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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.
Carbon Monoxide — From Tool to Neurotransmitter
Published in David G. Penney, Carbon Monoxide, 2019
Nanduri R. Prabhakar, Robert S. Fitzgerald
Long-term potentiation (LTP) is a mechanism that underlies certain forms of learning and memory. LTP requires activation of presynaptic sites via a retrograde messenger released from the postsynaptic site. It has been established that NO is one of the retrograde messengers mediating LTP (Bohme et al., 1991; Haley et al., 1992; Schuman and Madision, 1991; Zhuo et al., 1993; Zorumski and Izumi, 1993). Evidence that CO can serve as an intracellular messenger in the brain prompted several investigators to test its role in LTP. Stevens and Wang (1993) reported the involvement CO in LTP. Using hippocampal slices from rats and mice, these authors found that ZnPP-9, an inhibitor of heme oxygenase, prevented the induction of LTP without affecting long-term depression (LTD), another form of synpatic plasticity associated with memory. Heme oxygenase inhibitors also abolished LTP that was already established. Independent studies by other investigators reported similar results (Ikegaya et al., 1994; Zorumski and Izumi, 1993), and further demonstrated that exogenous CO enhances LTP. These observations support the idea that CO is a retrograde messenger in hippocampal pyramidal cells. Hippocampal pyramidal neurons contain not ony HO-2 (Verma et al., 1993), but also the endothelial type of NO synthase (Dinerman et al., 1994). The fact that inhibitors of both NO and CO synthesis abolish LTP suggest that both these gases may function in a coordinated fashion. In this context it is interesting to note that NO synthase structurally resembles cytochrome P-450 reductase (Bredt et al., 1991) .
Transcranial Magnetic and Electric Stimulation
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Shoogo Ueno, Masaki Sekino, Tsukasa Shigemitsu
Using a vascular dementia (VaD) rat model, Yang et al. (2015) determined whether low-frequency (1 Hz) 0.5 T rTMS protects pyramidal cell from apoptosis and promotes hippocampal synaptic plasticity. In this study, learning and memory were evaluated via Morris water maze (MWM), and the ultrastructure of hippocampal CA1 neurons was examined by electron microscopy. Hippocampal synaptic plasticity was assessed by long-term potentiation (LTP). The expression of N-methyl-D-aspartic acid receptor 1 (NMDAR1), Bcl-2, and Bax proteins was assessed by Western plot. Bcl-2 promotes cell survival and Bax promotes cell death. LTP is considered essential for cognition and the synaptic plasticity is the cellular basis for memory formation and cognition. Yang et al., applied rTMS for 600 s daily for 10 days during a 2-week period. Rats treated with rTMS had reduced escape latencies, increased swimming time and significantly less synaptic structure damage. The results show that rTMS improves learning and memory, protects the synapse, and increases synaptic plasticity in VaD model rats. In conclusion, increased Bcl-2 expression—upregulation—and reduced Bax expression—downregulation—may be a novel protective mechanism of rTMS treatment for VaD.
Neurophysiological and molecular approaches to understanding the mechanisms of learning and memory
Published in Journal of the Royal Society of New Zealand, 2021
Shruthi Sateesh, Wickliffe C. Abraham
Experimentally, LTP is a process whereby a brief period of high-frequency synaptic activity produces a long-lasting increase in synapse efficacy (Figure 2). The properties of LTP, such as cooperativity, input specificity, and associativity, are fundamental to its putative role in learning and memory in mammals. Cooperativity refers to the fact that LTP induction has a threshold, necessitating the cooperative interaction of multiple afferent fibres working together (McNaughton et al. 1978). LTP is input specific as its induction is restricted to the synapses activated by the high-frequency stimulation rather than all synapses that contact the same neuron (Andersen et al. 1977). The associativity property of LTP is particularly of interest, given its analogy to associative learning. Here, synapses that are unable to produce LTP due to a weak level of input activity can still undergo LTP when they are co-activated alongside strong input stimulation of neighbouring synapses, which will of course also undergo LTP induction (Bliss and Collingridge 1993). Note that in such paradigms, other synapses not activated by either set of stimulated inputs will not be potentiated, due to the input specificity property of LTP. Finally, both LTP and memory can be rapidly induced in regions throughout the brain, are reversible and can exist for shorter or longer periods of time (Eichenbaum et al. 1996; Abraham et al. 2002).
Cognitive and affective neuroscience: approaches and applications
Published in Journal of the Royal Society of New Zealand, 2021
Susan Schenk, Karen Waldie, Gina Grimshaw
Kirk et al. (2021) provides evidence to support the proposal that ‘LTP-like’ changes in EEG-derived human visual evoked potentials have the same characteristics (and are thus driven by the same mechanisms) as long-term potentiation (LTP) studied in experimental animals. The ability of to measure LTP mechanisms in humans allows for the exploration of the role of synaptic plasticity in human memory and other cognitive processes. This ability also allows for the direct study of synaptic plasticity in a number of human disorders (e.g. schizophrenia, depression, Alzheimers) in which LTP has been proposed to be atypical.
Human EEG and the mechanisms of memory: investigating long-term potentiation (LTP) in sensory-evoked potentials
Published in Journal of the Royal Society of New Zealand, 2021
Ian J. Kirk, Meg J. Spriggs, Rachael L. Sumner
Long-term potentiation (LTP) refers to a rapid strengthening of synapses in a neural network, thus increasing the efficacy of communication between particular cells in that network. LTP (and the inverse process, long-term depression (LTD)) allow for the storage of multiple memory items within a network (Neves et al. 2008). Thus, LTP is widely considered to be the principal candidate synaptic mechanism underlying learning and memory formation (Bliss and Lomo 1973; Bliss and Collingridge 1993; Martin et al. 2000; Abraham et al. 2002; Cooke and Bliss 2006; Abraham et al. 2019), and has been studied extensively in laboratory animals (Teyler and DiScenna 1987; Malenka and Nicoll 1999; Abraham et al. 2002). However, until the mid-2000s, there had been no direct demonstrations of LTP in the intact human brain, although LTP was generally thought to be the basis of declarative memory in humans (Squire 1986). Certainly, LTP has been demonstrated in isolated slices of human cortical tissue, where it displays properties very similar to those seen in nonhuman preparations (Chen et al. 1996; Beck et al. 2000). Although studied most often in hippocampal preparations of animals, LTP has also been demonstrated in the neocortex (Tsumoto and Suda 1979; Komatsu et al. 1988; Kirkwood and Bear 1994; Racine et al. 1995; Heynen and Bear 2001). Given these repeated demonstrations of LTP in sensory neocortex of experimental animals, it was thought that LTP might also be observed in human neocortex and measured via EEG-derived, sensory-evoked potentials. That is, it was thought that LTP in multiple synapses in human neocortical networks may be observable as changes in amplitude of sensory-evoked event-related potentials (ERPs) recorded from the scalp of adult humans. We therefore investigated whether it was possible to induce LTP-like amplitude increases of scalp-recorded visual or auditory ERPs in humans by rapid presentation of visual or auditory stimuli. These studies are discussed in the following sections.