Journal article
Dihydropyridines modulate K +-evoked amino acid and adenosine release from cerebellar neuronal cultures
Neuroscience letters, Vol.102(1), pp.97-102
1989
DOI: 10.1016/0304-3940(89)90314-5
PMID: 2476690
Abstract
Partial depolarization of primary cerebellar neuronal cultures with K
+ evoked the release of aspartate, glutamate, adenosine, serine, taurine, γ-aminobutyric acid (GABA), alanine and proline. The dihydropyridine calcium channel agonist, BAY K 8644, significantly augmented the K
+-induced release of adenosine, aspartate, glutamate and GABA, but not that of serine, taurine, alanine or proline. However, in all cases the dihydropyridine antagonist nifedipine decreased this BAY K 8644-enhanced, K
+-evoked efflux to below control levels. Neither BAY K 8644 nor nifedipine alone affected basal efflux levels. The phenylalkylamine calcium channel antagonist, verapamil, was ineffective in antagonizing K
+-evoked amino acid release except at very high concentration (100 μM). These findings suggest that L-type Ca
2+ channels are present in both excitatory (glutamatergic granule cells) and inhibitory (GABAergic stellate and basket cells) neurons in these cultures, and that they appear to be involved in regulating the release of not only neuroactive amino acids, but also some neutral amino acids and adenosine.
Details
- Title: Subtitle
- Dihydropyridines modulate K +-evoked amino acid and adenosine release from cerebellar neuronal cultures
- Creators
- Robert A PhilibertGary R Dutton
- Resource Type
- Journal article
- Publication Details
- Neuroscience letters, Vol.102(1), pp.97-102
- DOI
- 10.1016/0304-3940(89)90314-5
- PMID
- 2476690
- NLM abbreviation
- Neurosci Lett
- ISSN
- 0304-3940
- eISSN
- 1872-7972
- Publisher
- Elsevier Ireland Ltd
- Language
- English
- Date published
- 1989
- Academic Unit
- Roy J. Carver Department of Biomedical Engineering; Psychiatry; Iowa Neuroscience Institute; Neuroscience and Pharmacology
- Record Identifier
- 9984003456702771
Metrics
16 Record Views