Pharmacological HDAC3 inhibition alters memory updating in young and old male mice.

Long-term memories are not stored in a stable state but must be flexible and dynamic to maintain relevance in response to new information. Existing memories are thought to be updated through the process of reconsolidation, in which memory retrieval initiates destabilization and updating to incorporate new information. Memory updating is impaired in old age, yet little is known about the mechanisms that go awry.

Pharmacological HDAC3 inhibition alters memory updating in young and old mice.

Long-term memories are not stored in a stable state but must be flexible and dynamic to maintain relevance in response to new information. Existing memories are thought to be updated through the process of reconsolidation, in which memory retrieval initiates destabilization and updating to incorporate new information. Memory updating is impaired in old age, yet little is known about the mechanisms that go awry.

The clock gene Per1 may exert diurnal control over hippocampal memory consolidation.

The circadian system influences many different biological processes, including memory performance. While the suprachiasmatic nucleus (SCN) functions as the brain's central pacemaker, downstream "satellite clocks" may also regulate local functions based on the time of day. Within the dorsal hippocampus (DH), for example, local molecular oscillations may contribute to time-of-day effects on memory.

The clock gene Per1 is necessary in the retrosplenial cortex-but not in the suprachiasmatic nucleus-for incidental learning in young and aging male mice.

Aging impairs both circadian rhythms and memory, though the relationship between these impairments is not fully understood. Circadian rhythms are largely dictated by clock genes within the body's central pacemaker, the suprachiasmatic nucleus (SCN), though these genes are also expressed in local clocks throughout the body. As circadian rhythms can directly affect memory performance, one possibility is that memory deficits observed with age are downstream of global circadian rhythm disruptions stemming from the SCN.

Apoaequorin differentially modulates fear memory in adult and aged rats.

Introduction: Cognitive deficits during aging are pervasive across species and learning paradigms. One of the major mechanisms thought to play a role in age-related memory decline is dysregulated calcium (Ca ) homeostasis. Aging is associated with impaired function of several calcium-regulatory mechanisms, including calcium-binding proteins that normally support intracellular Ca regulation.

Infralimbic Estradiol Enhances Neuronal Excitability and Facilitates Extinction of Cocaine Seeking in Female Rats a BDNF/TrkB Mechanism.

Women are more susceptible to developing cocaine dependence than men, but paradoxically, are more responsive to treatment. The potent estrogen, 17β-estradiol (E), mediates these effects by augmenting cocaine seeking but also promoting extinction of cocaine seeking through E's memory-enhancing functions. Although we have previously shown that E facilitates extinction, the neuroanatomical locus of action and underlying mechanisms are unknown.