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Advanced Neurology MiR-195 regulates MS-dCA1 neural circuit in CBH rat

A B C D

E F G H

Figure 7. Upregulation of septal miR-195 expression improves the spatial learning and memory ability of CCH rats. (A) Comparison of swimming speed
among sham, 2VO, and 2VO + lenti-pre-miR-195 rats. (B) Comparison of the latency to hidden platform in the second, third, and fourth quadrant on the
1 day from rats of the three groups. (C–E) Comparison of the latency to hidden platform in the second, third, and fourth quadrant during the training
st
phase from rats of the three groups. (F and G) Differences of the platform crossing (F) and the percentage of swimming in the goal quadrant (G) during the
investigation trials from rats of the three groups. (H) Samples of swimming traces of the rats from the three groups in probe trial. n = 6. *P < 0.05 versus
sham rats. P < 0.05 versus 2VO rats.
#
+
+
induced the loss of Chat , GAD67 , or PV neurons in MS. or therapeutic drug for early AD or VaD. However, the
+
Next, we injected lenti-pre-miR-195 specific into the MS specific molecular mechanism of miR-195 modulating
region but not the hippocampus of 2VO rats and found that MS-dCA1 neural circuit function needs to be further
upregulation of miR-195 in MS region but not hippocampus investigated.
prevented the loss of neurons in the MS following CCH.
Taken together, the downregulation of septal miR-195 5. Conclusions
expression could impair the function of MS-dCA1 neural In our study, we found that knockdown of miR-195 in the
circuit that was associated with the neuronal losses in the MS region can impair MS-dCA1 neural circuit function,
MS area. while upregulation of miR-195 can rescue the impaired
Recent studies using both cellular and animal models function of MS-dCA1 neural circuit and spatial memory
demonstrated that miR-195 has positive effects on anti- ability in CCH rats. This provides a valuable reference for
apoptosis in injured neurons by suppressing Sema3A/ future anti-dementia therapy involving miR-195.
Cdc42/JNK signaling, promotes neural regeneration by
promoting neural stem cell proliferation and migration, Acknowledgments
and has anti-inflammation action by blocking the NF-κB None.
pathway . Furthermore, the cerebral stroke damage of
[27]
rats was improved by intravenously injecting miR-195 Funding
in the acute stage . These studies suggest that miR- This work was supported by the National Science and
[27]
195 may have the potential in the treatment of cerebral Technology Innovation 2030 - Major program of “Brain
ischemic diseases. Our previous studies found that Science and Brain-Like Research” 2022ZD0211804, the
upregulation of miR-195 expression in hippocampal National Natural Science Foundation of China (81870849
and cortical regions rescued the spatial cognitive ability to J.A.), the Key Research and Development Program
in 8-week 2VO rats by inhibiting Aβ deposition, tau of Heilongjiang Province (GA21C009 to J.A.), and
hyperphosphorylation, microglial polarization, synaptic Heilongjiang Touyan Innovation Team Program.
dysfunction, and neuronal death [7-10] . In the present study,
we demonstrated that upregulation of miR-195 expression Conflict of interest
through the injection of lenti-pre-miR-195 into MS region
successfully reversed the impaired function of MS-dCA1 The authors declare that they have no conflicts of interest
neural circuit as well as neuronal loss, and even attenuate to report.
the declined spatial learning memory ability induced Author contributions
by CCH. All these studies provide solid evidence that
miR-195 may have the potential to be a biomarker and/ Conceptualization: Jing Ai

Volume 1 Issue 2 (2022) 11 https://doi.org/10.36922/an.v1i2.116