Effects Of SDF-1 On GABA Releasing And Its Mechanisms In Cultured Hippocampal Cells

Hippocampus plays an important role in study and memory, which is the functions of the brain, and several parts of the brain contribute to this function. Hippocampus is located in the inferior horn and inside wall of lateral ventricle, and connects to the dentate gyrus, shaped like the letter C on the coronal plane. Hippocampus and the cortex of dentate gyrus are characterized by the regular arrange of the neurons. The cortex of hippocampus constitutes of CA1,CA2,CA3,CA4, among which CA1 relates to the functions of study and memory. The function requires accurate connections of the synapses among the neurons, which not only needs the synapse formation, but also relies on the neural transmitter releasing. GABA acting as one vital Inhibitory Neurotransmitter could regulate synaptic plasticity, and adjust Glu releasing as neuromodulator, meanwhile GABA could coexist with Glu. Some studies showed that the physiological properties of newborn neurons approximate immature neurons, GABA is one Inhibitory neurotransmitter to mature neurons, while one excitatory neurotransmitter to immature ones. Every part of hippocampus could release GABA. Granulocyte of DG could release Glu through mossy fiber, then wind up local inhibitory interneuron and release GABA. GABA releasing of the synapse of mossy fiber could protect nerves, wind up or inhibit neurons. Recent researches demonstrated that some cytokines could alter the synaptic plasticity, including the transmitter releasing. SDF-1 received public attention for its wide effects. SDF-1 belongs to the chemokines protein family, which has four conservative cysteine residues forming two pairs of disulfide species which are the specific structures of the chemokines, and there is one amino acid between the first cysteine residue and the second.Previous researches mainly focus on its chemotaxis on the immune system, and its effects on the angiopoiesis and hemopoiesis. However, recent researches demonstrated that SDF-1 and its receptor were expressed in the brain tissues, which suggested that it may regulate the nervous system they also found that SDF-1 could promote the growth of the CNS especially the DRG neurons'axon growth, which effected via its receptor-CXCR4. Some reported that the lack of SDF-1 and CXCR4 could inhibit cortex interneuron's migration towards the surface of the brain, which means SDF-1 may act as neurotransmitter. However, whether SDF-1 could regulate GAB A releasing and effect through SDF-1/CXCR4 axis remain uncertain. This article focuses on the expression and location of SDF-1 and CXCR4 in hippocampus neurons in vitro, and observes GABA releasing and its mechanism.Aim:To observe the effects of SDF-1 on GABA releasing and explore its mechanisms.Methods:Observe the distribution in hippocampus and the locations of SDF-1 and CXCR4 in hippocampal cells by immunohistochemistry. Determine the SDF-1 releasing changes in hippocampus neurons by ELISA. Realtime PCR is used to detect CXCR4 mRNA expression. Use AMD3100 to block down the receptor CXCR4, and then observe the GABA releasing and explore its mechanisms.Results:SDF-1 locates in the membrane of the hippocampus neurons, especially in the plasma, and its receptor CXCR4 is mainly expressed in the plasma and membrane, especially the membrane. During the procedure of the hippocampus neurons' invitroculture, during the time expansion(1,3,5,7,10day) SDF-1 decreased in the supernate gradually, and RT-PCR showed CXCR4mRNA was expressed both in control group and experimental group; with the time expansion the control group takes on time-dependent property: rise obviously at 7d, the highest at 10d, and the results have statistical meaning compared with the 1d; and the experimental group's results are similar. When compared between groups during the same time SDF-1 group and control group both rise; with the usage of 50ng/mL SDF-1 upon the hippocampus neurons, GABA releasing changes with the time changing, which takes on the trend that firstly decreases then increases slightly. The GABA releasing increases under the condition of AMD3100 blocking the receptor CXCR4.Conclusion:SDF-1 can affect GABA releasing of hippocampus neurons cultured in vitro, which is related to alterations of CXCR4 expression.