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

A D E F

B C

G H I

Figure 4. MiR-195 improves the basic neurotransmission process and presynaptic function of MS-dCA1 neural circuit in CCH rats. (A) Schedule of the
experiment plan. (B) The miR-195 level in the basal forebrain of 2VO rats treated with lenti-pre-miR-195. (C) Differences of minimum stimulus intensity
for triggering a measurable response of MS-dCA1 circuit in rats among sham, 2VO, and 2VO + lenti-pre-miR-195 rats. (D) Sample trace of fEPSP in the
hippocampal dCA1 with 8 and 20 V stimulations. (E) Comparison of input-output curves in the dCA1 region among three groups of rats. (F) Differences
of the fEPSP amplitude with 8- and 20-V stimulations in each group. (G) Samples of MS-dCA1 fEPSP trace after paired pulses stimuli with 20, 40, and 70
ms intervals between in rats from different groups. (H) The changes of PPR induced by lenti- pre-miR-195 injection. (I) The bar graph shows the largest
PPR in rats from different groups. n = 6. *P < 0.05 versus sham rats. P < 0.05 versus 2VO rats.
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in the hippocampi of 2VO rats were significantly decreased, three non-target quadrants of the localization navigation
which were recovered by lenti-pre-miR-195 injection test (Figure 7C-E). On the 6 day of the spatial exploration
th
(Figure 6F and G, Figure S2). These results suggest that test, we found that injection of lenti-pre-miR-195 reversed
upregulation of miR-195 expression can improve the the number of platform crossings (Figure 7F) and the
function of MS-dCA1 neural circuit of 2VO rats and percentage of swimming time in the target quadrant in 2VO
prevent the death of ChAT , GAD67 ,and PV neuron. rats (Figure 7G). The above results showed that upregulation
+
+
+
of miR-195 expression can attenuate the impairment of
3.4. Upregulation of miR-195 expression in the MS spatial learning memory ability in CCH rats (Figure 7H).
improves the spatial learning and memory ability of
CCH rats 4. Discussion
Our previous study found that exogenous supplementation With the aging of population and the prevalence of
of miR-195 in the hippocampus could prevent 2VO-induced cerebrovascular diseases, the incidence of VaD is increasing
cognitive decline . Therefore, we would like to evaluate year by year. However, the development of therapeutic drugs
[7]
[39]
whether upregulation of miR-195 expression in MS has the has not progressed much . At present, many scientists
similar effect using the Morris water maze test. First, we recognize that improving the function of neural circuits is
compared the swimming speed among the three groups a potential therapeutic approach to treat neurodegenerative
to exclude the influence of locomotor abnormalities on diseases [40,41] . Here, we found that loss-of-function of miR-195
the experimental results. The data showed that there was impaired the MS-dCA1 neural circuit in rats, while exogenous
no difference among the three groups (Figure 7A). On the supplementation of miR-195 rescued the dysfunction of the
1 day of the cued learning trial, basal forebrain injection MS-dCA1 neural circuit and declined spatial memory in
st
of lenti-pre-miR-195 reduced the latency to the platform CCH rats. We thus present in this paper a candidate strategy
of 2VO rats in the third and fourth quadrants (Figure 7B). for alleviating the impaired septohippocampal neural circuit
Exogenous supplementation of miR-195 also reduced the during the pathogenesis of dementia.
time spent by 2VO rats to find the hidden platform on the As the largest cerebral cholinergic nucleus and theta
2 –5 days after being released into the tank in all of the rhythm “pacemaker,” the basal forebrain forms a neural
nd
th
Volume 1 Issue 2 (2022) 8 https://doi.org/10.36922/an.v1i2.116