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Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
LTP is triggered by activation of NMDA glutamate receptors (NMDARs) concomitant with depolarization of the postsynaptic membrane. As mentioned earlier, the NMDA channel is blocked at the resting voltage by extracellular Mg2+. High-frequency stimulation causes prolonged depolarization of the postsynaptic membrane that removes the blockage, so that the glutamate-activated channel of the NMDA receptor conducts and allows the influx of Ca2+ and Na+ (Figure 6.14). The ensuing rise in [Ca2+]i triggers LTP through several mechanisms; the dominant one seems to be through CaMKII and, to a lesser extent, through PKC (Section 6.3.1). An interesting property of CaMKII is that its 12 subunits not only phosphorylate other proteins but can also phosphorylate each other. Because of this autophosphorylation, the activity of CaMKII can persist long after [Ca2+]i returns to its normal level. CaMKII phosphorylates AMPA receptors (AMPARs), thereby increasing the conductance of this receptor channel.
Advances in Understanding the Mechanisms Underlying Synaptic Plasticity
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Timothy J. Teyler, Idil Cavus, Chris Coussens, Pascal DiScenna, Lawrence Grover, Yi-Ping Lee, Zeb Little
The original descriptions of LTP were made in the hippocampus, particularly area CA1, and most mechanistic studies of LTP have been done in this region. Central to understanding the mechanisms underlying LTP is the role of the N-methyl-d-aspartate (NMDA) glutamate receptor subtype. When appropriately activated, the NMDA receptor (NMDAr) gates Ca2+ into the postsynaptic cell where Ca2+-dependent biochemical processes responsible for the expression of this enduring form of increased synaptic efficacy are activated. We shall term this form NMDA LTP. More recently, a second form of LTP was described that is independent of the NMDAr. This form of LTP gates Ca2+ into the cell through voltage-dependent calcium channels (VDCCs). We shall refer to this form as non-NMDA LTP. For both forms of LTP, the metabotropic glutamate receptor (mGLUr) may also play a role in the maintenance of the potentiated response. The most prevalent form of LTD is seen at synapses subjected to a long, low-frequency stimulus train (homosynaptic LTD). Heterosynaptic LTD is less reliably seen at inactive synapses when other synapses on the same cell are activated. Like LTP, LTD is a Ca2+-dependent phenomenon. The central question of this chapter concerns how a common second messenger, Ca2+, can initiate different physiological responses in the same cell.
Memory
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
Long-term potentiation (LTP) is operationally defined as a long-lasting increase in synaptic efficacy following high-frequency stimulation of the afferent fibers (Shors & Matzel, 1997). Changes in synaptic efficacy are thought to play a key role in the formation of long-lasting memories. LTP has a number of properties that make it suitable as a physiological substrate of memory: (1) synapse specificity: it occurs only at potentiated synapses that are activated by the tetanic stimulation; (2) cooperativity: multiple inputs must be activated simultaneously to produce sufficient postsynaptic depolarization to induce LTP; and (3) it is associative: when a weak input that is normally insufficient to induce LTP is paired with a strong input, the weak input will become potentiated (Mayford, Siegelbaum, & Kandel, 2012). LTP occurs prominently in the hippocampus, a structure important for memory. Long-term depression (LTD) of synaptic transmission is the opposite of LTP, i.e., a decrease in the strength of synaptic connections. The encoding of long-term memories is suggested to involve modification of synaptic connections through LTP and LTD.
Regulation of LTP at rat hippocampal Schaffer-CA1 in vitro by musical rhythmic magnetic fields generated by red-pink (soothing) music tracks
Published in International Journal of Radiation Biology, 2023
Zijia Jin, Lei Dong, Lei Tian, Mei Zhou, Yu Zheng
It is well known that when presynaptic afferent fibers are stimulated, the neurotransmitter glutamate is released into the synaptic gap, Na+, and K+ ion channels open the triggering postsynaptic membrane depolarization, removal of Mg2+ from NMDA receptor channels, and a large Ca2+ inward flow, leading to an increase in postsynaptic Ca2+ concentration and protein kinase activation, which triggers an increase in the number and conductivity of AMPA receptors on the postsynaptic membrane, and LTP is induced (Abbas et al. 2015). As a physical intervention, time-varying magnetic field has its effect on ions, receptors and other intermediate factors. Tokay et al. found that NMDA receptors are activated by high intensity 100 Hz magnetic field and directly induce LTP production (Tokay et al. 2014). Magnetic field stimulation at different frequencies may exert excitatory or inhibitory effects on cells by altering the ion distribution inside and outside the cell membrane or the permeability of channel proteins on the cell membrane (Hossmann and Hermann 2003), which may influence neuronal function. Maskey et al. found experimentally that magnetic field radiation at low frequencies may have an inhibitory effect on the function of cells. (Maskey et al. 2010) and even caused severe cellular damage if exposed to magnetic fields for a long time (Bas et al. 2009). The magnetic field stimulation with a frequency larger than 1500 Hz may have a different mechanism of action when acting on cells compared with that lower than 1500 Hz, resulting in different effects of the two.
Is tDCS a potential first line treatment for major depression?
Published in International Review of Psychiatry, 2021
Rachel Woodham, Rachael M. Rimmer, Julian Mutz, Cynthia H. Y. Fu
The neurophysiological effects of tDCS typically last beyond the immediate stimulation period (Nitsche et al., 2003a, 2003b). Long-term potentiation (LTP) describes the sustained increase in synaptic transmission that is the cellular correlate of learning and memory, first described in neuronal cells in the hippocampus (Bliss & Lømo, 1973). Cortical LTP and long-term depression (LTD)-like changes are modulated by glutamatergic and GABAergic neurons (Trepel & Racine, 2000). Anodal tDCS-enhanced excitability in the primary motor cortex is LTP-like, which is dependent on N-methyl-D-aspartate (NMDA) receptor and calcium channel activity (Liebetanz et al., 2002; Monte-Silva et al., 2013). Stimulation strength, duration and direction have a non-linear relationship impact on whether excitatory or inhibitory effects are generated (Batsikadze et al., 2013; Jamil et al., 2017; Monte-Silva et al., 2013).
The role of synaptic biomarkers in the spectrum of neurodegenerative diseases
Published in Expert Review of Proteomics, 2020
Sonia Mazzucchi, Giovanni Palermo, Nicole Campese, Alessandro Galgani, Alessandra Della Vecchia, Andrea Vergallo, Gabriele Siciliano, Roberto Ceravolo, Harald Hampel, Filippo Baldacci
Ng is a 78 aa neuron-specific post-synaptic somato-dendritic protein. It is one of the most abundant calmodulin-binding proteins and is mainly expressed by excitatory neurons of the cerebral cortex and hippocampus. High levels can be measured in amygdala, caudate, and putamen, whereas it is poorly expressed or absent in other brain regions as the thalamus, cerebellum, brainstem, and the spinal cord [5]. The protein can be found in neurons but is not expressed by glial cells. Ng regulates synaptic activity, mainly LTP, through its binding to calmodulin that is increased in the presence of low calcium concentrations and inhibited by large calcium amounts. In animal models, Ng overexpression demonstrated to enhance LTP and improve cognitive performances, whereas in Ng knockout mice memory deficits were reported, probably due to an impairment or even a block of LTP [8]. Furthermore, preclinical studies highlighted an age-dependent reduction of Ng mRNA in several brain regions, including the hippocampus [28].