海馬Racl活性與場景恐懼記憶的維持及遺忘
發(fā)布時間：2018-08-23 19:05
【摘要】：目的： 研究海馬Racl活性與場景恐懼記憶保持及遺忘的關(guān)系,探討PTSD病理性恐懼記憶不能遺忘的分子機(jī)制,為PTSD患者的治療提供新的理論指導(dǎo)。 方法： 實驗一：確定一個能誘導(dǎo)出相似學(xué)習(xí)曲線,但產(chǎn)生不同恐懼記憶的實驗方案。成年健康雄性SD大鼠在條件恐懼操作箱內(nèi)接受5次電擊強(qiáng)度為0.5、0.8或1.2mA的足底電擊,兩次電擊間隔時間為12s、122s或600s,24h后進(jìn)行恐懼記憶的檢測。 實驗二：探討0.8mA電擊強(qiáng)度學(xué)習(xí)后不同時間點產(chǎn)生的恐懼記憶及其與海馬Racl活性的關(guān)系。動物在條件恐懼操作箱內(nèi)接受5次電擊強(qiáng)度為0.8mA的足底電擊,兩次電擊間隔時間為12s,122s或600s,1h、24h或7d后進(jìn)行恐懼記憶的檢測,部分大鼠電擊結(jié)束后取材用于Rac-GTP的western blotting (WB)檢測及免疫組織化學(xué)(IF)染色。 實驗三：探討Racl的活性是否調(diào)節(jié)著大鼠的場景恐懼記憶。成年雄性SD大鼠在條件恐懼操作箱內(nèi)接受5次足底電擊,兩次電擊問隔時間為12s或122s,12s組大鼠電擊結(jié)束后立即雙側(cè)海馬CAl區(qū)予Racl抑制劑NSC23677,122s組大鼠雙側(cè)海馬CA1區(qū)予Racl激動劑CN04-A后行足底電擊,24h和(或)7天后進(jìn)行恐懼記憶的檢測。 實驗四：探討場景恐懼記憶的消退與海馬Racl活性的關(guān)系。成年雄性SD大鼠在條件恐懼操作箱內(nèi)接受5次足底電擊,24h后在條件恐懼操作箱內(nèi)接受6次每次5min的消退訓(xùn)練,兩次消退訓(xùn)練間隔時間為0min,10min或30min,消退結(jié)束后24h和16d進(jìn)行恐懼消退的檢測。部分大鼠消退結(jié)束后1h取材用于WB或IF。 實驗五：探討Racl活性是否直接調(diào)節(jié)場景恐懼記憶的消退。成年雄性SD大鼠在條件恐懼操作箱內(nèi)接受5次足底電擊,24h后在條件恐懼操作箱內(nèi)接受6次每次5min消退訓(xùn)練,兩次消退訓(xùn)練無間隔,消退訓(xùn)練結(jié)束后立即雙側(cè)海馬CA1區(qū)予Racl抑制劑NSC23677,24h和16d后進(jìn)行恐懼記憶的檢測。 實驗六：進(jìn)一步探討Racl活性是否調(diào)節(jié)著場景恐懼記憶的消退。成年雄性SD大鼠在條件恐懼操作箱內(nèi)接受5次足底電擊,24h后接受6次每次10min的強(qiáng)消退訓(xùn)練,兩次消退訓(xùn)練間隔時間為0min,10min或30min,消退結(jié)束后24h和16d進(jìn)行恐懼記憶的檢測；部分大鼠消退結(jié)束后1h取材用于WB或IF。結(jié)果： 實驗一：0.5mA電擊強(qiáng)度學(xué)習(xí)后,三組大鼠(12s,122s和600s)24小時恐懼記憶檢測無明顯差異,0.8mA或1.2mA電擊強(qiáng)度學(xué)習(xí)后,122s和600s組大鼠表現(xiàn)為場景恐懼記憶增強(qiáng),與12s組比具有統(tǒng)計學(xué)差異,此結(jié)果顯示0.8mA符合我們的實驗要求。 實驗二：學(xué)習(xí)后1小時恐懼記憶檢測結(jié)果顯示122s和600s組大鼠恐懼記憶明顯強(qiáng)于12s組,具有統(tǒng)計學(xué)差異；24h、7d恐懼記憶檢測結(jié)果類似1h,122s和600s組大鼠恐懼記憶顯著強(qiáng)于12s組。Western blot檢測結(jié)果顯示條件恐懼學(xué)習(xí)后0h時間點三組大鼠海馬Rac1-GTP的表達(dá)與正常對照大鼠相似；1h時間點間隔學(xué)習(xí)組(122s和600s組)大鼠海馬Rac1-GTP的表達(dá)顯著下調(diào),其中122s組低于600s組,集中學(xué)習(xí)組(12s)Rac1-GTP的表達(dá)類似正常組；24h時間點間隔學(xué)習(xí)組(122s和600s組)大鼠海馬Rac1-GTP的表達(dá)仍下調(diào),但與正常對照相比未達(dá)統(tǒng)計學(xué)差異,集中學(xué)習(xí)組Rac1-GTP的表達(dá)類似正常組。免疫熒光染色結(jié)果顯示正常大鼠Rac1-GTP的染色主要分布于神經(jīng)元的胞膜和突起,可見Rac1-GTP陽性的膠質(zhì)細(xì)胞及中間神經(jīng)元。集中學(xué)習(xí)組海馬CA1區(qū)Rac1-GTP的染色類似正常組,間隔學(xué)習(xí)組(122s和600s組)CA1區(qū)神經(jīng)元Rac1-GTP染色明顯減弱。此結(jié)果顯示間隔學(xué)習(xí)誘發(fā)海馬Racl活性下調(diào)及強(qiáng)的場景恐懼記憶。 