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No Exit: China’s State Surveillance over People Who Use Drugs

How can I buy cocaine online in Chengdu

Official websites use. Share sensitive information only on official, secure websites. Correspondence should be addressed to Xiaobo Cen at xbcen scu. Author contributions: X. Li, W. Zhang, Y. Li, Jie Zhang, Z. Zhao performed research; W. Li wrote the paper. SfN exclusive license. The development, persistence and relapse of drug addiction require drug memory that generally develops with drug administration-paired contextual stimuli. Adult hippocampal neurogenesis AHN contributes to cocaine memory formation; however, the underlying mechanism remains unclear. Male mice hippocampal expression of Tau was significantly decreased during the cocaine-associated memory formation. Genetic overexpression of four microtubule-binding repeats Tau 4R Tau in the mice hippocampus disrupted cocaine memory by suppressing AHN. Collectively, 4R Tau modulates cocaine memory formation by disrupting AHN, suggesting a novel mechanism underlying cocaine memory formation and provide a new strategy for the treatment of cocaine addiction. Previous studies have suggested that adult hippocampal neurogenesis AHN plays a role in cocaine memory formation. Here, we showed that Tau was significantly downregulated in the hippocampus in the cocaine memory formation. Tau knock-out KO promoted AHN in the hippocampal dentate gyrus DG , resulting in the enhanced memory formation evoked by cocaine-cue stimuli. In contrast, genetically overexpressed 4R Tau in the hippocampus disrupted cocaine-cue memory by suppressing AHN. In addition, 4R Tau interacted directly with phosphoinositide 3-kinase PI3K -p85 and hindered its nuclear translocation, eventually repressing PI3K-AKT signaling, which is essential for hippocampal neuronal proliferation. Drug addiction is characterized by compulsive drug seeking behaviors, repeated attempts at abstinence and high rates of relapse. Similar to the other memories, long-lasting drug-associated memory formation is closely associated with the rewarding effect of drugs and environmental cues related to drug exposure. Re-exposure to drug-associated contextual cues reactivates drug memory and promotes compulsive drug-seeking behaviors during the period of abstinence Wolf, An understanding of the neurobiological mechanisms underlying drug memory formation is important for exploring effective strategies for drug addiction treatment and relapse prevention. The hippocampus plays a critical role in the formation of drug-associated contextual memory Deschaux et al. In this process, new neurons undergo continual proliferation, migration, differentiation and integration into the existing neuronal circuitry of the dentate gyrus DG , eventually modulating the formation and updating of hippocampus-dependent memory Lazarov and Hollands, ; Toda and Gage, AHN has been recently considered an important factor in the establishment and maintenance of addiction memory Castilla-Ortega et al. When animals are subjected to pro-AHN manipulations, such as exercise, the subsequently acquired cocaine memory becomes stronger and more resistant to extinction Mustroph et al. However, the precise mechanism underlying the role of AHN in cocaine memories formation has not been completely elucidated. Tau is a microtubule-associated scaffolding protein whose major function is the stabilization of microtubules and promotion of microtubule polymerization Guo et al. Tau isoforms containing either three or four microtubule-binding repeats 3R Tau or 4R Tau exhibit approximately equal expression in the normal adult human brain; however, 4R Tau is the predominant isoform expressed in the adult murine brain. Tau was recently shown to be associated with the proliferation of newborn hippocampal granule neurons that require a high level of cytoskeletal plasticity to divide, proliferate and differentiate in response to external stimuli Pallas-Bazarra et al. During early brain development, 3R Tau predominates in the neonatal brain and exhibits a lower affinity for microtubules than 4R Tau. Therefore, 3R Tau participates in the morphologic differentiation and migration of immature neurons. In contrast, 4R Tau binds with higher affinity to microtubules, thereby maintaining the cytoskeletal stability and neuronal integrity Lu and Kosik, ; Tuerde et al. To date, the role of Tau isoforms in the formation of drug-associated memory is unknown. In the present study, our findings reveal a novel mechanism by which 4R Tau modulates cocaine memory formation by regulating AHN. All experimental procedures and use of the animals were conducted in accordance with the guidelines established by the Association for Assessment and Accreditation of Laboratory Animal Care and the Institutional Animal Care