Increasing age reduces expression of long-term depression and dynamic range of transmission plasticity in CA1 field of the rat hippocampus

Abstract

Abstract--Long-term depression, depotentiation and long-term potentiation of field excitatory postsynaptic potentials in the CA1 field of the hippocampus were studied in slices from two-, 12-, 24-and 36-week-old rats. Long-term potentiation was induced by stimulating afferent fibres for 1 s at 100 Hz. Long-term depression was induced either by stimulating the afferent pathways twice for 15 min at 1 Hz (protocol 1), giving in total 1800 pulses, or by stimulating the fibres at 5 min intervals twice at 1 Hz for 5 min followed by 5 min stimulation at 5 Hz (protocol 2), giving in total 2100 pulses. We found significant long-term depression in slices of all groups stimulated with protocol 1; however, the magnitude of long-term depression in slices from 24-and 36-week-old rats was significantly lower than that in slices from two-and 12-week old rats, although there was no such difference in the magnitude of long-term potentiation between slices. Stimulation protocol 2 induced long-term depression only in slices from twoand 12-week-old rats. Comparison of the dynamic range of transmission plasticity in slices from two-and 36-week-old rats, calculated as the difference between the nearly saturated long-term potentiation and nearly saturated depotentiation, revealed a significantly smaller dynamic range in slices from 36-week-old rats in comparison with slices from two-week-old animals. The decrease in the dynamic range in slices from 36-week-old rats was due to a diminished capacity to depotentiate the nearly saturated long-term potentiation and not due to a decreased long-term potentiation expression in these slices. In contrast to long-term depression, in which the slope of the field excitatory postsynaptic potentials consistently and significantly decreased below the baseline level, the nearly saturated depotentiation did not decrease below the original, pre-long potentiation baseline level.The results demonstrate that increasing age reduces expression of long-term depression and the dynamic range of transmission plasticity.1998 IBRO. Published by Elsevier Science Ltd.

Reduction in glutamate uptake is associated with extrasynaptic NMDA and metabotropic glutamate receptor activation at the hippocampal CA1 synapse of aged rats

“…Under our experimental conditions, the amount of LTD induced by 1 Hz stimulation was not different between young and aged rats in agreement with other studies indicating no change in LTD during aging (Kumar & Foster, 2007;Billard, 2010;Kollen et al 2010). However, others demonstrate an enhanced (Norris et al, 1996;Kumar & Foster, 2005) or a decreased susceptibility to LTD either in middleaged (Kamal et al, 1998) or aged animals (Lee et al, 2005). These discrepancies result from differences in methodology, including age, strain of the animals and the Ca ⁄ Mg ratio of the recording solution.…”

Contribution of the D-Serine-dependent pathway to the cellular mechanisms underlying cognitive aging

“…It is worth noting that VGCC activation is not related to memory acquisition, but only to the retention of information (Borroni et al, 2000) and that the excessive activation of the L-subtype of VGCCs may be detrimental to memory formation (Liu et al, 2003). Furthermore, we have shown that LTP is rapidly depotentiated in adult but not in aged animals, using an LFS protocol (Kamal et al, 1998). Since LTP saturation disrupts memory formation in young rats (Moser and Moser, 1999), a reduced capacity of hippocampal networks to be reset from potentiated levels may also constitute a synaptic mechanism contributing to cognitive aging.…”

Prenatal administration of morphine decreases CREBSerine‐133 phosphorylation and synaptic plasticity range mediated by glutamatergic transmission in the hippocampal CA1 area of cognitive‐deficient rat offspring

“…This finding appears to raise a possibility that prenatal exposure to morphine could significantly alter cytosolic downstream mechanisms, such as protein phosphatases that were important for the expression of LTD (Malenka, 1994). In addition, the magnitude of LTP and LTD and/or depotentiation can be seen as reflecting the dynamic range of long-term modulation of transmission strength in glutamatergic synapses (Baskys and Malenka, 1991;Kamal et al, 1998). This dynamic range may be of significance for information processing by the hippocampus.…”