ISSN:
1432-1912
Keywords:
Cerebral cortex
;
Noradrenaline release
;
Presynaptic α-receptors
;
Calcium ions
;
Hyperpolarization
;
Tetrodotoxin
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Brain cortical slices were superfused with Krebs-Ringer media and the effects of oxymetazoline (an α-adrenoceptor agonist) and phentolamine (an α-antagonist) on depolarization-induced 3H-NA release were examined. Depolarization was effected by various K+-concentrations or by electrical pulses. The effects of the α-receptor agents on stimulated 3H-NA overflow appeared to be dependent on the strength of the depolarizing stimulus. Thus, at low K+-concentrations (13 or 26 mM) oxymetazoline decreased and phentolamine increased the stimulated overflow, while at 56 mM K+ little or no modulation was found. The agents acting on α-receptors modulated 3H-NA release in a dose-dependent way (5 · 10−8–10−5 M). The lack of modulation by oxymetazoline of 3H-NA release induced by 56 mM K+ seems not to be due to a high concentration of NA released into the synaptic cleft, since reduction of the endogenous NA level by pretreatment with α-methyl-para-tyrosine did not reveal such modulation. However, oxymetazoline was found to decrease 56 mM K+-induced 3H-NA release effectively, if the Ca2+-concentration in the medium was lowered from 1.2 to 0.2 mM. This suggests that α-receptor mediated modulation of release may occur as a result of a change in Ca2+-availability to the depolarization-secretion process. In addition, hyperpolarization of nerve endings might be involved in the modulatory process, as concluded from calculations of the (theoretical) trans-membrane potential at various K+-concentrations. Although the α-receptors modulating NA release seem to be localized presynaptically, their precise location remains uncertain. Experiments with tetrodotoxin suggested that the α-receptor mediated modulation does not operate via a local interneuronal loop.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00498553
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