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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.
Remediating Brain Instabilities in a Neurology Practice
Published in Hanno W. Kirk, Restoring the Brain, 2020
When the training protocol and optimal reinforcement frequency (ORF) are ideal, the EEG-based neuromodulation and infra-low frequency brain training methods promote a powerful re-regulation of the patient’s brain networks, compelling them toward a recovery (or rediscovery or re-learning) of its inherent stability. This occurs after any productive session and may sustain only over the next day or two, thus requiring practice and repetition over time, as when learning a skill (like learning to play the guitar or to play golf), to eventuate toward a global brain homeostasis “reset” scenario wherein a new competence is incorporated in the system. Synaptic adaptation (Hebbian learning) and homeostatic plasticity mechanisms are implicated.6,7,8,9 The responsive results in the above vignettes serve to demonstrate the capacity for neuroplasticity at any age. Children self-report (or their parents report) immediate benefits that sustain more readily; the “re-learning” in children appears precipitous. At any age, the more severely dysregulated the central nervous system (CNS) has become, the more immediately the desired anticipated response becomes observable, as the above cases for patients A and B illustrate in elderly adults.
Multiple Commitments
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
The flexible explanatory powers of neuroplasticity are strained as addiction neuroscientists explore ontological and epistemological uncertainties. Dispensing with reductionism, addiction geneticists probe individual variation and population-wide differences. Social factors, including early-life trauma, take on importance as epigenetic understandings of stressful experiences are incorporated into mappings of addictive processes. Intense individual variation in response to opiates, long noted in the clinic, indicates existence of multiple plasticities ranging from “homeostatic” plasticity to “synaptic” or “wholesale” plasticity (the latter indicating overall change in neural excitability, rather than at specific synapses (Nestler 2013). Structural forms of neuroplasticity alter the number of synapses and expand or contract neuron size, a finding that changed the overall ecology of the addiction research field, creating new “trading zones.” “More than any other commonly studied form of experience-dependent plasticity, we are beginning to understand the potential causal relationships between the neural circuit adaptations elicited by drugs of abuse and the behavioural consequences of that experience” (Kauer & Malenka 2007: 855).
Does the tinnitus pitch correlate with the frequency of hearing loss?
Published in Acta Oto-Laryngologica, 2021
Natalia Yakunina, Eui-Cheol Nam
The association between the tinnitus pitch and the audiometric profile remains unclear despite extensive research on the topic; in addition, the two main neurophysiological models propose different types of association. The tonotopic model suggests that tinnitus is generated as a result of plastic reorganization in the auditory system following hearing loss (HL). After the loss of external auditory inputs, the cortical area (normally tuned to the frequencies corresponding to the damaged region of the cochlea) shifts its tuning toward the lower frequency adjacent to the HL area (the edge frequency) [1]. As a result, the edge frequency becomes overrepresented and gives rise to tinnitus percepts with a pitch corresponding to the edge frequency [1]. The second type of model (neural synchrony and homeostatic plasticity) suggests that the tinnitus pitch falls within the HL area. The neural synchrony model proposes that tinnitus arises due to spontaneous synchronous neural activity by hyperactive neurons in the HL region [2]. Recent studies have shown that, while the spontaneous firing rates of auditory cortical neurons were increased inside and outside of the frequencies affected by HL, the changes in phase-locked synchronous activity were confined to the HL region, where the tinnitus percept is localized [2]. The homeostatic plasticity model proposes that increased neuronal activity across the HL region serves as a compensatory mechanism that stabilizes the neural activity after HL, ultimately leading to an increase in neuronal noise and tinnitus percepts in the HL area [3].
Postsynaptic Syntaxin 4 negatively regulates the efficiency of neurotransmitter release
Published in Journal of Neurogenetics, 2018
Kathryn P. Harris, J. Troy Littleton, Bryan A. Stewart
One possible explanation for the potentiation we observe in Syx4 mutants is that it is the result of homeostatic compensation. Many studies have described homeostatic mechanisms of potentiation and depression at the fly NMJ. In presynaptic homeostatic potentiation (PHP), perturbations that inhibit the function of postsynaptic glutamate receptors by acute pharmacological blockade (Frank, Kennedy, Goold, Marek, & Davis, 2006) or genetic loss (Petersen, Fetter, Noordermeer, Goodman, & DiAntonio, 1997) are offset by compensatory increases in neurotransmitter release. These presynaptic changes include increases in the size and intensity of Brp clusters, increases in Ca2+ influx or increases in the readily releasable vesicle pool (Goel, Li, & Dickman, 2017; Kiragasi, Wondolowski, Li, & Dickman, 2017; Müller & Davis, 2012; Weyhersmuller et al., 2011). Moderate Cac increases have also been observed in conjunction with increases in Brp during PHP (Tsurudome et al., 2010), though most studies have not reported Cac levels. Presynaptic homeostatic depression (PHD) is a distinct phenomenon in which overexpression of the vesicular glutamate transporter, resulting in more glutamate packaged per synaptic vesicle, is offset by compensatory decreases in neurotransmitter release. PHD has been shown to involve a decrease in presynaptic Ca2+ influx and a decrease in Cac levels at active zones (Gaviño, Ford, Archila, & Davis, 2015). Thus, the synapse employs multiple mechanisms during homeostatic plasticity, including regulation of Cac channels and Ca2+ influx.
Pharmacologic agents directed at the treatment of pain associated with maladaptive neuronal plasticity
Published in Expert Opinion on Pharmacotherapy, 2022
Joseph V. Pergolizzi, Giustino Varrassi, Peter Magnusson, Frank Breve, Robert B. Raffa, Paul J. Christo, Maninder Chopra, Antonella Paladini, Jo Ann LeQuang, Kailyn Mitchell, Flaminia Coluzzi
Synaptic plasticity refers to transmission of messages along certain synapses which can modulate the pathways along which messages travel [10]. Synaptic plasticity allows neural activity to alter neutral circuity, which can play out in memory of transient events or modifications of behavior or feelings. Synaptic plasticity may play a role in early brain development. Synaptic plasticity is a complex and vast field; various subtypes have been described such as short-term synaptic plasticity, long-term, metaplasticity, homeostatic plasticity, and others. The molecular mechanisms underlying synaptic plasticity remain to be more thoroughly elucidated [10].