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iNature
The hippocampal CA2 region plays a key role
in social memory.
The encoding of this memory involves afferent activity
from the suprathalamic nucleus (SuM) to CA2.
However, the neural circuits needed to consolidate newly encoded social memories remain unknown
.
On October 21, 2022, Chen Xiaowei and Qin Han of the Army Medical University published a joint communication entitled "REM sleep-active hypothalamic neurons may contribute to hippocampal social-memory consolidation" online in Neuron (IF=19).
The research paper suggests that REM sleep-active hypothalamic neurons may contribute to social memory consolidation
in the hippocampus.
The study used circuit-specific optical and single-cell electrophysiology to record mice to explore the role of sleep in social memory consolidation and its underlying circuit mechanisms
.
The study found that SuM neurons projected to CA2 were highly active during REM sleep, but not during
non-REM sleep or restful wakefulness.
REM sleep-selective photogene silencing in these neurons impairs social memory
.
In contrast, silencing SuM neurons of REM sleep activity projected into the dentate gyrus had no effect
on social memory.
Thus, the study provides causal evidence that hypothalamic neurons projected into the REM sleep activity of CA2 are particularly needed for social memory consolidation
.
in the astrocyte subset of the auditory cortex by imaging two-photon Ca2+ in head-fixed mice and fibrophotometry in free-moving mice.
The study demonstrates that fear learning leads to de novo induction
of sound-induced Ca2+ transients in these astrocytes.
The reactivity of astrocytes persisted for several days along with fear memories and disappeared
in animals that experienced learned cryogenic extinction.
Deletion of the conditional gene for α7-nAChRs in astrocytes significantly impairs the persistence
of fear memories.
In summary, the study found that learn-acquired, α7-nAChR-dependent astrocyte responsiveness is a component of the cell matrix at the basis of memory persistence (click to read).
Social memory is a fundamental cognitive process that enables animals to recognize and remember members of their kind, often impaired
in neurological disorders.
The circuit mechanisms of how social memory is encoded, expressed, and consolidated are only partially understood
.
There is growing evidence that hippocampal CA2 neurons can respond to external social novelty signals and are necessary to
encode social memory.
These CA2 signals are transmitted to ventral CA1, where social memories
may be stored.
A recent study found that glutamatergic neuronal circuits from the supratypal nucleus of the hypothalamus papillary nucleus (SuM) to the CA2 region help detect new social signals
.
However, while photogene activation of the SuMCA2 circuit can affect social memory expression, inhibition of the same circuit does not appear to affect the same memory expression, suggesting that other unknown circuits may contribute to
the expression of social memory.
This possible redundancy at the circuit level raises a key question about how and through which specific circuits social memory is consolidated
in the hippocampus.
Mechanistic pattern diagram (Figure from Neuron) The study's understanding of the role of sleep in memory consolidation has been greatly improved
by the recent development of high-precision recording and manipulation methods.
Both non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM) sleep are thought to be essential
for memory consolidation.
These memory consolidation processes rely on multiple neural circuits
in the hippocampus and extra-hippocampal regions.
The prevailing view in the field is that the reactivation of hippocampal neurons during sharp wave ripples (SWRs) during non-REM sleep promotes memory consolidation
.
This reactivation in CA3-induced SWRs is necessary for
spatial memory consolidation.
In fact, in the case of spatial memory, REM sleep-dependent neuronal activity of sleep stage-specific perturbed septum or hippocampal dentate gyrus (DG) impairs its consolidation
.
The study combines opticalCa2+ recording, single-cell electrophysiology, and optogenetics in the hypothalamic-hippocampal circuit, defined under various behavioral conditions, to explore the possible role
of mouse NREM and REM sleep in consolidating social memory.
The study found a small group of CA2 projection neurons in the hypothalamus SuM that were active only during REM sleep and not during
non-REM sleep or restful wakefulness (QW).
Photogene silencing experiments reveal the important role
of these neurons in consolidating social memory.
In contrast, a distinct set of hypothalamic SuM neurons projected into DG was also highly active during REM sleep, selectively helping to consolidate spatial memory rather than social memory
.
Overall, the findings decisively expand the understanding of REM sleep memory function and highlight the importance of
clusters of hypothalamic neurons in consolidating hippocampal memories of specific content.
In addition, the data from the study contributed to the understanding
of the functional role of SuM.
Original link: (22) 00809-1
—END—
The content is 【iNature】
