| Autor: |
Soldo BL; Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622, USA. soldob@umich.edu, Moises HC |
| Jazyk: |
angličtina |
| Zdroj: |
Brain research [Brain Res] 1997 May 30; Vol. 758 (1-2), pp. 118-26. |
| DOI: |
10.1016/s0006-8993(97)00206-0 |
| Abstrakt: |
Opioid modulation of calcium currents was studied in acutely dissociated rat basal forebrain neurons using the whole cell patch-clamp recording technique. The mu-opioid receptor agonist DAGO reversibly suppressed high-voltage activated calcium currents and slowed their rate of activation, while neither delta- nor kappa-opioid receptor agonists were effective in modifying calcium current in these neurons. The inhibitory effect of DAGO on calcium current was abolished following irreversible blockade of N-type calcium channels by omega-conotoxin GVIA, whereas DAGO-induced inhibitory responses were not affected following blockade of L-type calcium channels by nifedipine. These findings indicate that mu-opioid receptors are negatively coupled to N-type calcium channels on the postsynaptic membrane of basal forebrain neurons. Calcium currents recorded from a significant number of large, mu-opioid sensitive neurons were also suppressed by muscarinic receptor activation, while smaller, mu-opioid sensitive neurons were not sensitive to muscarinic receptor activation. Thus, the present data demonstrate that voltage-activated calcium influx in several subpopulations of basal forebrain neurons can be regulated by mu-opioid receptor activation. These results suggest that mu-opioid regulation of calcium current may be an important functional mechanism in regulating neuronal excitability and synaptic transmission in the basal forebrain. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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