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Endogenous Activation and Neurophysiological Functions of Acid-Sensing Ion Channels
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Wei-Zheng Zeng, Yi-Zhi Wang, Tian-Le Xu
Accumulating evidence shows that ASIC1a channels are mainly expressed on neural soma and dendrites (1,3,85,93). Moreover, they were found to be present in synaptosome-enriched subcellular fractions and colocalize with postsynaptic proteins, such as postsynaptic density-95 (PSD-95), protein interacting with C-kinase-1 (PICK1), β-actin, and A kinase anchoring protein 79/150 (AKAP79/150), suggesting that ASIC1a channels are enriched in dendritic spines (85,94,95). It is interesting that ASIC1a is not directly bound to PSD-95, but rather associated with PSD-95 in dendritic spines via binding to the ASIC2a subunit (89). Although ASIC3 was also found to interact with PSD-95 (96), there is no information about its precise subcellular localization. Moreover, intracellular ASIC1a was recently identified in the mitochondrial membrane (mtASIC1a) of the mouse cortical neurons (97,98). Considering the key role of mitochondria in neuronal functions (99,100), mtASIC1a may contribute to neural physiological functions in a whole new way. In the following section, we present previous results on the neuronal physiological functions of ASICs in terms of synaptic roles and region-specific differences.
Role of Herbs and Their Delivery Through Nanofibers in Pharmacotherapy of Depression
Published in Anne George, Snigdha S. Babu, M. P. Ajithkumar, Sabu Thomas, Holistic Healthcare. Volume 2: Possibilities and Challenges, 2019
Ginpreet Kaur, Mihir Invally, Hiral Mistry, Parnika Dicholkar, Sukhwinder Bhullar
In humans, there are two zones subventricular zone and subgranular zone, an area in brain (hippocampus) is responsible for learning and memory.11,12 Due to aging, there is reduction of postsynaptic density in hippocampus resulting in a decrease in long-term potentiation (LTP) and increase in long-term depression which results in major depression.13,14 SSRIs (selective serotonin reuptake inhibitors) or atypical antidepressants (venlafaxine) in chronic treatment are found to be more beneficial than tricyclic antidepressants (TCAs) because they prevent stress induced LTP.15,16 In hippocampus and Cornu Ammonis pyramidal cells, cellular plasticity increases due to SSRIs (fluoxetine), while this neuroplastic activity is decreased by TCA due to its anticholinergic activity.17-19
Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
To assess the possibility that proBDNF was reduced at sites of release in dendritic spines, they examined the juxtaposition of proBDNF with postsynaptic density protein-95 (PSD95). PSD95 is a scaffolding protein that interacts with the NMDAR on dendritic spines and serves as a marker of the postsynaptic compartment. Their data show that Pb2+ significantly reduced proBDNF-PSD95 juxtaposition by ca. 15%–35% (n = 5 independent trials, F2, 81 = 7.914, p < 0.001) and increased the percent of PSD95 that is expressed alone by 1%–25% (n = 4 independent trials, F2, 66 = 4.009, p < 0.05) without affecting PSD95 puncta density (n = 5 independent trials, F2, 76 = 0.58, p > 0.05). These data indicate that proBDNF levels at putative sites of release in dendritic spines are decreased by Pb2+ exposure. In general, the results presented above support and extend our previous findings364 that hippocampal neurons exposed to Pb2+ during synaptogenesis exhibit decreased intracellular levels of proBDNF protein and this effect is present along the entire length of dendrites resulting in reduced levels of mBDNF in the extracellular media.
Oligomeric Aβ25–35 induces the tyrosine phosphorylation of PSD-95 by SrcPTKs in rat hippocampal CA1 subfield
Published in International Journal of Neuroscience, 2023
Gui-Mei Wu, Cai-Ping Du, Yan Xu
Numerous studies have shown that soluble Aβ oligomers disrupt glutamatergic synapses and plasticity [9, 16]. N-methyl-D-aspartate (NMDA) receptors, a subtype of ionotropic glutamate receptors, are involved in excitotoxic neuronal injury. Our previous reports have demonstrated that inhibition of NMDA receptors prevents Aβ-mediated neuronal damage and suppresses Aβ-induced mixed lineage kinase 3 (MLK3) signal pathway [11, 12]. However, how NMDA receptors activate the MLK3 signal pathway remains unclear. At postsynaptic sites, NMDA receptors are regulated by interaction with postsynaptic density-95 (PSD-95) [17, 18]. PSD-95 binds to NMDA receptors and other signal molecules, such as Src family protein tyrosine kinases (SrcPTKs), which sequentially regulates downstream signaling [18, 19]. We have found that PSD-95 is involved in the regulation of NMDA receptors in the Aβ neurotoxicity [15]. Furthermore, several studies have indicated that tyrosine phosphorylation of PSD-95 up-regulates the activity of NMDA receptors [20, 21]. But the regulation mechanisms of PSD-95 in Aβ neurotoxicity has not been clarified.
Homocysteine can aggravate depressive like behaviors in a middle cerebral artery occlusion/reperfusion rat model: a possible role for NMDARs-mediated synaptic alterations
Published in Nutritional Neuroscience, 2023
Mengying Wang, Xiaoshan Liang, Qiang Zhang, Suhui Luo, Huan Liu, Xuan Wang, Na Sai, Xumei Zhang
To observe whether HCY treatment could induce synaptic structural changes in the rat hippocampal region after MCAO, the number of synapses and the area of postsynaptic density were detected by TEM (Figure 3). In the SHAM group, the membranes of synapses were clear and had complete outlines, and abundant postsynaptic density was detected. Compared with the SHAM group, ultrastructure of synapsis in the MCAO group exhibited vague membranes, decreased quantity of synapse (P < 0.05, Figure 3(a)), and thinner postsynaptic densities (P = 0.004, Figure 3(b)). The administration of HCY further damaged the related synaptic morphology, including decreased number of synapses and downregulated postsynaptic density thickness, compared to the MCAO group (P = 0.019). These results suggested that HCY might cause synaptic loss and pathological changes in the hippocampus following ischemic injury.
Datumetine exposure alters hippocampal neurotransmitters system in C57BL/6 mice
Published in Drug and Chemical Toxicology, 2022
Azeez Olakunle Ishola, Aminu Imam, Moyosore Salihu Ajao
Electron microscopy technique was done to check for viable synapse in the hippocampus. Viable synapse was identified by the presence of pre- and post-synaptic membrane, postsynaptic density (PSD) and presynaptic vesicles (Figure 9(a)). The number of viable synapses was reduced in animals exposed to datumetine; this effect was more in animals exposed to 1.0 mg/kg body weight of datumetine. The number of presynaptic vesicles identified in the viable synapse was observed to reduce significantly (*p < 0.05) in datumetine exposed animals compared to control with 1.0 Datumetine animals with the least count (Figure 9(b)). PSD thickness was also measured in viable synapse identified in the micrograph of the experimental animals. Datumetine significantly (***p < 0.001) increased the thickness of PSD in the hippocampus of experimental animals compared to control with 1.0 Datumetine animals having the highest PSD thickness (Figure 9(c)).