EFFECT OF INTRACAROTID ADMINISTRATION OF ADENOSINE ON THE ACTIVITY OF AREA POSTREMA NEURONS IN BARODENERVATED RATS
10.3321/j.issn:0371-0874.1999.06.010
- VernacularTitle:颈动脉内注射腺苷对去缓冲神经大鼠最后区神经元放电的影响
- Author:
SHUANG CHEN
1
;
RUI-RONG HE
Author Information
1. Hebei Medical University
- Keywords:
adenosine;
area postrema;
spontaneous single-unit discharge;
8-phenyltheophylline;
8-cyclopentyl-1,3-dipropylxanthine;
glibenclamide
- From:
Acta Physiologica Sinica
1999;(6):667-674
- CountryChina
- Language:Chinese
-
Abstract:
To observe the effect of intracarotid administration of adenosine on the electrical activity of area postrema (AP) neurons, 76 spontaneous active units were recorded from 45 sino-aortic denervated Sprague-Dawley rats using extracellular recording technique. The results obtained are as follows. (1) Following intracarotid administration of adenosine (Ado, 25 μg/kg), the discharge rate of 29 out of 42 units decreased markedly from 6.26±0.75 to 4.74±0.76 spikes/s (P<0.01), whereas that of 6 units increased from 4.13±0.77 to 4.72±0.83 spikes/s (P<0.05), and the other 7 showed no response. Blood pressure (BP) and heart rate (HR) were unaltered throughout the experiment. (2) 8-phenyltheophylline (8-PT, 15 μg/kg), a nonselective adenosine receptor antagonist, completely blocked the inhibitory effect of Ado in 10 units. (3) Selective A1 adenosine receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 50 μg/kg), blocked the effect of Ado in 12 units to a remarkable extent. (4) Glibenclamide (500 μg/kg), a blocker of ATP-sensitive potassium channel, abolished the effect of Ado in 12 units. The above results indicate that Ado can inhibit spontaneous electrical activity of AP neurons, which is mediated by adenosine A1-receptor with the involvement of ATP-sensitive potassium channels.
