Abstract
Depression not only threatens the health and quality of life of patients but also brings a huge mental and economic burden to the patients' families. This paper mainly studies the mechanism of dopaminergic neurotransmission in different doses of morphine addiction and stress-induced depression. In the experiment, 40 male SD rats were selected. The experiment established a rat model of chronic stress depression. The rats used in this model are all raised in a single cage, and there will be various stimuli every day for 21 days, but high-intensity continuous stimuli must be avoided, and the same stimuli will not appear continuously. The experiment established a depression animal model through chronic unpredictable mild stress (CUMS), combined with the conditioned position preference (CPP) model of morphine addiction to detect the establishment of CPP in such animals, so as to explore certain stress stimuli or depression, the influence on morphine addiction, and the relationship between them. The second or third branches of pyramidal neurons were selected to analyze the PL and CA3 regions. When analyzing the density of dendrites, each animal selected at least 8 dendrites in order to count the number of dendrites and selected a length of 20 μm on each branch to record the number of dendrites. All measured values are expressed as average ± standard deviation and analyzed by SPSS17.0 statistical software, and Levene test is used in the scattered consistency test. The average NIV of PEN before injection was 11.92 ± 2.90 Hz, and the average latency was 0.16 ± 0.03 s. The results indicate that CUMS may reduce the conditioned learning and memory ability by damaging the learning loop, rather than affecting the reward loop to weaken the establishment of morphine-dependent CPP.
Highlights
Depression threatens the health and quality of life of patients and brings a huge mental and economic burden to the patients’ families. is paper mainly studies the mechanism of dopaminergic neurotransmission in different doses of morphine addiction and stress-induced depression
40 male SD rats were selected. e experiment established a rat model of chronic stress depression. e rats used in this model are all raised in a single cage, and there will be various stimuli every day for 21 days, but high-intensity continuous stimuli must be avoided, and the same stimuli will not appear continuously. e experiment established a depression animal model through chronic unpredictable mild stress (CUMS), combined with the conditioned position preference (CPP) model of morphine addiction to detect the establishment of CPP in such animals, so as to explore certain stress stimuli or depression, the influence on morphine addiction, and the relationship between them. e second or third branches of pyramidal neurons were selected to analyze the PL and CA3 regions
All measured values are expressed as average ± standard deviation and analyzed by SPSS17.0 statistical software, and Levene test is used in the scattered consistency test. e average NIV of PEN before injection was 11.92 ± 2.90 Hz, and the average latency was 0.16 ± 0.03 s. e results indicate that CUMS may reduce the conditioned learning and memory ability by damaging the learning loop, rather than affecting the reward loop to weaken the establishment of morphine-dependent CPP
Summary
Depression threatens the health and quality of life of patients and brings a huge mental and economic burden to the patients’ families. is paper mainly studies the mechanism of dopaminergic neurotransmission in different doses of morphine addiction and stress-induced depression. Suzuki S believes that patient-specific induced pluripotent stem cells (iPSCs) may be used as a tool for in vitro modeling of PD He tried to increase the efficiency of IPSC induced dopaminergic (DA) neurons by using surface markers expressed in Da progenitor cells, in order to increase the importance of phenotypic analysis. He used the MT mKeima reporting system to establish a quantitative system to monitor the mitochondrial phagocytosis of the fusion of mitochondria and lysosomes and combined the system with the above DA neuron induction method to determine the mitochondrial damage in PARK2 neurons. His research can generate calcium signals by activating TRPC1 channels, it does not explain the role of DA neurons [5]
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