The hippocampus plays a selective role in the retrieval of detailed contextual memories.

BACKGROUND: It is widely believed that the hippocampus plays a temporary role in the retrieval of episodic and contextual memories. Initial research indicated that damage to this structure produced amnesia for newly acquired memories but did not affect those formed in the distant past. A number of recent studies, however, have found that the hippocampus is required for the retrieval of episodic and contextual memories regardless of their age. These findings are currently the subject of intense debate, and a satisfying resolution has yet to be identified. RESULTS: The current experiments address this issue by demonstrating that detailed memories require the hippocampus, whereas memories that lose precision become independent of this structure. First, we show that the dorsal hippocampus is preferentially activated by the retrieval of detailed contextual fear memories. We then establish that the hippocampus is necessary for the retrieval of detailed memories by using a context-generalization procedure. Mice that exhibit high levels of generalization to a novel environment show no memory loss when the hippocampus is subsequently inactivated. In contrast, mice that discriminate between contexts are significantly impaired by hippocampus inactivation. CONCLUSIONS: Our data suggest that detailed contextual memories require the hippocampus, whereas memories that lose precision can be retrieved without this structure. These findings can account for discrepancies in the literature-memories of our distant past can be either lost or retained after hippocampus damage depending on their quality-and provide a new framework for understanding memory consolidation.

CREB regulates excitability and the allocation of memory to subsets of neurons in the amygdala.

The mechanisms that determine how information is allocated to specific regions and cells in the brain are important for memory capacity, storage and retrieval, but are poorly understood. We manipulated CREB in a subset of lateral amygdala neurons in mice with a modified herpes simplex virus (HSV) and reversibly inactivated transfected neurons with the Drosophila allatostatin G protein-coupled receptor (AlstR)/ligand system. We found that inactivation of the neurons transfected with HSV-CREB during training disrupted memory for tone conditioning, whereas inactivation of a similar proportion of transfected control neurons did not. Whole-cell recordings of fluorescently tagged transfected neurons revealed that neurons with higher CREB levels are more excitable than neighboring neurons and showed larger synaptic efficacy changes following conditioning. Our findings demonstrate that CREB modulates the allocation of fear memory to specific cells in lateral amygdala and suggest that neuronal excitability is important in this process.