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)

The present study investigates the effect of the mammalian tachykinin neurokinin A on salt intake in the rat. Intracerebroventricular injection of neurokinin A inhibited salt intake elicited by sodium depletion, by subchronic deoxycorticosterone treatment and by adrenalectomy. It also inhibited the need-free salt intake of female rats that had been previously depleted of sodium. Since different brain mechanisms elicit salt intake in these experimental models, it is concluded that neurokinin A exerts a general antinatriorexic effect. Apparently, its inhibitory effect on salt intake is not due to malaise or competing behaviors, as shown by the fact that the doses of neurokinin A which suppress salt intake do not suppress milk intake. In comparison to the amphibian tachykinin kassinin, neurokinin A possesses a similar spectrum of antinatriorexic activities, but is markedly less potent and less effective in all the experimental models investigated. These findings suggest that activation of neurokinin A receptors cannot solely account for the potent antinatriorexic effect of kassinin and of other nonmammalian tachykinins.
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PMID:Suppression of salt intake in the rat by neurokinin A: comparison with the effect of kassinin. 254 May 11

A patient with solar urticaria induced by wavelengths 290-420 nm is reported. Wheals appeared after a few seconds of exposure to the sun; longer exposure caused general malaise and syncope. Intradermal injection of in vitro irradiated plasma caused a local whealing which was not seen with plasma kept dark. The wheals induced by irradiation could be inhibited by local injection of an antihistamine. Local injection of lidocaine and hydrocortisone was ineffective. Depletion of substance P in the skin by topical application of capsaicin did not change the sensitivity to irradiation with 313 nm and a single PUVA treatment did not change the minimal urticarial dose (MUD). Sunscreens were in practice of limited value with the exception of a protective plastic helmet. Repeated daily irradiation with UVA in increasing doses normalized his response to sunlight.
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PMID:Solar urticaria: mechanism and treatment. 374 56

Using combined immuno-staining and retrograde tracing techniques many of the ascending visceral and taste pathways within the rat central nervous system have been shown to be composed of a variety of neuropeptide and catecholamine synthesizing enzyme containing neurones. The pathway we examined extended from the periphery to sensory cortex and included: the nodose ganglion (periphery)----solitary nucleus (medulla)----parabrachial nucleus (pons)----ventral posterior medial nucleus (thalamus)----visceral and taste sensory areas (cortex). In the solitary nucleus of the medulla many neuronal cell bodies could be shown to be both immuno-positive for one of 6 neuropeptides including avian pancreatic peptide (APP), cholecystokinin (CCK), enkephalin (ENK), neurotensin (NT), somatostatin (SOM) and substance P (SP) or the catecholamine synthesizing enzyme tyrosine hydroxylase (TOH) and to have a projection to the parabrachial nucleus of the pons. In the parabrachial nucleus of the pons many neuronal cell bodies could be shown to be immuno-positive for one of 5 neuropeptides (CCK, ENK, NT, SOM, SP) and have a projection to the ventral posterior medial nucleus of the thalamus. In the ventral posterior medial nucleus of the thalamus several neuronal cell bodies were shown to be immuno-positive for one of 3 neuropeptides (CCK, ENK, SOM) and project to the visceral and taste sensory cortex. This is the first report of neuropeptides being present in the projection neurones of any sensory system in the central nervous system and for the first time describes an entire set of putative neurotransmitters which extends from the periphery to the sensory cortex. From previous studies it also appears that in all cases examined the relevant receptors are present in these visceral and taste relay nuclei in order for the neuropeptide or catecholamine to produce an effect upon release. Comparisons between rat and other animals suggest that a similar organization of these visceral and taste pathways may also be present in other mammals including man. Functionally these neuropeptides containing projection neurones appear to be primarily involved in relaying visceral information rather than taste information. In this capacity activation of these neurones may produce such visceral sensations as malaise, well being, hunger, satiety or thirst.
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PMID:Neuropeptides are present in projection neurones at all levels in visceral and taste pathways: from periphery to sensory cortex. 673 52

Central injections of the selective tachykinin NK3 receptor agonist senktide (SENK) suppresses salt appetite. Also, following SENK, intraoral infusions of hypertonic NaCl elicit fewer ingestive taste reactivity responses and more aversive responses than following intraventricular injections of isotonic saline. This pattern of taste reactivity results suggest that SENK affects the oral stimulating properties of salt taste. Before accepting this interpretation, however, alternative explanations need to be examined. The following experiments evaluated whether the effects of intraventricular SENK injection on taste reactivity could be due to: 1) a general oral motor impairment that reduces ingestive responding to tastes (Experiment 1) or; 2) SENK having aversive consequences (Experiment 2). In Experiment 1, the effects of intraventricular injections of SENK (200 ng) on taste reactivity responses to 0.5 M NaCl and 0.1 M sucrose were measured in sodium deficient rats. Intraoral infusions of 0.5 M NaCl elicited fewer ingestive taste reactivity responses following SENK than injections of isotonic saline in sodium deficient rats. Sucrose continued to elicit the same high number of ingestive taste reactivity responses following intraventricular injections of isotonic saline and SENK. Thus, SENK did not cause a general decrease in ingestive responding. A conditioned taste aversion test was employed in Experiment 2 to determine if SENK had aversive consequences. Rats were given 30 min access to alanine (0.3 M) and were then administered either lithium chloride (LiCl) or intraventricular injections of SENK (200 ng) on three consecutive days. Rats avoided alanine that was paired with LiCl, but those rats that had alanine paired with SENK showed no avoidance of the taste even after three pairings. These results replicate findings that intraventricular injections of the NK3 agonist SENK decreases the palatability of NaCl (as measured by taste reactivity) and suggest that its effect on NaCl-elicited taste reactivity is not due to the treatment causing a motor impairment or malaise.
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PMID:Lateral ventricular injections of the NK3 agonist senktide affect salt taste-elicited responses. 949 64

The purpose of the present study was to determine whether central administration of substance P (SP), a tachykinin neuropeptide, influenced feeding behavior in layer chicks (Gallus gallus). Intracerebroventricular (ICV) injections of 5 nmol SP decreased food intake in 5- and 6-day-old chicks under both ad libitum and 3-h fasting conditions. There are 3 major subtypes of tachykinin receptors, namely, neurokinin 1, 2 and 3 receptors. Injection of neurokinin A and neurokinin B, which are respectively endogenous agonists for neurokinin 2 and 3 receptors, did not suppress feeding behavior in chicks, suggesting that the anorexigenic effect of SP might be mediated by the neurokinin 1 receptor rather than neurokinin 2 and 3 receptors. Chicks that received 5 nmol SP did not change their locomotion, standing, sitting or drinking time, suggesting that its anorexigenic action might not be due to SP-induced hyperactivity or sedation. ICV injection of SP increased water intake, also indicating that SP likely did not affect feeding behavior through malaise. In addition, the anorexigenic effect of SP might not be related to corticotrophin-releasing hormone (CRH) because plasma corticosterone concentration was not affected by ICV injection of SP and co-administration of the CRH receptor antagonist astressin did not affect the anorexigenic effect of SP. The present study suggests that central SP acts as an anorexigenic neuropeptide in chicks.
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PMID:Central administration of substance P inhibits feeding behavior in chicks. 1990 53