Abstract:
:Partial depolarization of primary cerebellar neuronal cultures with K+ evoked the release of aspartate, glutamate, adenosine, serine, taurine, gamma-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 microM). These findings suggest that L-type Ca2+ 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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Philibert RA,Dutton GRdoi
10.1016/0304-3940(89)90314-5subject
Has Abstractpub_date
1989-07-17 00:00:00pages
97-102issue
1eissn
0304-3940issn
1872-7972pii
0304-3940(89)90314-5journal_volume
102pub_type
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journal_title:Neuroscience letters
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doi:10.1016/j.neulet.2008.12.016
更新日期:2009-02-20 00:00:00
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journal_title:Neuroscience letters
pub_type: 杂志文章
doi:10.1016/j.neulet.2005.05.008
更新日期:2005-09-02 00:00:00
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