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)

Adult male mice of albino Swiss-derived CD-1 strain were used to assess the effects of capsaicin (a powerful agent that produces a marked depletion of the undecapeptide substance P) on both intraspecific aggressive behavior (induced by 8 weeks of individual housing) and pain sensitivity. Capsaicin was given SC, 48 h before behavioral testing. Aggressive behavior, scored during a 5-min session under red light, was significantly enhanced by capsaicin treatment (50 or 100 microliters of a 7.5 mg/ml solution). In fact, Total Aggressive Episodes, Attacks, and Upright Offensive Posture were significantly higher in the two capsaicin-treated groups, while Latency to the first Attack was decreased, when compared to both vehicle or unhandled controls. A concomitant decrease in Submissive Postures and Flee was also evident in capsaicin mice. Hot plate testing (55 +/- 0.1 degrees C, cutoff time 30 s), carried out on nonisolated mice, did not reveal any difference among the two capsaicin groups (same doses) and vehicle or unhandled controls.
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PMID:Capsaicin affects aggressive behavior, but not hot plate responding, of adult male mice. 188 75

Peptides with hormonal or neuronal activity are derived by enzymatic processing from pro-hormones, which by themselves are biologically inert. Processing and other enzymatic conversions may occur step-wise, leading to the formation of a cascade of biologically active (or inactive) peptides. The neurokin in substance P is known to be metabolically transformed both by amino- and endopeptidases. More N-terminal substance (1-7) has been found than C-terminal (2-11 to 5-11) fragments in various CNS areas. The substance P (1-7) fragment also shows biological activity e.g., providing analgesia, lowering blood pressure, inhibiting aggressive behavior and (in contrast to substance P) inhibiting grooming behavior. An endopeptidase generating substance P (1-7) and to a lesser extent, substance (1-8), has been isolated and characterized from human cerebrospinal fluid (CSF) and bovine spinal cord, as a metalloenzyme with essential SH-groups. Substance P co-exists with calcitonin gene related peptide (CGRP) in a large population of non-myelinated primary afferent ('pain') fibers. Intrathecal injection of substance P causes behavioral and physiological responses which are potentiated and prolonged by CGRP. It was found that CGRP competes with substance P for the endopeptidase. It is suggested that the main action of CGRP in the spinal cord is to inhibit substance P degradation.
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PMID:Modulation of endopeptidase activity by calcitonin gene related peptide: a mechanism affecting substance P action? 245 90

Administration of 10 and 30 micrograms methionine-enkephalin (MET-ENK)/g bw (n = 10/dose) affected the propensity towards fighting in H. bimaculatus; 10 micrograms increased, while 30 micrograms decreased the aggressive behavior. MET-ENK also affected a number of behavior patterns displayed by the fish. Moreover, the "wet-dog-shakes" observed suggest that MET-ENK acts on opiate-receptors. Treatment with substance P (SP)/g bw (n = 10/dose) induced chafing movements in the fish slightly. It also decreased fighting and increased biting of the air stone, which is evidence that H. bimaculatus is still aggressive, directing its attacks to different objects. When 4, 8, 12 micrograms somatostatin (SRIF)/g bw (n = 10/dose) were injected, H. bimaculatus stopped fighting for several hours after the onset of treatment, depending on the dosage. Somatostatin reduces blood glucose concentration, causing a sudden stop of aggressive behavior, 0.04, 0.1, 0.6, 1.0 and 3.0 IU prolactin (PRL)/g bw (n = 5/dose) eventually decreased fighting and affected a number of behavior patterns displayed by the fish.
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PMID:Effects of MET-ENK, substance P and SRIF on the behavior of Hemichromis bimaculatus. 258 Dec 33

Substance P (SP) significantly reduced fighting in mice made aggressive by prolonged isolation. The N-terminal heptapeptide fragment SP (1-7) also reduced fighting. The C-terminal fragment SP(4-11) was without activity, while the shorter C-terminal fragment analog less than E-SP(7-11) significantly increased isolation-induced fighting. The aggression-enhancing effect of less than E-SP(7-11) was antagonized by naloxone, which by itself had no significant effect. The aggression-reducing effect of SP(1-11) was significantly enhanced by naloxone, while the effect of SP(1-7) was unchanged. These results demonstrate that a behavioral effect of SP may be duplicated by an N-terminal fragment of the SP molecule, and that peptide fragments or analogs of the N- and C-terminal portions of the SP molecule can exert opposing effects on a specific behavior. These findings represent a structure/activity relationship that is strikingly different from any previously described for SP. The differing effects of naloxone on N- and C-terminal fragment analogs suggest that these two effects may be mediated by different mechanisms.
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PMID:Modulation of isolation-induced fighting by N- and C-terminal analogs of substance P: evidence for multiple recognition sites. 620 Aug 67

