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)

Directional behavioral and functional asymmetries (i.e., left-biased or right-biased in all or most animals of the population) induced by certain chemical substances are new types of brain and spinal cord asymmetry. The revealed asymmetry comprises: (1) left- or right-biased circle rotation in rat, (2) hind limb postural asymmetry resulting from alteration of the left or right flexion reflex in rat and cat, and (3) asymmetric alterations of the evoked potentials (EP) in the turtle visual cortex. Circle rotation of animals is induced by hypothalamic neurohormones (somatostatin, LH-RH, substance P, and TRH). Postural asymmetry develops under the effect produced by enkephalins and opioid kappa- and delta-agonists, sigma-agonist SKF 10.047, Arg-vasopressin. Endogenous peptide factors, the activity (or content) of which increased under brain and spinal cord unilateral injury, as well as the ones localized in the left or right hemisphere, also induced postural asymmetry. EP of the left and right turtle visual cortex were inhibited by enkephalins and opioid kappa-, and delta- and mu-agonists, and factors predominantly localized in the left or right turtle visual cortex in a different manner. The data reported here suggest the existence of a side-specific mechanism for a selective neurohormonal regulation of the neuronal activity and other processes in the left and right halves of brain and spinal cord which involves lateralized neuropeptides and their receptors. This mechanism might serve to maintain a certain balance between the activity of the left and right-side neurons, and other contralateral processes in the paired and bilateral structures in brain and spinal cord. Significant deviations from the balance occur most likely due to powerful unilateral stimuli, e.g., unilateral trauma. Many neuropeptides (opioid ones, somatostatin, MSH, ACTH) are, presumably, involved in the regeneration processes in the central and peripheral nervous system. In the case of brain lesions, some lateralized endogenous peptides may participate in the regulation of regeneration process on the left, whereas the other ones, on the right side of the midline, which depends on the side of the lesion. Some lateralized receptors and ligands may serve as positional markers of the left, whereas the other ones may serve as those of the right brain hemisphere. In ontogenesis, these markers are probably necessary to perform the function of the mechanism responsible for symmetrical brain formation.
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PMID:Neuropeptides induce directional asymmetry in brain and spinal cord: facts and hypotheses. 268 85

[125I-Tyr]Somatostatin [( 125I-Tyr]SRIH) binding was found in 11 GH-secreting pituitary adenomas [Kd = 0.46 +/- 0.15 (+/- SE) nM; maximum binding, 165 +/- 35 fmol/mg protein). This binding was specific, since it was displaced by somatostatin-14 (SRIH-14), N-Tyr-SRIH-14, and SRIH-28. In contrast, a number of peptides and drugs not structurally related to SRIH, such as bombesin, dopamine, LHRH, met-enkephalin, naloxone, neurotensin, secretin, substance P, TRH, or vasoactive intestinal peptide, did not affect [125I-Tyr]SRIH binding. [125I-Tyr]SRIH specific binding also was found in PRL-secreting pituitary adenomas. The kinetic characteristics of the specific binding were similar to those of GH-secreting adenomas. However, maximal binding was one quarter that of GH-secreting adenomas (37 +/- 9 fmol/mg protein). In contrast, nonsecreting (chromophobe) tumors were devoid of any specific binding. Finally, in acromegaly, the density of [125I-Tyr]SRIH-binding sites in the adenomas was negatively correlated with plasma GH levels before surgery (r = -0.80). This suggests that somatostatinergic control is involved in GH secretion in acromegalic patients.
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PMID:Somatostatin receptors in human growth hormone and prolactin-secreting pituitary adenomas. 286 Jan 20

The effects of neurotransmitters or drugs on the release of endogenous dopamine (DA) and extracellular levels of its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), were examined in vivo by intracerebral dialysis. A dialysis tube was implanted stereotaxically through bilateral caudate nuclei of rats and perfused with the Ringer solution. Amounts of DA, DOPAC and HVA in the perfusates were measured by high performance liquid chromatography (HPLC) with electrochemical detection. The basal level of DA was 2.76 +/- 0.64 pg/min, whereas the levels of DOPAC and HVA were 218.7 +/- 20.7 and 142.4 +/- 10.6 pg/min, respectively. Apomorphine (4 mg/kg, i.v.) reduced the efflux of DA and its metabolites. Haloperidol (0.4 mg/kg, i.v.) did not change DA release and produced only a minor increase of its metabolites. This increase of metabolites was inhibited by pargyline. Met-enkephalin (10(-4) M), substance P (10(-4) M) and acetylcholine chloride (10(-4) M) added to the perfusing medium increased the release of DA. Met-enkephalin also increased the release of DOPAC. gamma-Amino-n-butyric acid (GABA, 10(-4) M) reduced the release of DOPAC and HVA when added to the perfusing medium. Thyrotropin releasing hormone (TRH, 5 mg/kg, i.v.) increased the release of HVA. These findings indicated that different mechanisms mediated effects of neurotransmitters or drugs on the release and metabolism of DA in the rat striatum.
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PMID:Effects of neurotransmitters or drugs on the in vivo release of dopamine and its metabolites. 287 Feb 4