and Use Committee of Sichuan University. All efforts were made to minimize the suffering of the mice. Mice were acclimated for one week before experiments and habituated to handling for 2 d before each behavioral test. Conditioned place preference CPP and self-administration were used to assess cocaine-cue memory formation. All behavioral experiments were performed in a double-blind manner. The CPP test was conducted using a standard three-chambered apparatus equipped with two large conditioning compartments black and white that differed in their flooring bar and grid and a small middle chamber gray, smooth PVC floor that connected the two large compartments. Before each session, animals were habituated to the chambers for at least 10 min for a continuous 2 d. Baseline preference was assessed by placing the mice in the middle chamber and allowing them to habituate the entire chambers freely for 15 min; an initial measurement of baseline preference was defined as the time spent in the black chamber subtracted from the time spent in the white chamber Time pre-test. Animals were randomly assigned to two groups and trained for 6 d with alternating injections of cocaine 20 or 2. They were confined to the conditioning or unconditioning chambers for 30 min after the injection and then returned to their home cages. On the test day, the animals were placed in the middle compartment and the time of spent in the two compartments was recorded for 15 min. We defined the time spent in the black chamber minus the time spent in the white chamber as Time test. The CPP scores were calculated by Time test minus Time pre-test and defined as the extent of the shift in preference after cocaine injection. Mice were exposed to cocaine as described for consolidation training, and then they were not confined to the conditioning or unconditioning chambers, but were returned to their home cages without any context exposure to the test apparatus. On the test day, mice were placed in the middle connecting chamber, and the time spent in each chamber was calculated as described in previous experiments to evaluate the CPP score. The food CPP test used a similar apparatus and methodology as described above. During the food conditioning sessions, the food-induced CPP group was transferred to the food-paired chamber 2—3 g of food were placed in the chamber for 30 min. In the non-food conditioning sessions, mice were assigned to the non-food-paired chamber for 30 min. After conditioning training for 3 h, animals were only fed once daily 1 h. The alternating sessions of conditioning were repeated 3 times a total of 6 d. On the test day, mice were placed in the central chamber and allowed to freely explore both compartments for 15 min; the time spent in each chamber was recorded to calculate the CPP score. Mice were exposed to the CPP protocol, and the test day course was repeated each day until the preference of the cocaine group for the conditioned compartment had returned to the habituation baseline. The distance traveled was measured daily, and automated tracking was performed with EthoVision 7. The distal end of the catheter was threaded through the skin on the back of the mice and exited the skin via a stainless-steel guide cannula RWD Life Science. After surgery, catheters were flushed with 0. One week after recovering from surgery, animals were trained to self-administer intravenous injections of cocaine 0. The response to the active poke produced a cocaine injection and was accompanied with a blue light stimulus for 20 s and an audible tone for a 5-s timeout period. At the same time, the inactive poke failed to inject the drug and produce conditioning stimuli. The locomotor activity was measured as the distance traveled. Before the test, the baseline locomotor activity was not statistically different between groups. The distance traveled was measured daily for one week, and automated tracking was performed with EthoVision 7. Cocaine was purchased from the National Institute for the Control of Pharmaceutical and Biological Products and dissolved in saline. Dental cement was used to anchor the guide cannula and the stainless-steel stylet blocker was inserted into each cannula to prevent blockage and infection. All mice were used for subsequent training after one week of recovery from surgery. Point mutations of arginine , proline and proline to alanine were synthesized in the murine full-length Tau amino acid sequence, as these three residues are normally important for the interaction of PI3K-p85 SH3 domains, and their mutation has previously been shown to attenuate PI3K-p85 binding to human 2N4R Tau Reynolds et al. The vector was confirmed by sequencing. After shaving the hair and cleaning the incision site with medical-grade alcohol, the scalp was incised to expose the skull and the connective tissue