The present study was designed to test the hypothesis that a major excitatory mechanism for the expression of feline defensive rage behavior involves the medial nucleus of the amygdala which utilizes substance P as a neurotransmitter in a direct output pathway that supplies the medial hypothalamus. In phase I of the experiment, stimulating electrodes were implanted into the medial amygdala and cannula electrodes were implanted into the medial and lateral hypothalamus from which defensive rage and predatory attack behavior could be elicited by electrical stimulation, respectively. Response latencies for defensive rage were significantly lowered after dual stimulation of the medial amygdala and medial hypothalamus relative to single stimulation of the medial hypothalamus alone. In phase II, dose- and time-dependent decreases in medial amygdaloid-induced facilitation of defensive rage were observed after the i.p. administration of the NK1 antagonist, CP-96,345 (0.05, 2 and 4 mg/kg). In phase III of the study, the effects of microinjections of CP-96,345 placed directly into defensive rage sites within the medial hypothalamus (0.05, 0.5 and 2.5 nmol) upon medial amygdaloid modulation of this response were assessed. Again, intracerebral administration of this antagonist blocked the facilitatory effects of medial amygdaloid-induced facilitation of defensive rage in a manner parallel to that observed with peripheral administration of the NK1 antagonist. The results suggest that the medial amygdala facilitates defensive rage by acting through a substance P mechanism at the level of the medial hypothalamus. Other experiments revealed that peripheral administration of the NK1 antagonist: (1) had little upon the latency or threshold for elicitation of defensive rage, suggesting that the medial amygdaloid-substance P facilitatory mechanism acts in a phasic rather than tonic manner; and (2) also blocks the suppressive effects of medial amygdaloid stimulation upon predatory attack behavior elicited from the lateral hypothalamus. The latter finding suggest that similar neurochemical mechanisms regulate medial amygdaloid modulation of both forms of hypothalamically elicited aggression. The final aspect of this study utilized the combination of retrograde-tracing of amygdaloid neurons into the medial hypothalamus after microinjections of Fluoro-Gold into defensive rage sites, and the immunocytochemical analysis of substance P neurons within the amygdala. The data indicated that large numbers of retrogradely and immunocytochemically positive labeled cells were identified in the medial nucleus, including many that were double-labeled.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Evidence that substance P is utilized in medial amygdaloid facilitation of defensive rage behavior in the cat. 750 10

Many neurons within the ventrolateral hypothalamus in guinea pigs contain estrogen-induced progestin receptors as well as substance P. Retrograde tracing combined with immunocytochemistry was used to determine the specific projections of this subset of steroid-sensitive cells. Unilateral Fluoro-Gold injections into the dorsal midbrain, including the central gray, labeled a large proportion of the ventrolateral hypothalamic neurons immunoreactive for both progestin receptors and substance P (approximately 30%); substantially fewer of these neurons were labeled by unilateral Fluoro-Gold injections into the preoptic area (approximately 6%), medial amygdala (approximately 10%), or the bed nucleus of the stria terminalis (approximately 11%). The projections of progestin receptor-immunoreactive neurons in the ventrolateral hypothalamus were similar to those of progestin receptor/substance P double-labeled neurons, while a slightly lower percentage of the ventrolateral hypothalamic, substance P-immunoreactive neurons tended to project to each of these areas. These pathways may prove to be components of the neural circuitry underlying a variety of functions influenced by gonadal steroid hormones and substance P, such as female sexual behavior, salt intake, nociception and aggression.
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PMID:Projections from ventrolateral hypothalamic neurons containing progestin receptor- and substance P-immunoreactivity to specific forebrain and midbrain areas in female guinea pigs. 751 13

