Format

Send to

Choose Destination
Neurobiol Aging. 2012 Mar;33(3):627.e13-26. doi: 10.1016/j.neurobiolaging.2011.04.005. Epub 2011 Jun 12.

Learning capabilities and CA1-prefrontal synaptic plasticity in a mice model of accelerated senescence.

Author information

1
División de Neurociencias, Universidad Pablo de Olavide, Sevilla, Spain.

Abstract

SAMP8 mice represent a suitable model of accelerated senescence as compared with SAMR1 animals presenting normal aging. Five-month-old SAMP8 mice presented reflex eyelid responses like those of SAMR1 controls, but were incapable of acquiring classically-conditioned eye blink responses in a trace (230 milliseconds [ms] of interstimulus interval) paradigm. Although SAMP8 mice presented a normal paired-pulse facilitation of the hippocampal CA1-medial prefrontal synapse, an input/output curve study revealed smaller field excitatory postsynaptic potentials (fEPSPs) in response to strong stimulations of the CA1-prefrontal pathway. Moreover, SAMP8 mice did not show any activity-dependent potentiation of the CA1-prefrontal synapse across the successive conditioning sessions shown by SAMR1 animals. In addition, SAMP8 mice presented a functional deficit during an object recognition test, continuing to explore the familiar object when controls moved to the novel one. Alert behaving SAMP8 mice presented a significant deficit in long-term potentiation (LTP) at the CA1-medial prefrontal synapse. According to the present results, SAMP8 mice present noticeable functional deficits in hippocampal and prefrontal cortical circuits directly related with the acquisition and storage of new motor and cognitive abilities.

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center