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 was undertaken to quantify selected neuropeptides (thyrotropin releasing hormone, substance P, methionine and leucine enkephalin) in the cervical spinal cord and other regions of the central nervous system of Wobbler mice by radioimmunoassays during several stages of the motoneuron disease compared with age- and sex-matched normal phenotype littermates. In Wobbler spinal cord, thyrotropin releasing hormone is higher early in the disease, whereas in the brainstem it is higher at a later stage. Substance P in spinal cord is also higher late in the disease. Leucine enkephalin levels are greater at all stages in diseased spinal cord and brainstem, but methionine enkephalin increases only late in the disease. Highly significant increases of the peptides (except thyrotropin releasing hormone) appear in hypothalamus and midbrain only late in the motoneuron disease. Regression analyses show that thyrotropin releasing hormone in spinal cord and brainstem decreases normally with age in the control mice and at a faster rate related to the extent of motor impairment in Wobbler mice. Thyrotropin releasing hormone and methionine enkephalin in the Wobbler brainstem correlate (P less than 0.05) with the progress of the motoneuron disease. Methionine enkephalin increases faster in Wobbler brainstem and decreases faster in control spinal cord with age. The increase of leucine enkephalin in the Wobbler spinal cord correlates significantly with age and with the progress of the disease, but leucine enkephalin declines slightly with age in the controls. The changes of substance P in spinal cord and brainstem do not correlate significantly with the progress of the disease. In the hypothalamus, increasing values for substance P in control specimens and enkephalins in Wobbler specimens are significantly correlated with age. However, in the midbrain, higher methionine and leucine enkephalin levels are significantly associated with age only in the control mice. Alterations of neuropeptides in the Wobbler mouse spinal cord and brainstem may result from the degeneration of bulbospinal raphe neurons projecting to the ventral spinal cord, or from primary afferent or interneuronal nerve terminals. The data imply that the neuronal degeneration process in the Wobbler motoneuron disease is not limited to motoneurons. In the spinal cord, the data support our previous hypothesis that neuronal sprouting presynaptic to the motoneurons may account for increased neuropeptide concentrations. Alternatively, synthesis and/or degradation of these peptides may be altered. In addition, it is proposed that enkephalinergic neurons may develop abnormally in Wobbler mice. The early increase of leucine enkephalin in the Wobbler spinal cord possibly indicates its importance in the etiology of the motoneuron disease.
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PMID:Alteration in the levels of thyrotropin releasing hormone, substance P and enkephalins in the spinal cord, brainstem, hypothalamus and midbrain of the Wobbler mouse at different stages of the motoneuron disease. 138 70

These three neuropeptides were measured at daily baseline values by radioimmunoassay. Stimulated parotid saliva was collected from 31 subjects using a modified Carlson-Crittenden device affixed over Stenson's duct. Methionine enkephalin-like immunoreactivity ranged from 6.6 to 11.7 fmol/ml, with a mean of 9.3 fmol/ml. Substance P-like immunoreactivity ranged from 6.1 to 12.6 fmol/ml, with a mean of 9.3 fmol/ml. beta-Endorphin-like immunoreactivity ranged from 1.2 to 3.6 fmol/ml, with a mean of 2.6 fmol/ml. This is believed to be the first documentation of methionine enkephalin- and substance P-like activities in human parotid saliva and the first demonstration of beta-endorphin-like activity in any type of human saliva. Substance P-like activity was significantly higher in morning than evening samples; beta-endorphin-like activity also tended to be higher in the morning samples. Substance P and beta-endorphin-like immunoreactivities covaried in a significant positive manner, suggesting either common control mechanisms or similar responses to physiological variables.
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PMID:Methionine enkephalin-like, substance P-like, and beta-endorphin-like immunoreactivity in human parotid saliva. 138 60

The effects of a range of neuropeptides were investigated on the membrane potential of the Schwann cells of the giant nerve fibre of the tropical squid. Vasoactive intestinal peptide (VIP) produced a dose-dependent, long-lasting hyperpolarization of the Schwann-cell membrane potential. Among peptides structurally related to VIP, similar effects were produced by peptide histidine isoleucine (PHI) but not by secretin and glucagon. Substance P and somatostatin also hyperpolarized the Schwann-cell membrane potential but via receptor systems distinct from those activated by VIP. Methionine enkephalin ([Met]-enkephalin) blocked the actions of all the above peptides as well as the effects of DL-octopamine and carbachol. The actions of [Met]-enkephalin upon the VIP responses were antagonized by naloxone. VIP produces its effects on the Schwann-cell membrane potential via a receptor system that is independent from those described previously which mediate the effects of carbachol and DL-octopamine. However, VIP can potentiate the effects of the latter systems. The actions of VIP on the Schwann cell are unlikely to be mediated via changes in adenosine 3',5'-cyclic monophosphate (cyclic AMP) levels and are insensitive to changes in the level of extracellular calcium in the superfusate. The actions of VIP are, however, potentiated in the presence of low concentrations of lithium ions suggesting that the VIP receptor may mediate its effects by inducing the hydrolysis of polyphosphatidylinositols in the Schwann-cell membrane. Evidence is presented for the existence of an endogenous VIP-like component in the normal hyperpolarizing action of giant-axon activity on the membrane potential of the Schwann cell.
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PMID:Peptidergic modulation of the membrane potential of the Schwann cell of the squid giant nerve fibre. 243 97

Neuropeptidergic systems have been studied in human tissues and fluids, which include the pituitary and lumbar cerebrospinal fluid, respectively. This paper reviews the qualitative and quantitative mass spectrometric analytical data obtained from three areas of study. Methionine enkephalin (ME) and beta-endorphin (BE) were quantified in the human pituitary by liquid secondary ion mass spectrometry (LSI MS)-tandem mass spectrometry. Corresponding stable isotope-incorporated synthetic peptide internal standards were used. Proenkephalin A and proopiomelanocortin produce ME and BE, respectively. The analysis of neuropeptides in macroadenomas demonstrated a decrease in both of those neuropeptidergic systems relative to controls. An analysis of prolactin-secreting microadenomas showed an increase in the proenkephalin A system. Mass spectrometry was also used to detect opioid peptide-containing proteins in the pituitary. Enzymes that process the precursors of proenkephalin A and tachykinin (substance P) neuropeptides were studied in human lumbar cerebrospinal fluid. Electrospray ionization mass spectrometry was used to characterize the molecular mass of each peptide product.
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PMID:Mass spectrometric analysis of neuropeptidergic systems in the human pituitary and cerebrospinal fluid. 1049 85