Neuromodulation

Neuromodulation is the physiological process by which a given neuron uses one or more chemicals to regulate diverse populations of neurons. Neuromodulators typically bind to metabotropic, G-protein coupled receptors (GPCRs) to initiate a second messenger signaling cascade that induces a broad, long-lasting signal. This modulation can last for hundreds of milliseconds to several minutes. Some of the effects of neuromodulators include: altering intrinsic firing activity,[1] increasing or decreasing voltage-dependent currents,[2] altering synaptic efficacy, increasing bursting activity[2] and reconfigurating synaptic connectivity.[3]

Major neuromodulators in the central nervous system include: dopamine, serotonin, acetylcholine, histamine, norepinephrine, nitric oxide, and several neuropeptides. Cannabinoids can also be powerful CNS neuromodulators.[4][5][6] Neuromodulators can be packaged into vesicles and released by neurons, secreted as hormones and delivered through the circulatory system.[7] A neuromodulator can be conceptualized as a neurotransmitter that is not reabsorbed by the pre-synaptic neuron or broken down into a metabolite. Some neuromodulators end up spending a significant amount of time in the cerebrospinal fluid (CSF), influencing (or "modulating") the activity of several other neurons in the brain.[8] When discussing neuromodulation, there are two forms of non-invasive stimulation when treating migraines. One is electrical stimulation, and some of the characterizations include transcranial alternating stimulation and transcranial direct current stimulation. The other is magnetic stimulation, which includes single pulse and repetitive transcranial stimulation. [User:Ngwinn]/Editing User:Ngwinn/Neuromodulation - Wikipedia].[9]

  1. ^ DeRiemer SA, Strong JA, Albert KA, Greengard P, Kaczmarek LK (24–30 January 1985). "Enhancement of calcium current in Aplysia neurones by phorbol ester and protein kinase C". Nature. 313 (6000): 313–316. Bibcode:1985Natur.313..313D. doi:10.1038/313313a0. PMID 2578617. S2CID 4230710.
  2. ^ a b Harris-Warrick RM, Flamm RE (July 1987). "Multiple mechanisms of bursting in a conditional bursting neuron". The Journal of Neuroscience. 7 (7): 2113–2128. doi:10.1523/JNEUROSCI.07-07-02113.1987. PMC 6568948. PMID 3112322.
  3. ^ Klein M, Kandel ER (November 1980). "Mechanism of calcium current modulation underlying presynaptic facilitation and behavioral sensitization in Aplysia". Proceedings of the National Academy of Sciences of the United States of America. 77 (11): 6912–6916. Bibcode:1980PNAS...77.6912K. doi:10.1073/pnas.77.11.6912. PMC 350401. PMID 6256770.
  4. ^ Fortin DA, Levine ES (January 2007). "Differential effects of endocannabinoids on glutamatergic and GABAergic inputs to layer 5 pyramidal neurons". Cerebral Cortex. 17 (1): 163–174. doi:10.1093/cercor/bhj133. PMID 16467564.
  5. ^ Good CH (January 2007). "Endocannabinoid-dependent regulation of feedforward inhibition in cerebellar Purkinje cells". The Journal of Neuroscience. 27 (1): 1–3. doi:10.1523/JNEUROSCI.4842-06.2007. PMC 6672293. PMID 17205618.
  6. ^ Hashimotodani Y, Ohno-Shosaku T, Kano M (January 2007). "Presynaptic monoacylglycerol lipase activity determines basal endocannabinoid tone and terminates retrograde endocannabinoid signaling in the hippocampus". The Journal of Neuroscience. 27 (5): 1211–1219. doi:10.1523/JNEUROSCI.4159-06.2007. PMC 6673197. PMID 17267577.
  7. ^ Marder E (October 2012). "Neuromodulation of neuronal circuits: back to the future". Neuron. 76 (1): 1–11. doi:10.1016/j.neuron.2012.09.010. PMC 3482119. PMID 23040802.
  8. ^ Conlay LA, Sabounjian LA, Wurtman RJ (October 1992). "Exercise and neuromodulators: choline and acetylcholine in marathon runners". International Journal of Sports Medicine. 13 (Suppl 1): S141–S142. doi:10.1055/s-2007-1024619. PMID 1483754. S2CID 36276472. [verification needed]
  9. ^ Tiwari V, Agrawal S (November 2022). "Migraine and Neuromodulation: A Literature Review". Cureus. 14 (11): e31223. doi:10.7759/cureus.31223. PMC 9729750. PMID 36505141.

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