Signalling effect of elevated potassium concentrations and monoamines on brain energy metabolism at the cellular level.
The effects of elevated K+ concentrations and monoamine transmitters on different cell types in the CNS and on different subcellular structures in these cells are reviewed. Pronounced differences exist in the metabolic processes that are stimulated by excess K+ and by adrenergic agonists, e.g., noradrenaline. An elevation in the extracellular K+ concentration appears to enhance neuronal-astrocytic interaction by stimulating metabolic processes involved in (1) the promotion of supply of precursors for transmitter glutamate, and (2) reestablishment of resting ion distribution following neuronal excitation. The monoamine transmitters stimulate energy production and Na+,K(+)-ATPase activity in astrocytes in a complex manner and, in so doing, facilitate their role in ion regulation. However, in contrast to excess K+, they do not enhance the production of astrocytic precursors for neuronal glutamate production. Emphasis is placed on possible profound differences in metabolic effects on excitatory and inhibitory neurotransmission and on the importance of stimulation of glycolytic metabolism in astrocytes versus oxidative metabolism in neurons.
Huang
R
R
Department of Pharmacology, University of Saskatchewan, Saskatoon, Canada.
Peng
L
L
Chen
Y
Y
Hajek
I
I
Zhao
Z
Z
Hertz
L
L
D000818:Animals; D015306:Biogenic Monoamines / Q000502:physiology*; D001921:Brain / Q000166:cytology* / Q000378:metabolism; D004734:Energy Metabolism / Q000502:physiology*; D006801:Humans; D011188:Potassium / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology*
D015306:Biogenic Monoamines; D011188:Potassium