was gently removed from the skull surface with cotton swabs. After each injection, the syringe was left in place for an additional 5 min and then slowly withdrawn to allow the virus to diffuse. Mice recovered for at least three weeks before behavioral tests. Mice were killed by rapid decapitation at the end of the behavioral tests. Brain tissues and cells were lysed and proteins were extracted using a mammalian cell and tissue extraction kit K, Biovision containing phosphatase inhibitors , Roche according to the manufacturer's protocols. The total protein concentration was analyzed with a Bradford assay kit P, Beyotime. Twenty micrograms protein were loaded and separated on 10 or On the next day, after three washes with TBST for 15 min, the blots were incubated with the secondary antibody at room temperature for 2 h. The sections were washed with TBS 3 times 10 min each and incubated with a blocking solution containing 0. On the next day, the sections were also washed with TBS After another three washes with TBST, sections were coverslipped with anti-fade mounting medium containing DAPI H, Vector , and confocal images were acquired with a laser confocal microscope Nikon. The corresponding DG areas and cell numbers were determined using Image J software National Institutes of Health to assess the cell densities. Immunohistochemistry was then performed. Mice with misplaced cannulas were excluded from the statistical analysis. On the next day, coverslips were washed three times with PBS and incubated with the fluorescent dye-conjugated secondary antibodies for 1 h at room temperature. Afterwards, the retrieved brains were immersed in equal parts of Solutions A and B containing potassium dichromate, mercuric chloride, and potassium chromate and stored at room temperature for two weeks in the dark. Tissues were subsequently rinsed, placed in the cryoprotectant solution, and stored at room temperature for at least 72 h in the dark before cutting. The brain slices were cut in the coronal plane at approximately a mm thickness with the freezing microtome Leica. Tissue sections were placed on poly-D-lysine-coated slides and dried in the dark. Finally, the sections were defatted with a xylene substitute and coverslipped with DPX mounting medium , Sigma. Images were acquired from prepared slides using a confocal microscope Olympus. At least 20 neurons per mouse were selected for dendritic spine analysis in each group three mice per group , and the average of spine density of each mouse was collected for statistical analysis. Neuronal reconstruction was performed using a confocal microscope, and dendrite spine density was measured using ImageJ software National Institutes of Health. After the incubation, the protein supernatants extracted using the mammalian cell and tissue extraction kit were collected, and the protein concentration was determined using a Bradford assay kit. Elution buffer was used to elute the bound antigen, and neutralization buffer was used to neutralize the low pH. The supernatants were collected for Western blot analysis. N2a cells were grown in six-well plates to generate 2N4R Tau overexpression and Tau knock-down-resistant cells. Antibiotic-resistant clones were picked and cultured in DMEM containing puromycin or blasticidin. Harvested cells and tissues were extracted using the ProteoExtract Subcellular Proteome Extraction kit , Millipore. The cytoplasmic and nuclear fractions were separated according to the manufacturer's instructions. The brain tissue was dissected on ice and enzymatically digested using the Adult Brain Dissociation kit , Miltenyi. The single-cell suspension was prepared for the flow cytometry assay according to the manufacturer's instructions. Gating parameters and data analysis were performed using FlowJo 10 software Tree Star. BrdU and EdU immunostaining were performed to assess the proliferation of newborn hippocampal cells during cocaine memory formation. For the flow cytometry assay of proliferation, single-cell suspensions were prepared from mice injected intraperitoneally with EdU as described above. Data were analyzed as described above. The proteins were extracted and the co-IP procedures were conducted as described above. Samples were incubated at room temperature for 45 min in the dark. The tryptic peptides were dissolved in 0. The electrospray voltage applied was 2. Automatic gain control AGC was set to 5E4. Tandem mass spectra were searched in the SwissProt Mouse database. The mass error was set to 10 ppm for precursor ions and 0. Carbamidomethylation on Cys was specified as the fixed modification and oxidation on Met was specified as the variable modification. All interesting gene name identifiers mainly proteins involved in regulating cell proliferation were searched against the STRING database version Only interactions