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)

1. A morphological and physiological comparison was made between embryonically and postnatally derived superior cervical ganglion neurons (SCGN) grown in dissociated cell culture. It was found that while morphologically distinct, the physiological properties of the postnatal neurons were the same as their embryonic counterparts. 2. Intracellular injection of horseradish peroxidase (HPR) demonstrated that SCGN from any age of animal elaborated two basic types of processes, although the pattern of process ramification was unique for each neuron. The two types of proceses were 1) the large, smooth, rapidly tapering; and 2) the thin, nontapering variety, which often contained varicosities along its length. It is suggested that the former are dendritic in function, while the latter act as axons. 3. A difference was noted in somal size and the number of primary processes extended by the embryonic and postnatal neurons, with the latter more closely resembling the in vivo morphology. 4. Resting potentials and action-potential amplitudes of postnatal SCGN were comparable to those found previously for embryonic SCGN in vitro. 5. Iontophoretic application of putative neurotransmitter substances revealed the presence of acetylcholine receptors (AChR) on both embryonic and postnatal SCGN. Picrotoxin-sensitive depolarizing responses to iontophoresed gamma-aminobutyric acid (GABA) was seen on a few embryonic neurons, but not on the older cells. No responses were detected when norepinephrine (NE), glutamate, cAMP, substance P, or dopamine were applied to the SCGN of either age group. 6. Synatpic interaction between postnatal SCGN were found at an earlier in vitro age (12 days) than was the case for embryonic neurons (20 days). 7. Synaptic transmission was found to be chemical in nature. This was shown by 1) a dependence on external Ca2+ concentrations; 2) steplike fluctuations in synpatic potential amplitude, and 3) a variation in potential amplitude with changes in membrane potential. 8. It is concluded that the postnatal SCGN are able to survive in culture even when taken from animals up to 12.5 wk old. The elaboration of processes is in many ways strikingly similar to sympathetic neurons in the animal, and they are able to form functional synaptic interactions.
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PMID:Postnatal rat sympathetic neurons in culture. I. A comparison with embryonic neurons. 3 83

In vivo and in vitro perfusion techniques have been used to study the release of neurokinin A-like immunoreactivity from the rat substantia nigra. Potassium depolarization and electrical field stimulation evoked calcium-dependent release from nigral slices. Potassium depolarization was also effective in vivo. Tetrodotoxin (1 microM) completely blocked electrically stimulated release but only diminished release in response to depolarizing potassium. Neurokinin A-like immunoreactivity release showed frequency dependence and a clear facilitation phenomenon between 5 and 25 Hz. High-performance liquid chromatography analysis of the immunoreactivity released in vitro revealed the presence of neurokinin A, neuropeptide K and neurokinin B, along with their sulphoxide forms. A marked depletion of neuropeptide K and neurokinin B content was observed when the tachykinin content of the nigral slices was examined before and after stimulation. However, the neurokinin A content of the slices was unchanged or even increased, suggesting an accelerated processing of neurokinin A precursors during the stimulation. The tachykinin peptides were degraded at different rates by substantia nigra homogenates; degradation was fastest for neuropeptide K and slowest for neurokinin A. The addition of a mixture of peptidases inhibitors (thiorphan, phosphoramidon, bestatin and captopril) substantially reduced the degradation of all three tachykinins, but did not completely block degradation. GABA-A receptor antagonists such as bicuculline and, particularly, picrotoxin potentiated the stimulated neurokinin A-like immunoreactivity release in vitro, but the GABA-agonist muscimol had no effect. Picrotoxin was even more potent in vivo. The results presented in this study demonstrate that neurokinin A, neuropeptide K and neurokinin B can be released by depolarizing stimuli from rat substantia nigra. Furthermore, the features exhibited by this release suggest that these peptides may have a neurotransmitter/neuromodulator role in the rat substantia nigra.
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PMID:In vitro and in vivo release of neurokinin A-like immunoreactivity from rat substantia nigra. 290 88

Rat substantia nigra slices were superfused with a physiological medium containing a diluted substance P (SP) antiserum, bacitracin and serum albumin to measure SP released in superfusates. As shown by measuring the degradation of a SP-labelled derivative incubated with cerebellar slices, this medium prevented the enzymatic inactivation of SP. Potassium (K+, 50 mM) and veratridine (5 X 10(-5) M) stimulated SP release and these effects were respectively prevented in absence of calcium and in presence of tetrodotoxin (5 X 10(-7) M). GABA (5 X 10(-5) M), nicotine (10(-6) M) and L-glutamic acid (5 X 10(-5) M) reduced the K+ (50 mM)-evoked release of SP. In contrast, glycine (5 X 10(-5) M), oxotremorine (5 X 10(-5) M), D-glutamic acid (5 X 10(-5) M) and serotonin (5 X 10(-5) M) were without effect. Pempidine (10(-5) M) prevented the inhibitory effect of nicotine (10(-6) M) on the K+-evoked release of SP. Glutamic acid diethyl ester (10(-4) M) completely abolished the L-glutamic acid-induced inhibition of the K+-evoked release of SP. Picrotoxin (5 X 10(-5) M) did not influence the L-glutamic acid inhibitory effect excluding the intervention of GABAergic mechanisms.
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PMID:Inhibitory effects of GABA, L-glutamic acid and nicotine on the potassium-evoked release of substance P in substantia nigra slices of the rat. 616 87

Membrane potential changes induced by 5-hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA) and 1,1-dimethyl-4-phenyl piperazinium (DMPP) were recorded from nodose ganglia (NG) by the sucrose-gap method. An amount of 0.002-0.5 mumol of the depolarizing agent was injected into the superfusion stream to the ganglion. Responses to 5-HT were also evoked from superior cervical (SCG) and dorsal root ganglia (DRG). 5-Hydroxytryptamine elicited depolarizations of graded amplitude. Maximal responses were 4.5 +/- 0.4 mV in nodose ganglia compared to 2.2 +/- 0.2 mV in superior cervical and 0.6 +/- 0.1 mV in dorsal root ganglia (means +/- SEM). In nodose ganglia, GABA induced smaller maximal depolarizations than did 5-HT, similar to those evoked by DMPP; dopamine was a weak depolarizing agent while substance P was apparently inactive. The dose-response curve for 5-HT in nodose ganglia was parallel to that for 5-HT in superior cervical ganglia and significantly to the left (ED50 values 0.029 and 0.098 mumol). Curves for 5-HT and GABA in nodose ganglia were superimposable. The high sensitivity of nodose ganglia cells to 5-HT is briefly discussed. Analogues of 5-HT lacking a hydroxyl group at position 5 on the nucleus were relatively inactive as depolarizing agents. Picrotoxin (10(-6)-10(-5) M) reduced or suppressed responses in nodose ganglia to GABA, whereas responses to 5-HT and DMPP were not much affected or, in the case of 5-HT, sometimes somewhat reduced. Quipazine (10(-6) M) was a selective antagonist of 5-HT responses in nodose ganglia; those to GABA and DMPP were not significantly altered. Neither trazodone nor LSD displayed antagonist properties at 5-HT receptors in nodose ganglia.
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PMID:Depolarizing responses recorded from nodose ganglion cells of the rabbit evoked by 5-hydroxytryptamine and other substances. 706 7