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Biosynthesis and release of tachykinins from rat sensory neurons in culture.
J Neurosci Res. 1991 Oct; 30(2):288-99.JN

Abstract

A long-term culture system of dissociated rat dorsal root (DRG) and trigeminal ganglion cells with high cell density has been developed. Two to 3 weeks after plating, the cultures consist of a nearly pure population of sensory neurons, which can be kept for more than 2 months in culture. Cultured neurons synthesize and release the tachykinins substance P (SP) and substance K (SK, neurokinin A) with a time course similar to that observed in vivo. High-pressure liquid chromatography (HPLC) analysis of peptides extracted from neuronal cultures and synthetic tachykinins revealed identical retention characteristics. Northern blot analysis of mRNAs from cultured cells with a specific tachykinin-probe demonstrated that the preprotachykinin-gene is expressed in preparations of both DRG and trigeminal ganglia cells. Depolarizing stimuli such as high potassium (47 mM) evoked a peptide release from cultured neurons in a strictly Ca(++)-dependent manner. Capsaicin, a compound known to stimulate nociceptive sensory neurons, dose-dependently released tachykinins in concentrations as low as 10(-9) M. Only total absence of Ca++ ions from the incubation medium abolished the capsaicin-induced peptide release. Nifedipine, a blocker of voltage-dependent L-type Ca++ channels, completely blocked the potassium-induced release of SP but did not reduce the capsaicin-evoked release. Mediator substances of pain and inflammation, such as bradykinin, serotonin, and histamine, triggered the release of tachykinins from sensory neurons in vitro. These results clearly demonstrate that the neurons characterized express properties similar to those of sensory neurons in vivo and provide model systems for detailed studies of the biosynthesis and release of neuropeptides as well as the participation of sensory neurons in pain and inflammatory reactions.

Authors+Show Affiliations

Max Planck Institute for Psychiatry, Clinical Institute, Munich, Germany.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

1798053

Citation

Vedder, H, and U Otten. "Biosynthesis and Release of Tachykinins From Rat Sensory Neurons in Culture." Journal of Neuroscience Research, vol. 30, no. 2, 1991, pp. 288-99.
Vedder H, Otten U. Biosynthesis and release of tachykinins from rat sensory neurons in culture. J Neurosci Res. 1991;30(2):288-99.
Vedder, H., & Otten, U. (1991). Biosynthesis and release of tachykinins from rat sensory neurons in culture. Journal of Neuroscience Research, 30(2), 288-99.
Vedder H, Otten U. Biosynthesis and Release of Tachykinins From Rat Sensory Neurons in Culture. J Neurosci Res. 1991;30(2):288-99. PubMed PMID: 1798053.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Biosynthesis and release of tachykinins from rat sensory neurons in culture. AU - Vedder,H, AU - Otten,U, PY - 1991/10/1/pubmed PY - 1991/10/1/medline PY - 1991/10/1/entrez SP - 288 EP - 99 JF - Journal of neuroscience research JO - J. Neurosci. Res. VL - 30 IS - 2 N2 - A long-term culture system of dissociated rat dorsal root (DRG) and trigeminal ganglion cells with high cell density has been developed. Two to 3 weeks after plating, the cultures consist of a nearly pure population of sensory neurons, which can be kept for more than 2 months in culture. Cultured neurons synthesize and release the tachykinins substance P (SP) and substance K (SK, neurokinin A) with a time course similar to that observed in vivo. High-pressure liquid chromatography (HPLC) analysis of peptides extracted from neuronal cultures and synthetic tachykinins revealed identical retention characteristics. Northern blot analysis of mRNAs from cultured cells with a specific tachykinin-probe demonstrated that the preprotachykinin-gene is expressed in preparations of both DRG and trigeminal ganglia cells. Depolarizing stimuli such as high potassium (47 mM) evoked a peptide release from cultured neurons in a strictly Ca(++)-dependent manner. Capsaicin, a compound known to stimulate nociceptive sensory neurons, dose-dependently released tachykinins in concentrations as low as 10(-9) M. Only total absence of Ca++ ions from the incubation medium abolished the capsaicin-induced peptide release. Nifedipine, a blocker of voltage-dependent L-type Ca++ channels, completely blocked the potassium-induced release of SP but did not reduce the capsaicin-evoked release. Mediator substances of pain and inflammation, such as bradykinin, serotonin, and histamine, triggered the release of tachykinins from sensory neurons in vitro. These results clearly demonstrate that the neurons characterized express properties similar to those of sensory neurons in vivo and provide model systems for detailed studies of the biosynthesis and release of neuropeptides as well as the participation of sensory neurons in pain and inflammatory reactions. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/1798053/Biosynthesis_and_release_of_tachykinins_from_rat_sensory_neurons_in_culture_ L2 - https://doi.org/10.1002/jnr.490300203 DB - PRIME DP - Unbound Medicine ER -