Modern neuroanatomical methods, specifically immunocytochemistry and receptor autoradiography, have greatly increased our knowledge on the organization of the human nervous system. This review, based on the literature and largely on personal results, is devoted to the chemical neuroanatomy of the normal human spinal cord. It provides a comprehensive overview of the differential distribution of various chemical messengers, their metabolizing enzymes and their receptors (acetylcholine, amino acids, monoamines, neuropeptides) in the neuronal laminae of the spinal gray matter. At the level of the dorsal horn, lamina II, i.e. Rolando's substantia gelatinosa, is characterized by a heavy concentration of several transmitters and receptors. Within the intermediate gray matter the autonomic nuclei receive a dense peptidergic input, e.g. substance P, enkephalin and VIP afferents. In the ventral horn close contacts are numerous between serotonergic or peptidergic (SP, TRH, enkephalins...) fibers and motoneuronal perikarya or dendrites. The present knowledge on the putative role of certain neurotransmitters in spinal functions is summarized.
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PMID:[Chemical neuroanatomy of the human spinal cord]. 290 52

Recent developments in thyroid hormone metabolism have helped to understand the complex events which characterize the regulation of TSH secretion. Plasma T3 concentration as well as intrapituitary T3 generation from T4, exert a profound effect on TSH synthesis and release. Pituitary Type II deiodinase differs from Type I deiodinase found in other tissue such as liver and kidney, and in fact different conditions such as hypothyroidism and hyperthyroidism affect these enzymes in opposite direction. Thyroid hormones exert other effects on the pituitary such as increased synthesis of substance P, increased synthesis of GH, and decreased TRH receptors, TRH also modifies its own receptors in the pituitary and exerts modulatory effects on TSH molecule. Patients with non thyroidal illness may display TSH molecules with decreased biological activity. Various agents used in every day praxis may alter TSH and thyroid secretion. The physician must be aware of changes in order to avoid diagnostic pitfalls.
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PMID:Pituitary-thyroid interaction: effects of thyroid hormone, non thyroidal illness and various agents on TSH secretion. 314 May 59

Using an antiserum (no. 373) raised against a tyrosinated analog of preproTRH53-74 [( Tyr1]preproTRH53-74 or pYT 22), we have demonstrated the presence of a discrete population of immunoreactive neurons in the midbrain periaqueductal gray (PAG). Relative to the distribution of serotonin, somatostatin, peptide histidine isoleucine (PHI), methionine enkephalin, substance P and neurotensin-containing neuronal perikarya in the PAG, neurons containing immunoreactive pYT 22 occupied a unique location in the ventrolateral PAG. In contrast, terminal fields containing these neuroactive substances with the exception of PHI, were seen in abundance in the region of the ventrolateral PAG neurons. These studies indicate that a non-TRH sequence contained within the N-terminal portion of the TRH prohormone are expressed in a distinct group of neurons in the ventrolateral PAG. The location of these neurons in the PAG in a region richly innervated by nerve terminals containing analgesia-mediating substances, suggests a possible role for proTRH-derived peptides in the modulation of nociception.
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PMID:Neurons containing a N-terminal sequence of the TRH-prohormone (preproTRH53-74) are present in a unique location of the midbrain periaqueductal gray of the rat. 314 23

In experimental models of spinal cord trauma there is often a relatively poor correlation between light microscopic histological changes and motor recovery. Previously it was shown that spinal cord levels of immunoreactive TRH and substance P, by radioimmunoassay, are significantly reduced caudal to the injury site. Since much of the substance P and TRH in the spinal cord derives from cells within the ventral medulla, many of which also contain serotonin, we examined changes in serotonin immunoreactivity within the spinal cord caudal to the injury site in rats subjected to varying degrees of impact trauma to the thoracic cord. Reductions in immunocytochemical staining of serotonin in ventral gray matter of the lumbar region at two weeks after trauma were significantly correlated with the degree of injury severity as reflected by motor impairment. Changes in the region of the central canal, but not dorsal horn, were also correlated with injury severity. These findings indicate that serotonin immunocytochemical analysis may permit better correlation between anatomical and functional outcome after spinal cord injury than generally utilized light microscopic methods.
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PMID:Use of serotonin immunocytochemistry as a marker of injury severity after experimental spinal trauma in rats. 340 25