The experiments described in this review reveal that the expression and modulation of aggressive responses in the cat are organized by two distinct sets of pathways. One set of pathways is associated with the elicitation of a specific form of attack behavior. It includes the medial hypothalamus and its projections to the PAG for the expression of defensive rage behavior and the lateral hypothalamus and its descending projections for the expression of predatory attack behavior. The primary focus of the present review is upon the analysis of defensive rage behavior. It was demonstrated that the pathway from the medial hypothalamus to the PAG, which appears to be essential for elicitation of defensive rage, is powerfully excitatory and utilizes excitatory amino acids that act upon NMDA receptors within the PAG. The other pathways examined in this review arise from different nuclei of the amygdala and are modulatory in nature. Here, two facilitatory systems have been identified. The first involves a projection system from the basal complex of amygdala that projects directly to the PAG. Its excitatory effects are manifest through excitatory amino acids that act upon NMDA receptors within the PAG. The second facilitatory pathway arises from the medial nucleus of the amygdala. However, its projection system is directed to the medial hypothalamus rather than the PAG. Its neurotransmitter appears to be substance P that acts upon NK1 receptors within the medial hypothalamus (see Figure 10). It has yet to be determined whether substance P acts upon any of the other neurokinin receptor subtypes. It should also be pointed out that the substance P pathway from the medial amygdala to the medial hypothalamus functions to suppress predatory attack behavior elicited from the lateral hypothalamus. In this network, it is likely that the modulatory effects of the medial amygdala require the presence of a second, inhibitory pathway from the medial hypothalamus that innervates the lateral hypothalamus. At the present time, the neurochemical nature of this second pathway remains unknown, although it is suggested that such neurons may be GABAergic. One major inhibitory pathway was also identified. It arises principally from the central nucleus of the amygdala and projects to the PAG. Its powerful suppressive effects upon PAG elicited defensive rage behavior are mediated through opioid peptides that act upon mu receptors within the PAG. While the present series of studies have begun to define the structural and functional nature of the neural systems that regulate aggressive behavior, our understanding of the overall mechanisms regulating different forms of aggressive behavior remains incomplete.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitters regulating feline aggressive behavior. 763 40

Subcutaneous administration of capsaicin (50 mg/kg) at Postnatal Days 2 and 5 exerted long-term effects on isolation-induced aggressive behavior of adult mice (Mus musculus) of the CD-1 strain. Isolated capsaicin-treated mice (scored during a 10-min session) showed the highest frequency and the longest duration of total attacks, attacks, rattling, and offensive upright posture when compared with nonisolated capsaicin-treated subjects and both isolated and nonisolated vehicle control animals. Hypothalamic Substance P (SP) was assessed by radioimmunoassay. Capsaicin treatment significantly lowered hypothalamic SP content in both isolated and nonisolated mice. Moreover, individual scores of isolated capsaicin-treated subjects showed a significant correlation between SP depletion and expression of offensive upright posture. Isolation per se was revealed to play an important role in depleting SP from the hypothalamus.
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PMID:Neonatal capsaicin exposure affects isolation-induced aggressive behavior and hypothalamic substance P levels of adult male mice (Mus musculus). 768 73

Previous research demonstrates that intraseptal administrations of arginine vasotocin (AVT) inhibit male aggression in the territorial field sparrow (Emberizidae: Spizella pusilla) but facilitate aggression in the colonial zebra finch (Estrildidae: Taeniopygia guttata). In order to determine whether this difference may be related to the territorial and colonial social organizations of these two species, the effect of AVT infusions was examined in a territorial Estrildid species, the violet-eared waxbill (Uraeginthus granatina). This species is more closely related to the zebra finch than to the field sparrow and shares most critical features of breeding ecology in common with zebra finches, but differs in social organization. AVT infusions administered via chronic guide cannulae directed at the septum significantly inhibited aggressive behavior, consistent with results in the territorial field sparrow, supporting the hypothesis that social organization is correlated with AVT function. Similar experiments with mesotocin and substance P produced no effects on any of the behaviors measured, but infusions of vasoactive intestinal polypeptide (VIP) significantly facilitated aggression. This result contrasts with the inhibitory effect of septal VIP obtained in the colonial zebra finch, suggesting that VIP function may be correlated with social organization as well.
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PMID:Vasotocin and vasoactive intestinal polypeptide modulate aggression in a territorial songbird, the violet-eared waxbill (Estrildidae: Uraeginthus granatina). 967 95

Evidence is reviewed concerning the brain areas and neurotransmitters involved in aggressive behavior in the cat and rodent. In the cat, two distinct neural circuits involving the hypothalamus and PAG subserve two different kinds of aggression: defensive rage and predatory (quiet-biting) attack. The roles played by the neurotransmitters serotonin, GABA, glutamate, opioids, cholecystokinin, substance P, norepinephrine, dopamine, and acetylcholine in the modulation and expression of aggression are discussed. For the rat, a single area, largely coincident with the intermediate hypothalamic area, is crucial for the expression of attack; variations in the rat attack response in natural settings are due largely to environmental variables. Experimental evidence emphasizing the roles of serotonin and GABA in modulating hypothalamically evoked attack in the rat is discussed. It is concluded that significant progress has been made concerning our knowledge of the circuitry underlying the neural basis of aggression. Although new and important insights have been made concerning neurotransmitter regulation of aggressive behavior, wide gaps in our knowledge remain.
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PMID:Neuropharmacology of brain-stimulation-evoked aggression. 998 25


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