[Abstract Title]. - Society for Neuroscience

Topic: F.02.h. Memory modulation, consolidation, and reconsolidation
Support: NARSAD
National Institute of Mental Health F31 MH 081621-A1
National Institute of Mental Health R01 MH 74736
National Institute of Mental Health R01 MH 65635
Title: Temporal requirement of hippocampal BDNF for long-term memory consolidation
Authors: *D. Y. CHEN, G. POLLONINI, C. M. ALBERINI;
Neurosci., Mount Sinai Sch. Med., New York, NY
Abstract: Newly learned information becomes long-term memory through a process known as
consolidation, which depends on an initial phase of transcription and translation. However, little
is known about the temporal progression of the molecular requirements of consolidation. The
neurotrophin, brain-derived neurotrophic factor (BDNF) is known to play an important role in
memory consolidation. Recently, BDNF has been also reported to mediate memory maintenance
as dorsal hippocampal injection of function-blocking anti-BDNF antibodies 12 hours after
inhibitory avoidance (IA) training disrupted memory retention at 7 days, but not at 2 days after
training. To determine the role of hippocampal BDNF in long-term memory consolidation, using
2 distinct strategies, we disrupted hippocampal BDNF functions before or at several times points
after IA training. We found that dorsal hippocampal injection of either function-blocking anti-
BDNF antibody or BDNF scavenger (TrkB-Fc) 15 minutes before training blocked the
consolidation of long-term memory as the animals were amnesic when tested at 2 days after
training. The effect was persistent at 7 days after training and the memory did not recover
following a reminder foot-shock. Furthermore, dorsal hippocampal injection of the same anti-
BDNF antibody or TrkB-Fc immediately after training only modestly decreased long-term
memory retention at 2 days after training, but significantly disrupted the memory retention at 7
days after training. This memory impairment was not restored after a subsequent foot-shock
reminder. Conversely, disruption of hippocampal BDNF function at 2 and 7 days after IA
training did not affect memory retention. These results suggest that IA memory consolidation
critically requires hippocampal BDNF not only during training, but also after training when it is
needed to complete the consolidation process. Potential molecular mechanism underlying the
hippocampal BDNF-mediated long-term memory consolidation will be discussed.
Disclosures: D.Y. Chen , None; G. Pollonini, None; C.M. Alberini, None.
Poster
295. Memory Consolidation, Reconsolidation, Anatomy, and Mechanisms