Abstract
A mathematical model was developed based on the putative functional role of adrenergic autoreceptors for quantifying processes of synaptic depression, facilitation, stabilization of PSP amplitude, and rise in this amplitude produced by increased stimulation rate. Synaptic depression and facilitation are brought about by activation of α- and β-adrenergic autoreceptors respectively. A "steady release zone" is found between curves of adrenergic autoreceptor activity and this is responsible for stabilizing noradrenaline release during a series of presynaptic impulses. Experimental findings on labeled noradrenaline (3H-NA) release from rat brain slices showed that adrenergic autoreceptors do in fact form a stable release zone responsible for autofacilitation and stabilization of3H-NA release produced by 5-fold consecutive K+ depolarizations of slices spaced 30 min apart. Lack of a stable release zone in curves showing adrenergic autoreceptor activity produces destabilization of3H-NA release. These curves (together with the stable release zone) shift in the direction of high noradrenaline concentrations when stimulus intensity is increased.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