實驗三：24h恐懼記憶檢測結(jié)果顯示予Racl抑制劑(12s+NSC)組大鼠恐懼記憶明顯強(qiáng)于予生理鹽水(12s+sal)組,達(dá)到122s組水平,差異具有顯著性,7d再次檢測結(jié)果類似24h�？謶謱W(xué)習(xí)后7d第一次行恐懼記憶檢測的結(jié)果同樣顯示Racl抑制劑(12s+NSC)組大鼠恐懼記憶明顯高于生理鹽水對照(12s+sal)組,達(dá)統(tǒng)計學(xué)差異；Racl激動劑CN04-A (122s+CN04-A)組大鼠24h恐懼記憶檢測顯著低于生理鹽水對照組(122s+sal),7d再次檢測結(jié)果類似24h。此結(jié)果顯示調(diào)節(jié)海馬Racl活性可調(diào)節(jié)大鼠場景恐懼記憶的強(qiáng)弱。 實驗四：結(jié)果顯示0min組(集中消退)恐懼消退訓(xùn)練時成績明顯優(yōu)于10min和30min組(間隔消退),消退訓(xùn)練后24h檢測結(jié)果顯示三組大鼠(0min、10min、30min)恐懼記憶均出現(xiàn)明顯消退,組間無差異；消退后16d再次檢測結(jié)果顯示0min組大鼠恐懼記憶進(jìn)一步降低,10min組部分恢復(fù),30min組幾乎完全恢復(fù),三組間達(dá)統(tǒng)計學(xué)差異。WB檢測結(jié)果顯示0min組大鼠海馬Racl-GTP表達(dá)顯著上調(diào),30mmin組輕度下調(diào)；免疫熒光染色結(jié)果顯示0min組大鼠海馬CA1區(qū)Rac1-GTP染色增強(qiáng),30min組染色減弱。此結(jié)果顯示集中消退促進(jìn)大鼠海馬Racl的激活及明顯的場景恐懼記憶消退。 實驗五：24h恐懼消退結(jié)果顯示Racl抑制劑(0min+NSC)組大鼠恐懼記憶高于生理鹽水組(0min+sal),但未達(dá)統(tǒng)計學(xué)差異,16d再次檢測結(jié)果顯示Racl抑制劑(0min+NSC)組大鼠恐懼記憶明顯高于生理鹽水(0min+sal)組,兩組間具有統(tǒng)計學(xué)差異。此結(jié)果顯示抑制海馬Rac l的激活清楚了集中消退誘發(fā)的場景恐懼記憶較弱效應(yīng)。 實驗六：結(jié)果顯示0min組(集中消退)大鼠消退訓(xùn)練時消退成績明顯優(yōu)于10min和30min組(間隔消退),消退訓(xùn)練后24h檢測結(jié)果顯示三組大鼠(0min、10min、30min)恐懼記憶均出現(xiàn)明顯消退,其中10min組略高于0min組和30min組,但組問無統(tǒng)計學(xué)差異；消退后16d檢測結(jié)果顯示三組大鼠的恐懼記憶均出現(xiàn)明顯消退。WB檢測結(jié)果顯示與正常對照組相比,0min和10min組大鼠海馬Racl-GTP的表達(dá)均上調(diào),其中0min組達(dá)統(tǒng)計學(xué)差異。免疫熒光染色顯示0min和10min組大鼠海馬CA1區(qū)Racl-GTP染色均增強(qiáng),30min組染色與正常對照組相似。此結(jié)果顯示促進(jìn)海馬Racl活性的恢復(fù)促進(jìn)了場景恐懼記憶的消退。結(jié)論： 抑制海馬Racl活性導(dǎo)致大鼠場景恐懼記憶增強(qiáng)及場景恐懼記憶消退受損,激活海馬Racl致使大鼠場景恐懼記憶減弱及場景恐懼記憶消退增加,海馬Racl活性水平調(diào)節(jié)著場景條件恐懼學(xué)習(xí)大鼠場景恐懼記憶的強(qiáng)弱及場景恐懼記憶的消退效果。Racl活性調(diào)節(jié)著果蠅記憶的遺忘,因此,我們提出海馬Racl的活性調(diào)節(jié)著大鼠場景恐懼記憶的維持與遺忘,本研究提示PTSD患者病理性恐懼記憶增強(qiáng)可能與其海馬Racl不能正常激活,導(dǎo)致恐懼記憶的遺忘受損有關(guān)。
[Abstract]:Objective:
To study the relationship between the activity of Racl in hippocampus and the retention and forgetting of scene fear memory, and to explore the molecular mechanism of PTSD pathological fear memory.
Method:
Experiment 1: To determine an experimental scheme which can induce similar learning curve but produce different fear memory. Adult healthy male SD rats were subjected to 5 plantar shocks of 0.5, 0.8 or 1.2 mA in the conditioned fear operating box. The interval between the two shocks was 12 s, 122 s or 600 s, and the fear memory was tested 24 hours later.
