Neuroscientists who study memory have long believed that when we recall these memories, our brains turn on the same hippocampal circuit that was activated when the memory was originally formed. However, MIT neuroscientists have now shown, for the first time, that recalling a memory requires a “detour” circuit that branches off from the original memory circuit.
Susumu Tonegawa, Dheeraj Roy, Takashi Kitamura are the lead authors of the paper, which appears in the Aug. 17 online edition of Cell. The researchers note the following. Episodic memories are formed and retrieved through distinct hippocampal pathways.
It is generally thought that formation and retrieval of a memory are accomplished by activation and reactivation of memory-holding cells (engram cells), respectively, by a largely common set of neural circuits that convey relevant sensory and processed information. However, this hypothesis has not been well studied.
Here, we have shown that optogenetic inhibition of dSub during recall, but not during encoding, impairs behavioral performance in three hippocampal-dependent memory paradigms: CFC, trace fear conditioning, and conditioned place preference. The activity of dSub neurons is capable of regulating memory recall bidirectionally: its inhibition impairs recall, and its activation enhances recall. To our knowledge, this is the first identification of the specific causal role of dSub neurons in episodic memory recall.
Another possible merit of distinct circuits for encoding and retrieval of memory may be to perform rapid memory updating. When a new salient stimulus (such as footshock) is delivered while a subject is recalling a previously acquired memory, the original memory is known to be modified (or updated) by incorporating the concurrently delivered salient stimulus.