NDLI: Reflections on glycogen and β-amyloid: why does glycogenolytic β$_{2}$-adrenoceptor stimulation not rescue memory after β-amyloid?

Content Provider	Springer Nature Link
Author	Gibbs, Marie
Copyright Year	2014
Abstract	Normally noradrenaline release ~30 min after training in the day-old chick is essential for memory consolidation by simultaneously increasing both glycogenolysis, by its stimulation of β$_{2}$-adrenergic (AR) receptors, and glycogen synthesis, by its stimulation of α$_{2}$-AR receptors in astrocytes. At the same time noradrenaline stimulation of β$_{3}$-AR receptors increases glucose uptake solely in astrocytes. Intracerebral injection of small oligomeric β-amyloid protein (Aβ$_{1–42}$) (Aβ) 45 min before one-trial bead discrimination learning in day-old chicks abolishes consolidation of memory 30 min post-learning. The ensuing memory loss can be rescued by injection of selective β$_{3}$- and β$_{2}$-AR agonists (CL316243 and zinterol), which also have the ability to consolidate weakly-reinforced learning into long-term memory. However, although CL316243 rescues Aβ-induced memory loss over a similar time period to when it consolidates weak learning (up to 25 min post training), zinterol is effective over a more limited time period and unexpectedly it does not rescue at the time it promotes glycogenolysis. Injection of Aβ into the hippocampus and the locus coeruleus (LoC) also produces similar memory deficits and injection of both AR agonists into a cortical area can rescue memory from LoC Aβ. We have previously shown that β$_{3}$-AR stimulation increases astrocytic glucose uptake and have suggested there may be sensitization or upregulation of the receptor. Since β$_{2}$-AR stimulation does not rescue memory at the time it promotes glycogenolysis, but the receptor does not appear to be impaired, it is suggested that Aβ may be causing an impairment in the synthesis of readily available glycogen.
Starting Page	345
Ending Page	352
Page Count	8
File Format	PDF
ISSN	08857490
Journal	Metabolic Brain Disease
Volume Number	30
Issue Number	1
e-ISSN	15737365
Language	English
Publisher	Springer US
Publisher Date	2014-05-09
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Glycogen Memory formation Beta-amyloid β-adrenergic receptors Neurosciences Neurology Metabolic Diseases Biochemistry Oncology
Content Type	Text
Resource Type	Article
Subject	Biochemistry Neurology (clinical) Cellular and Molecular Neuroscience

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