D-Amphetamine Causes Dual Actions on Catecholamine Release from the Rat Adrenal Medulla

The present study was designed to examine the effect of d-amphetamine on CA release from the isolated perfused model of the rat adrenal gland, and to establish its mechanism of action. D- amphetamine (10~100microM), when perfused into an adrenal vein of the rat adrenal gland for 60 min, enhanced the CA secretory responses evoked by ACh (5.32x10-3 M), excess K+ (5.6x10-2 M, a membrane depolarizer), DMPP (10-4 M, a selective neuronal nicotinic Nn-receptor agonist) and McN-A-343 (10-4 M, a selective M1-muscarinic agonist) only for the first period (4 min), although it alone has weak effect on CA secretion. Moreover, d-amphetamine (30microM) in to an adrenal vein for 60 min also augmented the CA release evoked by BAY-K-8644, an activator of the dihydropyridine L-type Ca2+ channels, and cyclopiazonic acid, an inhibitor of cytoplasmic Ca2+ ATPase only for the first period (4 min). However, in the presence of high concentration (500microM), d-amphetamine rather inhibited the CA secretory responses evoked by the above all of secretagogues. Collectively, these experimental results suggest that d-amphetamine at low concentrations enhances the CA secretion from the rat adrenal medulla evoked by cholinergic stimulation (both nicotininc and muscarinic receptors) as well as by membrane depolarization, but at high concentration it rather inhibits them. It seems that d-amphetamine has dual effects as both agonist and antagonist at nicotinic receptors of the isolated perfused rat adrenal medulla, which might be dependent on the concentration. It is also thought that these actions of d-amphetamine are probably relevant to the Ca2+ mobilization through the dihydropyridine L-type Ca2+ channels located on the rat adrenomedullary chromaffin cell membrane and the release of Ca2+ from the cytoplasmic store.

Noradrenergic Drugs in Cerebral Infarction and Rehabilitation Therapy / 中国康复理论与实践

@#The efficacy of physical therapy for cerebral infarction is outstanding. This paper is to introduce that if physical therapy is combined with NA-gic drug-d-amphetamine,the latter will promote recovery of motor function in stroke patients. D-amphetamine can also enhance recovery from aphasia and poor motivation syndrome in patients after ischemic stroke. The recovery of hemiplegia in strok patient after treatment of d-amphetamine is proposed owing to dispel inhibition in the contralateral cerebellar hemisphere. This corresponds to the concept of diachisis.

Effect of D-amphetamine on apoptosis and GAP-43 expression of rat brain cells after focal cerebral ischemia / 第三军医大学学报

Objective To observe the protection of D-amphetamine on rat brain after focal cerebral ischemia.Methods The unilateral middle cerebral artery occlusion(MCAO) models were established by using Koizumi's method.TUNEL was applied to detect quantitatively brain cell apoptosis at 1st,3rd and 6th week after operation.Immunohistochemical staining and RT-PCR were respectively used to detect the expression of growth-associated protein 43(GAP-43) and GAP-43 mRNA around ischemic area.Results Apoptosis of brain cells reduced evidently in the group treated with D-amphetamine.GAP-43 protein detection demonstrated statistically significant increase in immunoreaction product as determined by optical density measurements in D-amphetamine treated group compared with the group without any agent treatment.The same results appeared in RT-PCR product.Conclusion D-amphetamine can reduce brain cell apoptosis and promote GAP-43 expression.