These results have permitted the design of specific probes to differentiate between substance P and neurokinin B transcripts by using in situ hybridization histochemistry [34].
• Further analysis by high pressure liquid chromatography revealed that increases in both neurokinin A and neurokinin B concentrations contributed to the increases in total neurokinin immunoreactivity 30 days after kainic acid [35].
• Peptide 2 antiserum specificity was determined by western blot analysis (which showed antibody cross-reactivity to a neurokinin B fusion protein from a cloned neurokinin B-encoding complementary DNA) and by the elimination of immunoreactive product in brain tissue sections upon preabsorption with a 10 microM concentration of Peptide 2 peptide [33].

References