TY - JOUR
T1 - Short-term environmental enrichment enhances synaptic plasticity in hippocampal slices from aged rats
AU - Stein, Liana R.
AU - O'Dell, Kazuko A.
AU - Funatsu, Michiyo
AU - Zorumski, Charles F.
AU - Izumi, Yukitoshi
N1 - Publisher Copyright:
© 2016 IBRO.
PY - 2016/8/4
Y1 - 2016/8/4
N2 - Age-associated changes in cognition are mirrored by impairments in cellular models of memory and learning, such as long-term potentiation (LTP) and long-term depression (LTD). In young rodents, environmental enrichment (EE) can enhance memory, alter LTP and LTD, as well as reverse cognitive deficits induced by aging. Whether short-term EE can benefit cognition and synaptic plasticity in aged rodents is unclear. Here, we tested if short-term EE could overcome age-associated impairments in induction of LTP and LTD. LTP and LTD could not be induced in the CA1 region of hippocampal slices in control, aged rats using standard stimuli that are highly effective in young rats. However, exposure of aged littermates to EE for three weeks enabled successful induction of LTP and LTD. EE-facilitated LTP was dependent upon N-methyl-. d-aspartate receptors (NMDARs). These alterations in synaptic plasticity occurred with elevated levels of phosphorylated cAMP response element-binding protein and vascular endothelial growth factor, but in the absence of changes in several other synaptic and cellular markers. Importantly, our study suggests that even a relatively short period of EE is sufficient to alter synaptic plasticity and molecular markers linked to cognitive function in aged animals.
AB - Age-associated changes in cognition are mirrored by impairments in cellular models of memory and learning, such as long-term potentiation (LTP) and long-term depression (LTD). In young rodents, environmental enrichment (EE) can enhance memory, alter LTP and LTD, as well as reverse cognitive deficits induced by aging. Whether short-term EE can benefit cognition and synaptic plasticity in aged rodents is unclear. Here, we tested if short-term EE could overcome age-associated impairments in induction of LTP and LTD. LTP and LTD could not be induced in the CA1 region of hippocampal slices in control, aged rats using standard stimuli that are highly effective in young rats. However, exposure of aged littermates to EE for three weeks enabled successful induction of LTP and LTD. EE-facilitated LTP was dependent upon N-methyl-. d-aspartate receptors (NMDARs). These alterations in synaptic plasticity occurred with elevated levels of phosphorylated cAMP response element-binding protein and vascular endothelial growth factor, but in the absence of changes in several other synaptic and cellular markers. Importantly, our study suggests that even a relatively short period of EE is sufficient to alter synaptic plasticity and molecular markers linked to cognitive function in aged animals.
KW - Aging
KW - Environmental enrichment
KW - Long-term depression
KW - Long-term potentiation
KW - N-methyl-d-aspartate receptor
UR - http://www.scopus.com/inward/record.url?scp=84973514630&partnerID=8YFLogxK
U2 - 10.1016/j.neuroscience.2016.05.020
DO - 10.1016/j.neuroscience.2016.05.020
M3 - Article
C2 - 27208617
AN - SCOPUS:84973514630
SN - 0306-4522
VL - 329
SP - 294
EP - 305
JO - Neuroscience
JF - Neuroscience
ER -