Neuraminidase Inhibition Primes Short-Term Depression and Suppresses Long-Term Potentiation of Synaptic Transmission in the Rat Hippocampus

Neuraminidase (NEU) is a key enzyme that cleaves negatively charged sialic acid residues from membrane proteins and lipids. Clinical and basic science studies have shown that an imbalance in NEU metabolism or changes in NEU activity due to various pathological conditions parallel with behavior and c...

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Bibliographic Details
Published in:Journal of neural transplantation & plasticity 2015-01, Vol.2015 (2015), p.466-475-141
Main Authors: Isaeva, Elena, Sydorenko, Vadym, Maximyuk, Oleksandr, Isaev, Dmytro, Romanov, Arthur, Savotchenko, Alina, Holmes, Gregory L.
Format: Article
Language:English
Subjects:
Acids
Animals
Depression, Mental
Experiments
Hippocampus (Brain)
Hippocampus - drug effects
Hippocampus - enzymology
Hippocampus - physiology
Mental depression
Neural transmission
Neuraminidase - antagonists & inhibitors
Neuraminidase - physiology
Neurogenesis
Neuronal Plasticity - drug effects
Neuropeptides
Physiology
Rats
Rats, Wistar
Short term
Software
Synaptic Transmission - drug effects
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Summary:Neuraminidase (NEU) is a key enzyme that cleaves negatively charged sialic acid residues from membrane proteins and lipids. Clinical and basic science studies have shown that an imbalance in NEU metabolism or changes in NEU activity due to various pathological conditions parallel with behavior and cognitive impairment. It has been suggested that the decreases of NEU activity could cause serious neurological consequences. However, there is a lack of direct evidences that modulation of endogenous NEU activity can impair neuronal function. Using combined rat entorhinal cortex/hippocampal slices and a specific inhibitor of NEU, 2-deoxy-2,3-dehydro-N-acetylneuraminic acid (NADNA), we examined the effect of downregulation of NEU activity on different forms of synaptic plasticity in the hippocampal CA3-to-CA1 network. We show that NEU inhibition results in a significant decrease in long-term potentiation (LTP) and an increase in short-term depression. Synaptic depotentiation restores LTP in NADNA-pretreated slices to the control level. These data suggest that short-term NEU inhibition produces the LTP-like effect on neuronal network, which results in damping of further LTP induction. Our findings demonstrate that downregulation of NEU activity could have a major impact on synaptic plasticity and provide a new insight into the cellular mechanism underlying behavioral and cognitive impairment associated with abnormal metabolism of NEU.
ISSN:0792-8483
2090-5904
1687-5443
DOI:10.1155/2015/908190