| pubmed-article:1696960 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0242726 | lld:lifeskim |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0017067 | lld:lifeskim |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0038585 | lld:lifeskim |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0441472 | lld:lifeskim |
| pubmed-article:1696960 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:1696960 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:1696960 | pubmed:dateCreated | 1990-9-24 | lld:pubmed |
| pubmed-article:1696960 | pubmed:abstractText | 1. Responses of primary sensory neurons to substance P applications by perfusion were studied with intracellular recording techniques in in vitro slice preparations of trigeminal root ganglia (guinea pigs). Application of substance P in micromolar doses produced reversible depolarizations of 2-47 mV in 48 out of 64 neurons. The depolarizing influence facilitated repetitive spike discharge evoked by current-pulse injection. Evidence of desensitization was observed during prolonged or repeated applications of the peptide. 2. The responses to substance P were associated with decreased input resistance, although increased input resistance was observed in neurons where the resting membrane potential was compensated with DC injection. In single-electrode voltage-clamp (SEVC) recordings, substance P evoked an inward shift in the holding current and reduced an outwardly rectifying component in the I-V relationships. The reversal potential for the substance P response could not be determined. These results suggested that the perikaryal response to substance P has a complex ionic mechanism involving activation and deactivation of membrane conductances. 3. Substance P-induced depolarizations were greatly attenuated during perfusion with solutions that were deficient in [Na+] or [Mg2+] and were not significantly affected during perfusion with low-[Ca2+]-, CO2(+)-containing solutions. 4. In the voltage-clamp investigations, an inward current contributed to the substance P responses during combined application with the K(+)-channel blockers, 4-aminopyridine (4-AP) and tetraethylammonium (TEA). This current was not abolished by the inclusion of CsCl in the perfusing solution or by internal Cs+ application from the recording electrode, suggesting that an anomalous inward rectifier was not involved in the responses to substance P.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
| pubmed-article:1696960 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1696960 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1696960 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1696960 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1696960 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1696960 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1696960 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1696960 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1696960 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:1696960 | pubmed:issn | 0022-3077 | lld:pubmed |
| pubmed-article:1696960 | pubmed:author | pubmed-author:PuilEE | lld:pubmed |
| pubmed-article:1696960 | pubmed:author | pubmed-author:SpigelmanII | lld:pubmed |
| pubmed-article:1696960 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1696960 | pubmed:volume | 64 | lld:pubmed |
| pubmed-article:1696960 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1696960 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1696960 | pubmed:pagination | 273-81 | lld:pubmed |
| pubmed-article:1696960 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:meshHeading | pubmed-meshheading:1696960-... | lld:pubmed |
| pubmed-article:1696960 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:1696960 | pubmed:articleTitle | Ionic mechanism of substance P actions on neurons in trigeminal root ganglia. | lld:pubmed |
| pubmed-article:1696960 | pubmed:affiliation | Department of Pharmacology and Therapeutics, Faculty of Medicine, University of British Columbia, Vancouver, Canada. | lld:pubmed |
| pubmed-article:1696960 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1696960 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1696960 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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