PT - JOURNAL ARTICLE AU - Anthony Lanahan AU - Gregory Lyford AU - Gail S. Stevenson AU - Paul F. Worley AU - Carol A. Barnes TI - Selective Alteration of Long-Term Potentiation-Induced Transcriptional Response in Hippocampus of Aged, Memory-Impaired Rats AID - 10.1523/JNEUROSCI.17-08-02876.1997 DP - 1997 Apr 15 TA - The Journal of Neuroscience PG - 2876--2885 VI - 17 IP - 8 4099 - http://www.jneurosci.org/content/17/8/2876.short 4100 - http://www.jneurosci.org/content/17/8/2876.full SO - J. Neurosci.1997 Apr 15; 17 AB - Normal human aging is associated with selective changes in cognition that are attributable, in part, to dysfunction of hippocampal pathways. Rodents also exhibit age-dependent hippocampal dysfunction that results in spatial memory deficits and a correlated reduction in the maintenance of long-term potentiation (LTP). Although suprathreshold stimulus protocols result in normal LTP induction in aged rats, the ability to sustain this increase in synaptic efficacy is reduced in the old animals. The maintenance phase of LTP is known to be dependent on rapid, transcriptional events, and recent studies have identified signal transduction mechanisms that link glutamate-induced responses at the synapse with transcriptional responses at the nucleus. To examine the integrity of these signaling pathways in aged hippocampus, we monitored the induction of a panel of immediate early genes (IEGs) that are known to be transcriptionally activated after LTP-inducing stimuli, using a “reverse Northern” strategy. Here we report that a broad representation of IEGs are similarly induced in awake, behaving young adult and aged, memory-impaired rats. This indicates a general preservation of these presumptive signaling pathways during the aging process. Induced levels ofc-fos mRNA, however, are significantly higher in the aged animals. These observations suggest that age-dependent hippocampal dysfunction may be associated with a selective change in the dynamic activity of signaling pathways upstream of c-fos, possibly involving calcium regulation.