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Ketamine Use in Pain Management
Published in Sahar Swidan, Matthew Bennett, Advanced Therapeutics in Pain Medicine, 2020
Sahar Swidan, Charles E. Schultz
Ketamine is an N-methyl-d-aspartate (NMDA) non-competitive receptor antagonist that acts as an analgesic agent and has notable use in anesthesia, psychiatry, and pain management, among other disease states. N-methyl-d-aspartate amplifies pain signals, the development of central sensitization, and opioid tolerance.1 The NMDA receptor is integral in learning, memory, and synaptic plasticity.
Pain Sensitization
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
NMDA receptors are involved in a number of phenomena that may contribute to the medium- or long-term changes observed in chronic pain states. These phenomena include the development of wind-up, facilitation, central sensitization, changes in peripheral receptive fields, induction of immediate early genes and long-term potentiation. Long-term potentiation, in particular, relates to the changes in synaptic efficacy that occur as part of the process of memory and may play a role in the development of a cellular ‘memory’ for pain or enhanced responsiveness to noxious inputs. NMDA antagonists can attenuate these responses, indicating a role for such compounds in the prevention of chronic pain states.
Computational Neuroscience and Compartmental Modeling
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
Note that, the N-methyl-D-aspartate receptor (also known as the NMDA receptor or NMDAR), is a glutamate receptor and ion channel protein found in nerve cells. The NMDA receptor is one of three types of ionotropic glutamate receptors, the others being the AMPA and kainate receptors. It is activated when glutamate and glycine (or D-serine) bind to it, and when activated it allows positively charged ions to flow through the cell membrane.99 The NMDA receptor is very important for controlling synaptic plasticity and memory function.100
Neural Plasticity in the Ventral Tegmental Area, Aversive Motivation during Drug Withdrawal and Hallucinogenic Therapy
Published in Journal of Psychoactive Drugs, 2023
Hector Vargas-Perez, Taryn Elizabeth Grieder, Derek van der Kooy
Another possible route of action of 5-HT2A receptors is the long-term regulation of the expression of NMDA-like glutamate receptors (Zhong, Yuen, and Yan 2008). NMDA receptors are directly related to learning, particularly to the production and maintenance of potentiated glutamatergic signaling. Blockade of NMDA receptors with selective antagonists, such as ketamine, produces a relief of depressive symptoms almost instantaneously after their administration (Lapidus, Soleimani, and Murrough 2013; Niciu et al. 2014). However, because the regulation of the NMDA receptor is at the synaptic level, its therapeutic effects are generally short-term (around a week), and at best a couple of months (Lapidus, Soleimani, and Murrough 2013; Niciu et al. 2014). On the other hand, the long-term effects (more than 6 months (Griffiths et al. 2011)) of the action of agonists at 5-HT2A receptors could be due to a modification in the genetic transcription of glutamatergic NMDA receptors (Yuen et al. 2008), however this hypothesis needs to be corroborated experimentally.
Multi-targeted drug design strategies for the treatment of schizophrenia
Published in Expert Opinion on Drug Discovery, 2021
Piotr Stępnicki, Magda Kondej, Oliwia Koszła, Justyna Żuk, Agnieszka A. Kaczor
Increasing evidence indicates that the glutamatergic system is involved in the development of schizophrenia. Glutamate is involved in the formation of the memory pathway, which means it has a significant effect on synaptic plasticity and cortical microcircuits [19]. Originally, this hypothesis was based on the assumption that there was a glutamatergic neurotransmission deficit in schizophrenia. For many years, the concept has been modified and developed, involving many glutamate receptors. However, the most important role in this hypothesis is fulfilled by dysfunction of N-methyl-D-aspartate (NMDA) receptor [12]. The NMDA receptor is a glutamate-gated ionotropic receptor that plays an important role in the development of neuronal plasticity. Postmortem examinations show that patients with schizophrenia are characterized by lower density of glutamatergic receptors. The combination of NMDA receptor deficiency and dopaminergic neurotransmission dysfunction can be a simple explanation for most clinical aspects of schizophrenia. Many studies indicate that the activation of D1 and D2 dopamine receptors is responsible for the regulation of NMDA receptor function. In addition, it is suggested that activation of D1 receptor is associated with increased expression of the NMDA receptor NR2B subunit in the prefrontal cortex and affects the subcellular location of NMDA receptors [20].
Low-dose ethanol ameliorates amnesia induced by a brief seizure model: the role of NMDA signaling
Published in Neurological Research, 2019
Azam Alinaghipour, Tahereh Mazoochi, Abolfazl Ardjmand
It is strongly established that the beneficial effect of EtOH-PC on the nervous system occurs via its neuroprotective effects [32]. In addition, the NMDA receptors are involved in the neuroprotective effect of EtOH-PC [33]. Moreover, it is assumed that in preconditioning, Eth modulates the NMDA receptors [33] via theNR1 subunit of these receptors [17]. The NMDA receptors are glutamate-dependent ion channels, which are crucial for learning and memory as well as neuronal communication [34]. While at the present time there is no clear explanation and mechanism for the acute and chronicversuslow-dose effects of Eth on NMDA subunits [35], among multiple promising mechanisms mentioned either for its chronic or acute events, the event may be best explained by the neuroprotective mechanism. From this point of view, Eth acting as an NMDA antagonist [36] and via decreasing the NMDA receptor expression, conditions the receptor, that is, the state referred as preconditioning [18]. The molecular findings of our study revealed increased NR1 mRNA expression in the group that received Eth+PTZ coadministration, while the NR1 mRNA expression was decreased after the PTZ per se.