Experiment 2: To explore the relationship between fear memory and Racl activity in the hippocampus at different time points after 0.8 mA shock intensity learning. After completion, Western blotting (WB) detection and immunohistochemical staining (IF) were applied to Rac-GTP.
Experiment 3: To investigate whether the activity of Racl regulates the memory of scene fear in rats. Adult male SD rats received 5 plantar shocks in the conditioned fear operating box. The interval time between the two shocks was 12 s or 122 s. Rats in the 12s group were given Racl stimulation in bilateral hippocampal CAl area immediately after the shock. After CN04-A, the foot was electrocuted, and 24h and (or) 7 days later, the fear memory was detected.
Experiment 4: To investigate the relationship between the deterioration of scene fear memory and the activity of Racl in hippocampus.Adult male SD rats were subjected to five plantar shocks in the conditioned fear operating box. After 24 hours, they were subjected to six 5-minute withdrawal training sessions in the conditioned fear operating box. The intervals of the two withdrawal training sessions were 0 minutes, 10 minutes or 30 minutes. After the recession, they were terrorized for 24 hours and 16 days. Detection of fear extinction. After withdrawal of some rats, 1H was taken for WB or IF..
Experiment 5: To investigate whether Racl activity directly regulates the decline of scene fear memory. Adult male SD rats received five plantar shocks in the conditioned fear operating box. After 24 hours, they received six 5-minute regression training sessions in the conditioned fear operating box. There was no interval between the two regression training sessions. NSC23677,24h and 16d were used to detect fear memory.
Experiment 6: To further explore whether Racl activity regulates the decline of scene fear memory. Adult male SD rats were subjected to five plantar shocks in the conditioned fear manipulation box and six 10-minute intensive regression training sessions after 24 hours. The intervals of the two regression training sessions were 0 minutes, 10 minutes or 30 minutes. Fear memory was tested 24 hours and 16 days after the regression. After the extinction of some rats, 1H was taken for WB or IF..
