| Objection:From the two different view of memory ethology and temporal coding ofhippocampal neuron, the preventing effect of low-frequency repetitive transcranialmagnetic stimulation (rTMS) on dysfunction of memory for Alzheimer's disease (AD)rat model is studied.Methods:(1)Making model: 33 normal SD rats were randomly divided into two groups. One isthe control(n=8), the left(n=25) would be microinjected amyloid protein into bilateralMeynert nucleus to make AD rat model. From the AD rat model, 15 rats would bechose to be given rTMS, as rTMS group.(2)Giving rTMS: 3 sessions of rTMS with frequency of 1Hz were given to the rTMSgroup, with each session including 20 trains with 20 pules of it during continuous 5days. The time of inter-session is 2day. The stimulation intensity is 0.5 Tesla.(3)Morris water maze test: Befor and after making model, and a third times, aftergiving rTMS, Morris water maze behavioral test, including place navigation andSpatial probe test, were performed among normal control group, AD group and rTMsgroup.(4)Getting spontaneous spike in hippocampat CA3 neuron: Original signal of all threegroups were recorded using microelectrode extracellular recording technology.Spontaneous spike were chose via Chart5.0 software after pre-disposal.(5)Temporal coding of interspike interval of spontaneous spike: The qualitativeindex——interspike interval was quantified in scatterplot coding and joint intervalhistogram coding by using IMAX which is the max of interspike interval in 70%intensive point of interspike interval.(6)Statistics: Repeated Two-ways ANOVA analysis was used to compare the result ofplace navigation of three groups; t test was used to compare the result of spatial probetest and the IMAX of three groups. P＜0.05 means there have statistic meaning. Results:(1) AD rat model: AD rat model were chose as followed criteria. The average latencyof all normal rats were 9.17±1.89s, the criteria was 11.06s, and the average latency ofeach rat microinjecting Aβcompared with it. Finally 16 out of 25 rats were regardedas AD rat model. The success rate was 64%.(2)Morris water maze behavioral test:①Out of syn comparison among three groups:In the place navigation, F is 7.58(P＜0.01). The average latency of AD was muchlonger than that of normal group (P＜0.01); the average latency of rTMS group wasmuch decreased than that of normal group and AD group (P＜0.01).In spatial probe test, the swim time in platform quadrant, the swim distance precentin platform quadrant, the memory mark of 3 circles in AD group and rTMS groupwere much lower than that of normal group (P＜0.05); the corresponding parameter inrTMS group were much lower than that of AD group(P＜0.05).③Synchronic comparison among three groups:In place navigation, F between AD and normal group is 14.48 (P＜0.01); F betweenrTMS group and AD group is 5.64(P＜0.05).In spatial probe test, the swim time in platform quadrant, the swim distance precentin platform quadrant, the memory mark of 3 circles in AD group were much lowerthan that of normal group (P＜0.05); the corresponding parameter in rTMS group weresimilar with that of AD group(P＞0.05).(3)ISI coding of neuron spike among three groups:①ISI histogram coding: Comparing with normal spike, the percent of 100ms intervalof ISI in rTMS group decreased markedly, while increased highly in the intervallarger than 200ms; the percent of 50ms,100ms,150ms interval of ISI in AD group decreased highly, much increased in the interval larger than 200ms. Comparing withAD group, the percent of 100ms interval of ISI in rTMS group increased markedly,similar at the interval of 150ms,200ms,250ms,decreased highly at the interval largerthan 300ms. (All: P＜0.05)②ISI scatterplot coding: Imax in normal group, AD group and rTMS group wererespectively 0.123±0.005ms, 0.163±0.013ms, 0.239±0.032ms. P＜0.01③ISI histogram coding: Imax in normal group, AD group and rTMS group wererespectively 0.193±0.019ms, 0.253±0.020ms, 0.387±0.072ms. P＜0.01(4)average frequency coding: The average frequency coding of normal group, ADgroup and rTMS group were respectively 9.51±0.86Hz, 7.54±0.55Hz, 5.31±0.50Hz.P＜0.01Conclusion:(1) The AD rat model was successfully made via microinjecting Aβinto bilateralMeynert nucleus, with rate of 64%, which support the cholinergic damaged theoryand Aβdeposited theory.(2)Learning and memory of the AD rat model decreased markedly, and improvedafter rTMS verified by the result of place navigation and spatial probe test of Morriswater maze, indicating that rTMS can repair the failed learning and memory.(3)From the ISI coding mode of three group rats, the spike mode of AD rats presentlower spike frequency and larger interspike interval. While the spike mode of rTMSrats shows increasing spike frequency and shorter interspike interval; The ISIdistribution of AD rats scattered more than normal rats, while rTMS rats show theassembly trend toward normal rats.(4)The ultrastructure of hippocampus: There are bulks of cellular necrosis, neurite edema, and lack of tigroid body, much vacuole, swelled and dissolved chondrosome,and rare microfilament in hippocampus of AD rat model. After rTMS, edemalocalized, and conferted neurite including chondrosome with cristal could be seenhere and there around edema area.(5) rTMS can improve the learning and memory function of AD rat. The probablereason is that rTMS could promote the expression of BDNF, c-fos and sAPP; andincrease the activation of AMPA and NMDA in hippocampus. In all, rTMS canimprove the memory failure in AD rat.
|
PDF Full Text Request