AtT20/D16v is a clonal strain of mouse pituitary tumor cells which synthesizes and secretes ACTH. Somatostatin, a hypothalamic tetradecapeptide, has been shown to inhibit the release of PRL, GH, and TSH from the pituitary gland. We have characterized specific binding sites for somatostatin on AtT20/D16v cells and demonstrate that somatostatin inhibits stimulated ACTH release by these cells. Equilibrium binding studies with [125I]Tyr1]somatostatin showed the presence of a single class of noninteracting binding sites on AtT20/D16v cells. Half-maximal binding of somatostatin occurred at 1.7 X 10(-9) M, and there were 26,300 binding sites/cell. The binding of [125I]Tyr1]somatostatin was not significantly inhibited by the hypothalamic peptides TRH, LHRH, and substance P. Somatostatin had no consistent effect on basal ACTH secretion by AtT20/D16v cells, but it inhibited ACTH secretion stimulated with either 50 mM KCl or a hypothalamic extract. Half-maximal inhibition occurred with 4 X 10(-10) M somatostatin. TRH, LHRH, and substance P at concentrations of 10(-7) M were without effect. Somatostatin had no effect on either basal or stimulated hormone secretion by GH12C1 or F4C1 cells, two cell strains which lack specific somatostatin-binding sites. A critical concentration of extracellular calcium was required for the stimulation of ACTH secretion in AtT20/D16v cells. No response to 50 mM KCl occurred in the presence of EGTA or cobalt. Increased extracellular calcium overcame the inhibition of stimulated hormone secretion by EGTA, cobalt, and somatostatin. Therefore, we conclude that the inhibition of stimulated ACTH secretion by somatostatin involves the interaction of the peptide with specific binding sites on AtT20/D16v cells and the inhibition of stimulus-elicited calcium influx.
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PMID:Inhibition of adrenocorticotropin secretion by somatostatin in pituitary cells in culture. 610 20

[125I]Iodo-Tyr1-somatostatin (SRIF) binds with high affinity to one class of sites in the rat anterior pituitary with a KD of 0.91 +/- 0.22 nM and a receptor concentration of 104.4 +/- 1.9 fmol/mg protein. This binding is saturable with respect to tissue concentration and is time-, temperature-, pH-, and calcium-dependent. It is also reversible as a function of time. The rates of association and dissociation were calculated to be 5.98 X 10(7) M-1 min-1 and 0.578 min-1, respectively. Binding of [125I]iodo-Tyr1-SRIF is not inhibited by morphine, beta-endorphin, [D-Ala2]Met-enkephalin, LHRH, TRH, histidylproline diketopiperazine, neurotensin, substance P, bombesin or vasoactive intestinal peptide. In contrast SRIF, [Tyr1]SRIF, and [D-Trp8,D-Cys14]SRIF displace [125I]iodo-Tyr1-SRIF binding with Ki values 0.10 +/- 0.05, 0.46 +/- 0.18, 0.05 +/- 0.01 nM, respectively. The constants of inhibition of a series of alanine monosubstituted analogs of SRIF are correlated (r = 0.89) with their biological potency on GH secretion. Furthermore, postnatal development patterns of [125I]iodo-Tyr1-SRIF binding sites follow the ability of SRIF to inhibit GH release. Thus, [125I]iodo-Tyr1-SRIF binding to adenohypophyseal membranes seems to reflect interaction with SRIF receptors on adenohypophyseal cells. Since biological effects of the peptide have been reported on GH, thyrotropin-stimulating hormone, and PRL secretion, further studies are required to determine the cell types upon which this binding occurs.
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PMID:Somatostatin receptors on rat anterior pituitary membranes. 612 57

Male Sprague-Dawley rats were trained to discriminate ethanol (2 g/kg, PO: EtOH) from saline (10 ml/kg, PO: SAL) in a two-bar positively reinforced operant task on a VI 15 sec schedule. After the rats reached criterion performance (greater than 90% correct responses on the appropriate lever), thyrotropin releasing hormone (pyroGlu-His-Pro-NH2: TRH), a metabolite of TRH (His-Pro diketopiperazine: HP), and a structural analog of TRH (HPCA-His-ThiaPro-NH2: OHT) were tested for their ability to antagonize the EtOH cue. These peptides were chosen for their reported ability to reverse ethanol-induced narcosis. However, at doses that did not disrupt performance, TRH, HP, and OHT did not affect the stimulus properties of ethanol at any dose tested, nor did they change the stimulus properties of saline. Naloxone and ACTH(1-10)-NH2 were also tested as ethanol antagonists of the training dose. Pretreatment with either of these compounds failed to alter ethanol-appropriate responding. In addition, (DA1a2-Met5)-enkephalin-ol, (DAla2-Met(O)5)-enkephalin-ol, substance P, delta sleep-inducing peptide, and bombesin were tested for their ability to elicit ethanol appropriate responding. The EtOH cue generalized to none of these peptides.
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PMID:The effects of peptides on the stimulus properties of ethanol. 615 98


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