Experiment 1: After 0.5mA shock intensity learning, there was no significant difference in 24-hour fear memory test among the three groups (12s, 122s and 600s). After 0.8mA or 1.2mA shock intensity learning, the rats in 122s and 600s groups showed enhanced scene fear memory, which was significantly different from that in 12S group. The results showed that 0.8mA met our experimental requirements.
Experiment 2: The results of fear memory test showed that the fear memory of rats in 122s and 600s groups was significantly stronger than that of 12S group, and the difference was statistically significant. The results of fear memory test in 24h and 7d groups were similar to that in 1h, 122s and 600s groups were significantly stronger than that in 12S group. Rac1-GTP expression in hippocampus was similar to that in normal control rats; Rac1-GTP expression in hippocampus was significantly down-regulated in 1-hour interval learning group (122 s and 600 s groups), of which 122 s group was lower than 600 s group, and Rac1-GTP expression in concentrated learning group (12s) was similar to that in normal group; Rac1-GTP expression in hippocampus was still down-regulated in 24-hour interval learning group (122 s and 600 s groups). The expression of Rac1-GTP in the central learning group was similar to that in the normal control group. Immunofluorescence staining showed that Rac1-GTP staining was mainly distributed in the membranes and processes of neurons, and Rac1-GTP positive glial cells and intermediate neurons were observed. Rac1-GTP staining in the hippocampal CA1 region of the central learning group was observed. Similar to the normal group, the Rac1-GTP staining of CA1 neurons in the interval learning group (122s and 600s) was significantly decreased. The results showed that interval learning induced a decrease in Racl activity in the hippocampus and a strong memory of scene fear.
Experiment 3: The results of 24-hour fear memory test showed that the fear memory of rats treated with Racl inhibitor (12s + NSC) was significantly stronger than that of rats treated with normal saline (12s + sal), and the difference was significant. The results of 7-day repeat test were similar to those of 24-hour repeat test. Fear memory of rats was significantly higher than that of normal saline group (12s+sal), and the fear memory of rats in Racl agonist CN04-A (122s+CN04-A) group was significantly lower than that of normal saline group (122s+sal) at 24h, and the result of repeat test was similar to that of normal saline group (122s+sal) at 7d.
Experiment 4: The results showed that the scores of fear subsidence training in 0-minute group were significantly better than those in 10-minute and 30-minute groups (interval subsidence). The results of 24 hours after subsidence training showed that the fear memory of the three groups of rats (0, 10, 30 minutes) had evident subsidence, and there was no difference between the three groups 16 days after subsidence. WB test showed that the expression of Racl-GTP in the hippocampus of rats in 0 min group was significantly up-regulated, but slightly down-regulated in 30 mmin group. Immunofluorescence staining showed that the expression of Rac1-GTP in CA1 area in the hippocampus of rats in 0 min group was enhanced and the staining was weakened in 30 min group. Regression promoted the activation of hippocampal Racl and the extinction of scene fear memory in rats.
Experiment 5: The results of 24-hour fear subsidence showed that the fear memory of rats in Racl inhibitor group (0 min + NSC) was higher than that of normal saline group (0 min + sal), but there was no significant difference. The results of 16-day re-test showed that the fear memory of rats in Racl inhibitor group (0 min + NSC) was significantly higher than that of normal saline group (0 min + sal). The activation of Rac L in hippocampus made clear the weak effect of fear of memory evoked by concentrated regression.
Experiment 6: The results showed that the extinction performance of 0-minute group was significantly better than that of 10-minute and 30-minute group (interval extinction). The results of 24 hours after extinction training showed that the fear memory of the three groups of rats (0, 10, 30 minutes) had evident extinction, of which 10-minute group was slightly higher than that of 0-minute group and 30-minute group, but there was no significant difference between the two groups. WB test showed that the expression of Racl-GTP in the hippocampus of rats in 0 min and 10 min groups was up-regulated compared with the normal control group, and the expression of Racl-GTP in the hippocampus of rats in 0 min and 10 min groups was statistically different. Immunofluorescence staining showed that the expression of Racl-GTP in the CA1 area of the hippocampus of rats in 0 min and 10 min groups was enhanced, and that in 30 min group was up-regulated. Similar to the normal control group, this result showed that the recovery of Racl activity in hippocampus promoted the decline of scene fear memory.
