Chronic caffeine consumption prevents diabete-induced neuropathy in hipocampus of NONCNZO10/LTJ mice
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1
University of Coimbra, Center for Neuroscience, Portugal
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2
University of Coimbra, Inst Biochemistry, Portugal
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3
University of Coimbra, Faculty of Medicine, Portugal
Diabetes is associated with modified brain function, namely with cognitive deficits. More than understanding the underlying mechanism, it is important to devise novel strategies to alleviate diabetes-induced cognitive deficits. Caffeine (a mixed antagonist of adenosine A1 and A2A receptors) is a promising candidate since caffeine consumption reduces the risk of diabetes and prevents memory deficits caused by different noxious stimuli. We used a novel model of type 2 diabetes, NONcNZO10/LtJ mice, to investigate the behavioural, neurochemical and morphological modifications present in the hippocampus and test if caffeine consumption might prevent these changes. Eleven months-old NONcNZO/LtJ mice, kept under an 11% fat diet, became diabetic (enhanced plasma levels of glucose) and displayed decreased spontaneous alternation in the Y- maze (with no change in locomotion assessed in an open field arena) accompanied by decreased density of nerve terminal markers (synaptophysin and SNAP-25 evaluated by Western blot analysis) and increased astrogliosis (GFAP immunoreactivity both in Western blot analysis and in immunohistochemical staining of brain sections) compared to their wild type littermates kept under the same diet. Furthermore, diabetic mice displayed up-regulated A2A receptors and down-regulated A1 receptors in the hippocampal nerve terminal membranes, evaluated by receptor binding assays with selective antagonists of A1 (3H-DPCPX) and A2A receptors (3H-SCH58261). Caffeine consumption (1 g/L) in the drinking water during 4 months, with onset at 7 months, was devoid of effects in control (non-diabetic mice) but restored cognitive performance and abrogated the diabetes-induced loss of nerve terminals and astrogliosis. These results show that chronic caffeine consumption prevents synaptic dysfunction and cognitive impairment in type 2 diabetes. (Supported by FCT and Fundacao Oriente).
Conference:
11th Meeting of the Portuguese Society for Neuroscience, Braga, Portugal, 4 Jun - 6 Jun, 2009.
Presentation Type:
Poster Presentation
Topic:
Abstracts
Citation:
Duarte
JM,
Carvalho
RA and
Cunha
RA
(2009). Chronic caffeine consumption prevents diabete-induced neuropathy in hipocampus of NONCNZO10/LTJ mice.
Front. Neurosci.
Conference Abstract:
11th Meeting of the Portuguese Society for Neuroscience.
doi: 10.3389/conf.neuro.01.2009.11.088
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Received:
10 Aug 2009;
Published Online:
10 Aug 2009.
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Correspondence:
Rodrigo A Cunha, University of Coimbra, Center for Neuroscience, Alicante, Portugal, cunharod@gmail.com