ISSN:
1432-1912
Keywords:
Noradrenaline
;
Dopamine
;
Utilization
;
Synthesis
;
Central alpha-adrenoreceptors
;
Presynaptic receptors
;
Postsynaptic receptors
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary 1. FLA 136 [4-amino-3-(2,6-dichlorobenzylidenehydrazino)-1,2,4-triazol] did not change the hindlimb flexor reflex of spinal rats, but it reduced the clonidine-induced increase in this reflex at high doses. 2. The α-methyltyrosine-induced disappearance of noradrenaline in the rat central nervous system was decelerated by FLA 136, with a peak effect after 15 mg/kg i.p. The accumulation of Dopa following decarboxylase inhibition was inhibited by FLA 136 (15 mg/kg i.p.) in a noradrenaline-predominant region (brain stem). The effect on the utilization appeared to be greater than that on the synthesis in agreement with a slight increase observed in the concentration of noradrenaline in the brain and the spinal cord. 3. FLA 136 reduced the α-methyltyrosine-induced disappearance of dopamine, decreased the Dopa accumulation following decarboxylase inhibition in the dopamine-rich corpus striatum and increased the concentration of dopamine. These effects might be secondary to inhibition of the noradrenergic neurotransmission. 4. Yohimbine almost completely inhibited the effect of FLA 136 on the utilization and on the synthesis of noradrenaline whereas phenoxybenzamine was much less effective on the change in the utilization. Yohimbine and phenoxybenzamine were about equipotent, however, in accelerating the disappearance of noradrenaline produced by α-methyltyrosine alone. 5. FLA 136 does not stimulate the postsynaptic α-adrenoreceptors mediating the increase in flexor reflex activity but it probably decelerates the utilization of noradrenaline by a stimulation of another kind of α-adrenoreceptors sensitive to yohimbine. The latter receptors might occur on the noradrenergic neurones (presynaptic receptors).
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00500894