Inhibition of Racl activity in hippocampus leads to the enhancement of scene fear memory and the deterioration of scene fear memory in rats. Activation of Racl in hippocampus leads to the decrease of scene fear memory and the increase of scene fear memory in rats. Racl activity in hippocampus regulates the intensity of scene fear memory and the deterioration of scene fear memory in scene conditioned fear learning rats. Therefore, we suggest that the activity of hippocampal Racl regulates the maintenance and forgetting of scene fear memory in rats. This study suggests that the enhancement of pathological fear memory in PTSD patients may be related to the inability of hippocampal Racl to activate normally, resulting in impaired forgetting of fear memory.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2014
【分類號】：R749.7
[Abstract]:Objective:
To study the relationship between the activity of Racl in hippocampus and the retention and forgetting of scene fear memory, and to explore the molecular mechanism of PTSD pathological fear memory.
Method:
Experiment 1: To determine an experimental scheme which can induce similar learning curve but produce different fear memory. Adult healthy male SD rats were subjected to 5 plantar shocks of 0.5, 0.8 or 1.2 mA in the conditioned fear operating box. The interval between the two shocks was 12 s, 122 s or 600 s, and the fear memory was tested 24 hours later.
Experiment 2: To explore the relationship between fear memory and Racl activity in the hippocampus at different time points after 0.8 mA shock intensity learning. After completion, Western blotting (WB) detection and immunohistochemical staining (IF) were applied to Rac-GTP.
Experiment 3: To investigate whether the activity of Racl regulates the memory of scene fear in rats. Adult male SD rats received 5 plantar shocks in the conditioned fear operating box. The interval time between the two shocks was 12 s or 122 s. Rats in the 12s group were given Racl stimulation in bilateral hippocampal CAl area immediately after the shock. After CN04-A, the foot was electrocuted, and 24h and (or) 7 days later, the fear memory was detected.
Experiment 4: To investigate the relationship between the deterioration of scene fear memory and the activity of Racl in hippocampus.Adult male SD rats were subjected to five plantar shocks in the conditioned fear operating box. After 24 hours, they were subjected to six 5-minute withdrawal training sessions in the conditioned fear operating box. The intervals of the two withdrawal training sessions were 0 minutes, 10 minutes or 30 minutes. After the recession, they were terrorized for 24 hours and 16 days. Detection of fear extinction. After withdrawal of some rats, 1H was taken for WB or IF..
Experiment 5: To investigate whether Racl activity directly regulates the decline of scene fear memory. Adult male SD rats received five plantar shocks in the conditioned fear operating box. After 24 hours, they received six 5-minute regression training sessions in the conditioned fear operating box. There was no interval between the two regression training sessions. NSC23677,24h and 16d were used to detect fear memory.
Experiment 6: To further explore whether Racl activity regulates the decline of scene fear memory. Adult male SD rats were subjected to five plantar shocks in the conditioned fear manipulation box and six 10-minute intensive regression training sessions after 24 hours. The intervals of the two regression training sessions were 0 minutes, 10 minutes or 30 minutes. Fear memory was tested 24 hours and 16 days after the regression. After the extinction of some rats, 1H was taken for WB or IF..
Experiment 1: After 0.5mA shock intensity learning, there was no significant difference in 24-hour fear memory test among the three groups (12s, 122s and 600s). After 0.8mA or 1.2mA shock intensity learning, the rats in 122s and 600s groups showed enhanced scene fear memory, which was significantly different from that in 12S group. The results showed that 0.8mA met our experimental requirements.
