α1-Adrenergic modulation of synaptic input to Purkinje neurons in rat cerebellar brain slices
Article first published online: 19 OCT 2005
Copyright © 2005 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 82, Issue 4, pages 571–579, 15 November 2005
How to Cite
Herold, S., Hecker, C., Deitmer, J. W. and Brockhaus, J. (2005), α1-Adrenergic modulation of synaptic input to Purkinje neurons in rat cerebellar brain slices. J. Neurosci. Res., 82: 571–579. doi: 10.1002/jnr.20660
- Issue published online: 20 OCT 2005
- Article first published online: 19 OCT 2005
- Manuscript Accepted: 22 AUG 2005
- Manuscript Revised: 18 JUL 2005
- Manuscript Received: 26 APR 2005
- Deutsche Forschungsgemeinschaft. Grant Numbers: BR-1831/2-1, DE-231/17-1, 19-1
- spontaneous postsynaptic currents;
- interneuron activity
The inhibitory activity in the cerebellar network, as investigated in acute brain slices from 14–20 days old rats, is modulated by α1-adrenergic stimulation. The specific α1-adrenoceptor agonist phenylephrine (PhE; 10 μM) or the α-adrenoceptor agonist 6-fluoronoradrenaline (10 μM) increases the frequency and the amplitude of spontaneous postsynaptic currents (sPSC) in Purkinje neurons. The effects are sensitive to the α1-adrenoceptor antagonists prazosin (30 μM) and phentolamine (10 μM). The PhE-induced augmentation is suppressed when phospholipase C is blocked by preincubation with U73122 (10 μM) but is not affected by inhibition of protein kinases with H7 (10 μM) or GF109203X (10 μM). Involvement of intracellular Ca2+ stores was shown by a reduced PhE effect after blocking of SERCA pumps with cyclopiazonic acid (30 μM) and thapsigargin (1 μM). The persistence of the PhE effect on the frequency of miniature postsynaptic currents, as recorded in presence of tetrodotoxin, indicates a presynaptic localization of the α1-adrenoceptors. A block of voltage-gated Ca2+ channels with nifedipine, verapamil, or ω-conotoxin MVIIC did not suppress the PhE-induced increase of the frequency and amplitude of sPSC. The results suggest that α1-adrenoceptors at presynaptic terminals mediate an increase of the spontaneous synaptic inhibition of Purkinje neurons in the cerebellar cortex via release of Ca2+ from intracellular stores. © 2005 Wiley-Liss, Inc.