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Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ming-Gang Liu, Michael X. Zhu, Tian-Le Xu
Synaptic strength is determined by both the amount of presynaptic neurotransmitter release and postsynaptic receptor abundance and responsiveness. Current knowledge on the involvement of ASIC1a in synaptic plasticity mainly concentrates on the postsynaptically localized ASICs. However, it still remains obscure whether ASIC1a is also expressed in the presynaptic axonal terminals. If so, does it have any effect on the probability or dynamics of transmitter release? Almost all forms of synaptic plasticity (LTP, LTD, structural plasticity and homeostatic plasticity) have been reported to have a presynaptic component92, but whether ASICs function in these forms of presynaptic plasticity remains unknown. Moreover, not only do excitatory synapses on pyramidal neurons exhibit activity-dependent plastic changes, but also excitatory synapses on inhibitory neurons and inhibitory synapses onto pyramidal neurons can equally undergo LTP or LTD93. Then, it would be tempting to ask whether and how ASIC1a contributes to synaptic plasticity at these synapses.
The Neurobiology of Central Sensitization
Published in Robert M. Bennett, The Clinical Neurobiology of Fibromyalgia and Myofascial Pain, 2020
Like the vast majority of excitatory synapses in the central nervous system [CNS], most presynaptic excitatory terminals in the dorsal horn release glutamate which activates ionotropic glutamate receptors that are strategically-localized in the postsynaptic neurons (1). The excitatory postsynaptic potentials [EPSPs] resulting from single presynaptic action potentials is caused primarily by activation of the alpha-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate [AMP A] and kainate [KAI] subtypes of glutamate receptor. The N-methyl-D-aspartate [NMDA] subtype of glutamate receptor, which is also localized at excitatory synapses, contributes little to the responses to single presynaptic action potentials because these receptors are tonically suppressed by extracellular magnesium [Mg2+] which blocks NMDA channels. This type of fast excitatory synaptic transmission occurs even at synapses of “slow” primary afferent which are predominantly nociceptors [Figure 1]. With low frequency activation of nociceptors produced by mild noxious stimuli, these EPSPs signal the onset, duration, intensity, and location of noxious stimuli to dorsal horn neurons.
Review of the Human Brain and EEG Signals
Published in Teodiano Freire Bastos-Filho, Introduction to Non-Invasive EEG-Based Brain–Computer Interfaces for Assistive Technologies, 2020
Alessandro Botti Benevides, Alan Silva da Paz Floriano, Mario Sarcinelli-Filho, Teodiano Freire Bastos-Filho
Neurons that connect the nervous system and different layers of the brain form the neuronal circuits, which transmit information through excitatory and inhibitory synapses. Excitatory synapses may be mediated by the neurotransmitter acetylcholine (ACo), dopamine (DA), noradrenaline (NA), adrenaline, serotonin, glutamate (Glu), and glycine (Gly), whereas the inhibitory synapses are mediated by the neurotransmitter gamma-aminobutyric acid (GABA).
Subanesthetic ketamine: the way forward for pain management in sickle cell disease patients?
Published in Expert Review of Hematology, 2022
Raissa Nobrega, Veronica Carullo, Swee Lay Thein, Zenaide M.N. Quezado
A dissociative anesthetic, ketamine has been used since the 1960s and proven safe and effective in many clinical settings including battlefield rescues, emergency departments, and operating rooms [11]. Ketamine’s principal mechanism of action is the noncompetitive blockade of the NMDA receptor, a cation channel mostly located in excitatory synapses (Figure 1). However, ketamine also affects opioidergic, GABAergic, monoaminergic, and muscarinic neurotransmissions, as well as substance P, alpha-amino-3-hydroxyl-5-methyl-4-isoxazole propionate (AMPA), and sigma receptors signaling [11]. The understanding that activation of NMDA receptors has been implicated in the development of central sensitization, inflammatory, nociceptive, and neuropathic pain, as well as of opioid tolerance and opioid-induced hyperalgesia provides the rationale for the use of subanesthetic ketamine for the treatment of acute and chronic pain [12–14].
Combination of tea polyphenols and proanthocyanidins prevents menopause-related memory decline in rats via increased hippocampal synaptic plasticity by inhibiting p38 MAPK and TNF-α pathway
Published in Nutritional Neuroscience, 2022
Qian Yang, Yusen Zhang, Luping Zhang, Xuemin Li, Ruirui Dong, Chenmeng Song, Le Cheng, Mengqian Shi, Haifeng Zhao
Dendritic spines are the major sites of excitatory synaptic input, the number of synapses is closely related to the transmission efficiency and the transmission efficiency of nerve impulses [40]. In the model group, decreased density of dendritic spines and decreased number of excitatory synapses impaired the efficiency of nerve conduction. Therefore, we further observed the ultrastructure of synapses by transmission electron microscope. Structural plasticity of synapses is the basis of functional plasticity, mainly manifested as the size of presynaptic and postsynaptic contact area, the number of active areas in the synaptic contact area, the change of synaptic gap (affecting synaptic transmission efficiency) [41]. Classical parameters of synaptic structure include synapse interface curvature, synapse gap width, postsynaptic density (PSD) thickness and numerical density per unit volume (Nv) [42]. Narrow synaptic cleft is advantageous to the pre-synaptic membrane release of neurotransmitters, larger interface curvature can reduce the neurotransmitters into the surrounding interstitial diffusion ensure the neurotransmitter release further to reach the target, improve the transfer function.
Change in gene expression levels of GABA, glutamate and neurosteroid pathways due to acoustic trauma in the cochlea
Published in Journal of Neurogenetics, 2021
Meltem Cerrah Gunes, Murat Salih Gunes, Alperen Vural, Fatma Aybuga, Arslan Bayram, Keziban Korkmaz Bayram, Mehmet Ilhan Sahin, Muhammet Ensar Dogan, Sevda Yesim Ozdemir, Yusuf Ozkul
For our investigation of the effect of AT on the genetic level Gls, Slc1a2, Slc17a8, Grin2b, Gabra1, Gad1, Slc6a1, Sult1a1 and Cyp11a1 genes were selected. Gls encodes the major enzyme that converts glutamine to glutamate, so it is responsible for the majority of glutamate synthesis (Prusiner, 1981). Slc1a2 encodes the protein required for the removal of glutamate from the synapse and termination of its excitatory effect (Shashidharan, Wittenberg, & Plaitakis, 1994). Slc17a8 encodes the protein that carries glutamate to presynaptic vesicles (Takamori, Malherbe, Broger, & Jahn, 2002). Grin2b encodes a glutamate-activated ion channel receptor located in excitatory synapses in the brain (Endele et al., 2010). Gabra1 encodes one of the GABA receptors (Garrett et al., 1988). Gad1 encodes the enzyme that catalyzes the conversion of glutamic acid to GABA, the main inhibitory neurotransmitter (Erlander & Tobin, 1991). Slc6a1 encodes the carrier that removes GABA from the synaptic cleft to presynaptic terminals (Hirunsatit et al., 2009). Cyp11a1 encodes the enzyme that catalyzes the conversion of cholesterol to pregnenolone which is the first and rate-limiting step in the synthesis of steroid hormones (John et al., 1984). Sult1a1 encodes the enzyme that converts pregnenolone to pregnenolone sulfate (PREGS) which is a neurosteroid in the brain (Wilborn et al., 1993). The genes and their pathways are shown in Table 1.