Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20366 (substance P)
 21,176 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An immunocytochemical analysis with 33 antisera was undertaken to investigate the localization of 25 different neurotransmitter-related antigens in the hypothalamic suprachiasmatic nucleus in the rat. To obtain estimates of relative densities of immunoreactive axons a stereological approach was used involving counting of intersections of immunoreactive axons with a superimposed semi-circle test grid. All neurotransmitter-related antigens found in perikarya within the suprachiasmatic nucleus, including those stained with antisera against bombesin, gastrin-releasing peptide, neurophysin, vasopressin, somatostatin, gamma-aminobutyrate, glutamate decarboxylase and vasoactive intestinal polypeptide were also found in axons within the nucleus. A greater number of these immunoreactive axons was found within the nucleus than in the adjacent anterior hypothalamus. The size of all immunoreactive axons in the suprachiasmatic nucleus was consistently small; immunoreactive axons were found ramifying widely in the nucleus, often ending with terminal boutons near perikarya immunoreactive for the same antigen. All neurotransmitter-related substances found in perikarya of the suprachiasmatic nucleus were also found in axons crossing over the midline to innervate the contralateral nucleus, providing an anatomical substrate for a high degree of communication between the paired nuclei. Axons immunoreactive for other putative transmitters including serotonin arising outside the nucleus were also found in high densities within the nucleus and crossing over the midline between the nuclei. Immunoreactivity for some transmitters was found in axons of similar densities within and outside the nucleus, including antisera against tyrosine hydroxylase; a small number of dopamine beta-hydroxylase and a few phenylethanolamine N-methyltransferase-immunoreactive axons were found in the SCN, suggesting that dopamine, norepinephrine and epinephrine may occur in a limited number of axons in the nucleus. Small numbers of axons immunoreactive with antisera raised against cholecystokinin, prolactin, substance P, thyrotropin-releasing hormone and choline acetyltransferase were found within the suprachiasmatic nucleus. Axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, alpha-melanocyte-stimulating hormone and neurotensin were rarely found within the suprachiasmatic nucleus; axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, cholecystokinin and tyrosine hydroxylase were found in both horizontal and coronal sections in the area between the left and right suprachiasmatic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitters of the hypothalamic suprachiasmatic nucleus: immunocytochemical analysis of 25 neuronal antigens. 241 88

In this article I have examined various aspects of the complex spatio-temporal patterning of peptidergic signaling that lead to synchronized development of neural events for the preovulatory LHRH discharge on proestrus. Undoubtedly, the integration of these events is orchestrated by both ovarian steroids, E2 and P. Evidence accumulated in recent years has failed to affirm the perceived notion that E2 is an adequate peripheral signal for the timely, robust discharge of LHRH on proestrus. The current understanding is shaped by the thesis that the concerted central actions of E2 and P are mediated by a host of regulatory peptides produced locally in the hypothalamus, and steroids, in general, augment the production and release of both inhibitory and excitatory peptides in a timely fashion to facilitate the preovulatory LHRH discharge. Since these peptidergic pathways appear mandatory for signal transfer, considerable recent research has been devoted first to identifying the signals that selectively participate in the induction of preovulatory LHRH (LH) surge, and then to trace the route of signal transmission that ultimately leads to LHRH hypersecretion on the afternoon of proestrus (Fig. 1). The peptidergic pathways that propagate and transmit impulses for the preovulatory LHRH discharge reside in the SCN-MPN-MPOA-ARC-ME neural complex (Fig. 1). The timely initiation of these impulses is entrained to the photo-periodic input reaching the SCN by the retino-hypothalamic tract. The evidence is already in place to show that further information processing is transduced in the MPN; however, the nature of neurochemical signaling between the two sites remains to be deciphered. The available evidence favors a mandatory participation of inhibitory (EOP and NPK) and excitatory (NPY, GAL, NT, and AII) messenger molecules within the SCN-MPN-MPOA-ARC-ME complex (Fig. 1). It is possible that the relevant information from the SCN-MPN is conveyed caudally to the ARC in order to initiate a chain of events for disinhibition/excitation of the NPY-EOP network and to affect LHRH neurosecretion at the perikaryal level in the MPOA and at axon terminals in the ME. Also, either concurrently or on a time-delayed basis, the relevant information from the MPN may be relayed to the MPOA via the local peptidergic network comprised of NT, EOP, NPK, and GAL. This transmission may initially be critical for elicitation of antecedent neurosecretory events in the ME and to ultimately evoke the preovulatory LHRH surge.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mandatory neuropeptide-steroid signaling for the preovulatory luteinizing hormone-releasing hormone discharge. 826 4

Substance P (SP) is a neuromodulator which may participate in the photic regulation of the circadian timing system in mammals. The biological effects of SP are mediated by interaction with specific receptors, designated as NK1, NK2, and NK3. The NK1 subtype receptor is expressed in the circadian system. Experiment 1 was designed to test whether an NK1 antagonist mimics the effects of dark pulses. Hamsters were housed in constant lighting conditions, either constant darkness or constant light (around 250 lx), and they received an i.p. injection of either the specific NK1 receptor antagonist, L-760,735 (5 mg/kg), or saline during the mid-subjective day, a time when dark pulses cause a phase-advance in circadian rhythm of locomotor activity. After treatment with the NK1 antagonist, significant phase-advances of wheel-running activity rhythm were found in constant light, but not in constant darkness. Experiment 2 was designed to test the ability of the NK1 antagonist to block the phase-delaying and/or the phase-advancing effects of light in animals kept in constant darkness. Phase-advances of locomotor activity rhythm that can normally be induced by light pulses given during the late subjective night were markedly reduced by pre-treatment with the NK1 antagonist. By contrast, phase-delays that can be induced by lights pulses given during the early subjective night were unaffected by the NK1 antagonist. These data support the hypothesis that SP within the circadian system may, by interacting with NK1 receptors, modulate photic responses of the SCN pacemaker.
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PMID:An NK1 receptor antagonist affects the circadian regulation of locomotor activity in golden hamsters. 968 77