between the proteins belonging to the searched dataset were selected, thereby excluding external candidates. For simple comparisons, an unpaired two-tailed Student's t test was used. For multiple comparisons, one-way or repeated-measures two-way ANOVA test was used for each experiment. In all cases, n refers to the number of animals. CPP test, an associative memory model linking drug reward with environment cues, is widely used to assess the formation of drug-associated memory Zhou et al. In the present study, we first investigated the effect of cocaine on the expression of Tau in the hippocampus during the cocaine memory formation. We next performed two other reward tests, the home cage intraperitoneal injection test and food CPP tests, to investigate whether the changes in Tau level was specific to the formation of cocaine CPP memory. We further measured Tau level after cocaine CPP extinction. Cocaine-cue memory downregulates the expression of Tau in the hippocampus. A , Experimental schedule for cocaine CPP. B , Cocaine CPP score was significantly increased in cocaine group when compared with control group. D , Timeline of cocaine self-administration experiment. E—G , Number of active pokes, inactive pokes and infusions in the cocaine self-administration. H , Expression of Tau in the hippocampus of cocaine self-administered mice. I , Schematic of the locomotor-activity procedure. J , Distance during the 15 min after daily cocaine administration. K , Expression of Tau in the hippocampus in cocaine-induced hyperlocomotion. Hab, habituation. Tau downregulation may play an important role in cocaine-associated memory formation. A , Experimental schedule for home cage intraperitoneal injections. B , CPP score of mice after home cage intraperitoneal injections test. C , Western blotting of Tau in the hippocampus of mice with home cage intraperitoneal injections training. D , Experimental schedule for food CPP. G , Timeline of cocaine CPP extinction experiment. J , Experimental schedule for cocaine behavioral sensitization. K , Distance during the 15 min after daily cocaine administration. L , Western blotting of Tau in the hippocampus of mice with cocaine behavioral sensitization. M , Schematic of tissue collection after cocaine CPP. We continued to investigate the role of Tau in cocaine self-administration, a paradigm that incorporates memories of drug experience and drug-associated environmental cues. Cocaine-associated memory was formed when an instrumental action active pokes resulted in cocaine delivery unconditioned stimulus paired with an audiovisual cue conditioned stimulus. Mice were trained on a FR1 schedule, where a single active poke produced an infusion of cocaine or saline. We further detected Tau level in the hippocampus of cocaine-treated mice subjected to a locomotor activity test that lacks cocaine-associated contextual stimuli. To further explore the role of Tau in cocaine memory formation, Tau-KO mice and non-transgenic WT mice were injected a low dose of cocaine 2. Collectively, Tau downregulation may play an important role in cocaine-associated memory formation. Tau-KO mice show increased proliferating rates in hippocampal neuronal subpopulations with a low dose of cocaine CPP paradigm. B , Tau-KO mice more easily for cocaine memory formation compared with WT mice with a low dose of cocaine. The upper right quadrants show the corresponding positive subpopulations. It has been known that AHN contributes to the formation of memory, including cocaine-associated memory Castilla-Ortega et al. To explore the role of Tau in AHN and cocaine memory formation, a flow cytometry assay was performed to investigate whether Tau ablation would affect the proliferation of newborn hippocampal neurons during cocaine memory formation. Thus, Tau deficiency may enhance AHN and facilitate cocaine memory formation. Because the neuroanatomy of the hippocampus supports the segregation of neuronal outputs along a dorsal-ventral axis Fanselow and Dong, , the dDG and ventral DG vDG were separated from the hippocampus for immunoblotting analysis after CPP training, respectively. Collectively, 4R Tau, but not 3R Tau, may specifically modulate cocaine-induced memory formation. We next explored the function of genetically overexpressed 4R Tau in AHN during cocaine memory formation. We further determined the effect of 4R Tau overexpression on the proliferation of newborn hippocampal neurons in the dDG during cocaine memory formation. These results support the hypothesis that 4R Tau overexpression inhibits the proliferation and activity of adult hippocampal neurons in the dDG during cocaine memory formation. AAV-mediated 4R Tau overexpression attenuates the proliferation of adult hippocampal neurons during cocaine memory formation. D—G , Representative flow cytometry plots depict the effect of