High sucrose consumption induces memory impairment in rats associated with electrophysiological modifications but not with metabolic changes in the hippocampus.

C. Lemos, D. Rial, F.Q. Gonçalves, J. Pires, H.B. Silva, F.C. Matheus, A.C. da Silva, J.M. Marques, R.J. Rodrigues, I. Jarak, R.D. Prediger, F. Reis, R.A. Carvalho, F.C. Pereira, R.A. Cunha
Neuroscience. 2016-02-01; 315: 196-205
DOI: 10.1016/j.neuroscience.2015.12.018

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High sugar consumption is a risk factor for metabolic disturbances leading to
memory impairment. Thus, rats subject to high sucrose intake (HSu) develop a
metabolic syndrome and display memory deficits. We now investigated if these
HSu-induced memory deficits were associated with metabolic and
electrophysiological alterations in the hippocampus. Male Wistar rats were
submitted for 9 weeks to a sucrose-rich diet (35% sucrose solution) and
subsequently to a battery of behavioral tests; after sacrifice, their hippocampi
were collected for ex vivo high-resolution magic angle spinning (HRMAS) metabolic
characterization and electrophysiological extracellular recordings in slices. HSu
rats displayed a decreased memory performance (object displacement and novel
object recognition tasks) and helpless behavior (forced swimming test), without
altered locomotion (open field). HRMAS analysis indicated a similar hippocampal
metabolic profile of HSu and control rats. HSu rats also displayed no change of
synaptic transmission and plasticity (long-term potentiation) in hippocampal
Schaffer fibers-CA1 pyramid synapses, but had decreased amplitude of long-term
depression in the temporoammonic (TA) pathway. Furthermore, HSu rats had an
increased density of inhibitory adenosine A1 receptors (A1R), that translated
into a greater potency of A1R in Schaffer fiber synapses, but not in the TA
pathway, whereas the endogenous activation of A1R in HSu rats was preserved in
the TA pathway but abolished in Schaffer fiber synapses. These results suggest
that HSu triggers a hippocampal-dependent memory impairment that is not
associated with altered hippocampal metabolism but is probably related to
modified synaptic plasticity in hippocampal TA synapses.

Auteurs Bordeaux Neurocampus