Alpha 1 adrenoceptor activation potentiates taurine response mediated by protein kinase C in substantia nigra neurons. Nabekura, Junichi, Tomohiro Omura, Naoki Horimoto, Tetsuro Ogawa and Norio Akaike. Department of Physiology, Kyushu University, Faculty of Medicine, 3-1-1 Maidashi, Higashiku Fukuoka, 812, Japan, Department of Physiology, Akita University, School of Medicine, 1-1-1 Hondou, Akita, 010 Japan.
APStracts 3:0143N, 1996.
SUMMARY AND CONCLUSIONS
1. The potentiation of glycine receptor-mediated taurine response (I tau ) by [alpha] 1 adrenoceptor activation was investigated in neurons freshly dissociated from the rat substantia nigra (SN) using a nystatin perforated patch recording. 2. Norepinephrine (NE) at a concentration of 10 -4 M in the presence of 10 -5 M yohimbine and 10 -5 M propranolol potentiated the peak amplitude of I tau (10 -3 M) at a holding potential of -40mV under voltage clamp conditions. NE could be substituted by phenylephrine at this potentiation. 3. This potentiation of the taurine response persisted in the treatment with pertussis toxin (500ng/ml) for 18 hrs. The intracellular application of GDP- [beta] S (100 [mu] M) with a conventional whole-cell patch recording mode abolished the effect of [alpha] 1 adrenoceptor activation on the I tau . 4, Staurosporine (10 -7 M) blocked the enhancement of I tau by 10 -4 M NE with 10 -5 M yohimbine and 10 -5 M propranolol. In addition, phorbol- 12-myristate 13-acetate (10 -5 M) potentiated I tau . 5. The intracellular application of 0.275U/ml protein kinase C (PKC) with a conventional whole cell configuration gradually increased the peak amplitude of I tau . On the other hand, intracellular perfusion either without PKC or with PKC plus 4 [mu] M PKC (19-36), a PKC inhibitor, did not potentiate I tau . 6. A single channel recording in a cell attached configuration revealed that NE (10 -4 M) with 10 -5 M yohimbine and 10 -5 M propranolol increased the total open time of the taurine-activated channel. This increase of the channel opening was antagonized by staurosporine (10 -7 M). 7. Neither tapsigargin (10 -6 M), LiCl (10 -4 M), trifluoperazine (10 -5 M) nor KN-62 (10 -4 M) applied in the perfusate were found to affect the potentiation of I tau by [alpha] 1 adrenoceptor. The intracellular application of inositol triphosphates (10 -4 M) in a conventional whole cell recording also had no effect on I tau . 8. These findings thus indicate that [alpha] 1 adrenoceptor coupled with pertussis-insensitive G protein increases the intracellular PKC activity, thus leading to an increase in the channel opening activated by taurine and an enhancement of the peak amplitude of I tau in the SN neurons. 

Received 5 February 1996; accepted in final form 11 June 1996.
APS Manuscript Number J94-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996