AAV-mediated 4R Tau overexpression on the proliferation rates of hippocampal neuron. A , Schematic representation of experiment timeline for mice receiving BrdU injection. J , Immunoblotting for c-fos in the dDG. We continued to investigate the effect of 4R Tau overexpression on the levels of memory formation-related proteins and the synaptic structure of granule neuron in dDG. Thus, 4R Tau upregulation disrupts the formation of cocaine-associated memory and dendritic structural plasticity of granule neuron. AAV-mediated 4R Tau overexpression modulates the expression of memory formation-related proteins and granule neurons morphology during the cocaine memory formation. C , Golgi staining showed the dendritic spines density of granule neurons in the dDG. K , Total distance within 15 min after daily cocaine administration. C—F , Representative flow cytometry plots depict the effect of AAV-mediated 4R Tau overexpression on the proliferation rates of hippocampal neuron. Tau is able to bind to a variety of other proteins, including a number of proteins functioning in cell signaling transduction Brandt and Leschik, ; Reynolds et al. Tau-interacting proteome was analyzed to investigate the underlying mechanisms by which Tau regulates AHN. Interestingly, 20 specific Tau-interacting proteins, which are intimately involved in regulating cell proliferation, were identified Extended Data Fig. Based on these results, the interaction of 4R Tau with PI3K-p85 may specifically modulate cocaine memory. Rabbit immunoglobulin G IgG was used as control. Extended Data Figure is supporting thus figure. We subsequently performed immunofluorescence staining to track the cellular localization of these two proteins in the cultured N2a cells in vitro and to further clarify the interaction of 4R Tau with PI3K-p An association of human Tau with PI3K-p85 has been shown in COS-7 cells, and the replacement of prolines and and arginine of human Tau with alanine drastically decreased its binding to PI3K-p85 Reynolds et al. By comparing the amino acid sequences of human and mouse Tau, prolines and and arginine in human Tau correspond to prolines and and arginine in mouse Tau, respectively. We then replaced these three amino acid residues of murine Tau with alanine and performed a co-IP assay. LV-mediated 4R Tau overexpression decreases the proliferating number of N2a cells. N2a cells were serum-starved overnight, and then cultured with EdU, an exogenous proliferation marker, for 2 h before the cells were collected for flow cytometry detection. We further used a Tau shRNA to silence Tau expression in N2a cells and determined whether the downregulation of Tau expression promotes cell proliferation by reducing its association with PI3K-p G , Proteins in the cytosolic and nuclear fraction of N2a cells were analyzed by immunoblotting. Immunofluorescence staining revealed the even distribution of endogenous PI3K-p85 red in the cytosol and nucleus of N2a cells. Similarly, exogenously expressed PI3K-p85 was also mainly expressed in the cytoplasm. We further separated cytosolic and nuclear fractions for Western blot analysis. I , Immunoblotting of 2A expression. J , Total distance within 15 min after daily cocaine administration. A , Schematic representation of the injection sites and photomicrographs of representative cannula placements in the dDG. B , Experimental timeline for cocaine CPP procedure. E , F , LY inhibited hippocampal neuronal proliferation. Tau accumulation plays an important role in memory impairment Yin et al. In the present study, we found a decreased expression of hippocampal Tau during cocaine memory formation; however, Tau expression remained unchanged in response to non-cocaine-conditioned stimuli. Furthermore, 4R Tau overexpression in the dDG disrupted cocaine memory formation, hippocampal neuronal proliferation and activity, and cocaine-seeking behaviors. In addition, cocaine-induced downregulation of 4R Tau clearly increased the expression of phosphorylated CREB, which is preferentially recruited or allocated to cocaine engram cells to encode memory consolidation Hsiang et al. These findings suggest a novel mechanism that 4R Tau modulates cocaine-associated memory formation. The segregation of neuronal outputs along the dorsal-ventral axis and their connectivity affect neurogenesis in the DG and hippocampus-associated memory Pierard et al. The difference observed in these two brain regions may be attributed to the functional dissociation that exists along the dorsal-ventral gradient in the hippocampus Fanselow and Dong, Indeed, the dorsal hippocampus is more important for spatial learning and contextual discrimination than the ventral region Wells et al. In contrast, the ventral hippocampus is strongly associated with negative affective symptoms, such as emotional behavior and stress