Experiment 2: The results of fear memory test showed that the fear memory of rats in 122s and 600s groups was significantly stronger than that of 12S group, and the difference was statistically significant. The results of fear memory test in 24h and 7d groups were similar to that in 1h, 122s and 600s groups were significantly stronger than that in 12S group. Rac1-GTP expression in hippocampus was similar to that in normal control rats; Rac1-GTP expression in hippocampus was significantly down-regulated in 1-hour interval learning group (122 s and 600 s groups), of which 122 s group was lower than 600 s group, and Rac1-GTP expression in concentrated learning group (12s) was similar to that in normal group; Rac1-GTP expression in hippocampus was still down-regulated in 24-hour interval learning group (122 s and 600 s groups). The expression of Rac1-GTP in the central learning group was similar to that in the normal control group. Immunofluorescence staining showed that Rac1-GTP staining was mainly distributed in the membranes and processes of neurons, and Rac1-GTP positive glial cells and intermediate neurons were observed. Rac1-GTP staining in the hippocampal CA1 region of the central learning group was observed. Similar to the normal group, the Rac1-GTP staining of CA1 neurons in the interval learning group (122s and 600s) was significantly decreased. The results showed that interval learning induced a decrease in Racl activity in the hippocampus and a strong memory of scene fear.
Experiment 3: The results of 24-hour fear memory test showed that the fear memory of rats treated with Racl inhibitor (12s + NSC) was significantly stronger than that of rats treated with normal saline (12s + sal), and the difference was significant. The results of 7-day repeat test were similar to those of 24-hour repeat test. Fear memory of rats was significantly higher than that of normal saline group (12s+sal), and the fear memory of rats in Racl agonist CN04-A (122s+CN04-A) group was significantly lower than that of normal saline group (122s+sal) at 24h, and the result of repeat test was similar to that of normal saline group (122s+sal) at 7d.
Experiment 4: The results showed that the scores of fear subsidence training in 0-minute group were significantly better than those in 10-minute and 30-minute groups (interval subsidence). The results of 24 hours after subsidence training showed that the fear memory of the three groups of rats (0, 10, 30 minutes) had evident subsidence, and there was no difference between the three groups 16 days after subsidence. WB test showed that the expression of Racl-GTP in the hippocampus of rats in 0 min group was significantly up-regulated, but slightly down-regulated in 30 mmin group. Immunofluorescence staining showed that the expression of Rac1-GTP in CA1 area in the hippocampus of rats in 0 min group was enhanced and the staining was weakened in 30 min group. Regression promoted the activation of hippocampal Racl and the extinction of scene fear memory in rats.
Experiment 5: The results of 24-hour fear subsidence showed that the fear memory of rats in Racl inhibitor group (0 min + NSC) was higher than that of normal saline group (0 min + sal), but there was no significant difference. The results of 16-day re-test showed that the fear memory of rats in Racl inhibitor group (0 min + NSC) was significantly higher than that of normal saline group (0 min + sal). The activation of Rac L in hippocampus made clear the weak effect of fear of memory evoked by concentrated regression.
Experiment 6: The results showed that the extinction performance of 0-minute group was significantly better than that of 10-minute and 30-minute group (interval extinction). The results of 24 hours after extinction training showed that the fear memory of the three groups of rats (0, 10, 30 minutes) had evident extinction, of which 10-minute group was slightly higher than that of 0-minute group and 30-minute group, but there was no significant difference between the two groups. WB test showed that the expression of Racl-GTP in the hippocampus of rats in 0 min and 10 min groups was up-regulated compared with the normal control group, and the expression of Racl-GTP in the hippocampus of rats in 0 min and 10 min groups was statistically different. Immunofluorescence staining showed that the expression of Racl-GTP in the CA1 area of the hippocampus of rats in 0 min and 10 min groups was enhanced, and that in 30 min group was up-regulated. Similar to the normal control group, this result showed that the recovery of Racl activity in hippocampus promoted the decline of scene fear memory.
Inhibition of Racl activity in hippocampus leads to the enhancement of scene fear memory and the deterioration of scene fear memory in rats. Activation of Racl in hippocampus leads to the decrease of scene fear memory and the increase of scene fear memory in rats. Racl activity in hippocampus regulates the intensity of scene fear memory and the deterioration of scene fear memory in scene conditioned fear learning rats. Therefore, we suggest that the activity of hippocampal Racl regulates the maintenance and forgetting of scene fear memory in rats. This study suggests that the enhancement of pathological fear memory in PTSD patients may be related to the inability of hippocampal Racl to activate normally, resulting in impaired forgetting of fear memory.
【學(xué)位授予單位】：中南大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2014
【分類號】：R749.7
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