responses Anacker et al. The functional neuronal expression of Tau isoforms has been a subject of controversy and debate. Interestingly, cocaine decreased hippocampal 4R Tau expression, but had little effect on 3R Tau expression, suggesting different functions of Tau isoforms in specific neuron populations. Indeed, 3R Tau binds with a lower affinity to microtubules, potentially contributing to the cytoskeletal plasticity. In contrast, 4R Tau is mainly expressed in the adult brain, exhibits higher affinity for microtubules, and functions in the establishment and maintenance of the synaptic structure of newly integrated neurons Lu and Kosik, Therefore, based on our findings, 4R Tau may contribute to the structural remodeling and integration of newborn neurons into the hippocampal circuit in response to drug conditioning. AHN is also a process in which adult-born hippocampal neurons are functionally integrated into the addiction network by interacting with addiction-related brain regions to contribute to cocaine memory formation Castilla-Ortega et al. In our study, AHN in the dDG was tightly regulated by 4R Tau during cocaine memory formation, and a reduction in cell proliferation inhibited memory formation in both the cocaine-paired CPP and self-administration paradigms. However, these results were obtained from experiments in which rodents were forcibly administered cocaine in their home cage; moreover, the measurement of cell proliferation was usually performed immediately or soon after cocaine administration in an open-field environment Xie et al. More importantly, these experiments lacked the cocaine-associated contextual stimuli that is critical for cocaine-cue memory formation. Besides, AHN induced by a genetic, pharmacological or environmental approach is able to exacerbate cocaine-seeking behavior, showing a role of AHN in increasing the vulnerability to the action of drugs Castilla-Ortega et al. For example, through reducing AHN, mice exhibited higher motivation to cocaine self-administration and drug-seeking behaviors in the phase of reinstatement Deroche-Gamonet et al. Therefore, we infer that that if cocaine CPP conditioning is conducted in the animals with increased numbers of adult-born hippocampal neurons, more young neurons might be recruited for CPP memory formation. It would explain why the cocaine-associated memory is more easily formed after increasing AHN Mustroph et al. However, once cocaine memory has been formed, such as in cocaine withdrawal phase, reducing AHN may fail to weaken the previous cocaine memory, which further trigger animal drug seeking and relapse during the period of abstinence Deroche-Gamonet et al. Our findings highlight the existence of a dynamic population of proliferating neurons in the DG, and AHN clearly emerges as a robust phenomenon during the cocaine memory formation. Although accumulating studies have shown that PI3K-AKT signaling regulates hippocampal neuron survival and proliferation in the DG on exposure to external chronic stress, the role of PI3K-AKT signaling in cocaine memory formation has not been completely elucidated Tiwari et al. Only one study published to date reported an association of human Tau with PI3K-p85 in COS-7 cells, and the replacement of a few amino acid residues of human Tau drastically decreased its binding with PI3K-p85 Reynolds et al. In turn, the cocaine-induced downregulation of 4R Tau may diminish the cytoplasmic localization of PI3K-p85 and subsequently increase its nuclear transportation, which is essential for cell proliferation and AHN. In the present study, the cellular distribution of PI3K-p85 was tightly regulated by 4R Tau, and the 4R Tau deficiency induced PI3K-p85 nuclear translocation, thus promoting neuronal proliferation. This finding suggests the presence of unexplored mechanisms of cocaine-induced circuit plasticity in the hippocampus, and may have implications for the development of novel therapeutic strategies aimed at restoring a normal level of AHN or the disruption of the Tau-mediated synaptic plasticity that occurs in response to cocaine. This section collects any data citations, data availability statements, or supplementary materials included in this article. As a library, NLM provides access to scientific literature. J Neurosci. Find articles by Hongchun Li. Find articles by Wei Xu. Find articles by Denian Wang. Find articles by Liang Wang. Find articles by Qiyao Fang. Find articles by Xuemei Wan. Find articles by Jiamei Zhang. Find articles by Yiming Hu. Find articles by Huifang Li. Find articles by Jie Zhang. Find articles by Zhen Yang. Find articles by Chunqi Liu. Find articles by Xiaocong Liu. Find articles by Yonghai Wang. Find articles by Bin Liu. Find articles by Zhengtao Hu. 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How can I buy cocaine online in Chengdu