Neuromodulation#Volume transmission

{{see also|Neural pathways}}

The major neurotransmitter systems are the noradrenaline (norepinephrine) system, the dopamine system, the serotonin system, and the cholinergic system. Drugs targeting the neurotransmitter of such systems affect the whole system, which explains the mode of action of many drugs.{{cn|date=January 2025}}

Most other neurotransmitters, on the other hand, e.g. glutamate, GABA and glycine, are used very generally throughout the central nervous system.

{{Further|Norepinephrine#Norepinephrine system}}

File:Norepinephrine.svg

The noradrenaline system consists of around 15,000 neurons, primarily in the locus coeruleus.{{cite journal | vauthors = Sara SJ, Bouret S | title = Orienting and reorienting: the locus coeruleus mediates cognition through arousal | journal = Neuron | volume = 76 | issue = 1 | pages = 130–141 | date = October 2012 | pmid = 23040811 | doi = 10.1016/j.neuron.2012.09.011 | doi-access = free }} This is diminutive compared to the more than 100 billion neurons in the brain. As with dopaminergic neurons in the substantia nigra, neurons in the locus coeruleus tend to be melanin-pigmented. Noradrenaline is released from the neurons, and acts on adrenergic receptors. Noradrenaline is often released steadily so that it can prepare the supporting glial cells for calibrated responses. Despite containing a relatively small number of neurons, when activated, the noradrenaline system plays major roles in the brain including involvement in suppression of the neuroinflammatory response, stimulation of neuronal plasticity through LTP, regulation of glutamate uptake by astrocytes and LTD, and consolidation of memory.{{cite journal | vauthors = O'Donnell J, Zeppenfeld D, McConnell E, Pena S, Nedergaard M | title = Norepinephrine: a neuromodulator that boosts the function of multiple cell types to optimize CNS performance | journal = Neurochemical Research | volume = 37 | issue = 11 | pages = 2496–2512 | date = November 2012 | pmid = 22717696 | pmc = 3548657 | doi = 10.1007/s11064-012-0818-x }}

{{Further|Dopamine#Functions in the brain}}

The dopamine or dopaminergic system consists of several pathways, originating from the ventral tegmentum or substantia nigra as examples. It acts on dopamine receptors.{{cite journal | vauthors = Scheler G | title = Regulation of neuromodulator receptor efficacy--implications for whole-neuron and synaptic plasticity | journal = Progress in Neurobiology | volume = 72 | issue = 6 | pages = 399–415 | date = April 2004 | pmid = 15177784 | doi = 10.1016/j.pneurobio.2004.03.008 | arxiv = q-bio/0401039 | bibcode = 2004q.bio.....1039S }}

File:Dopamin - Dopamine.svg

Parkinson's disease is at least in part related to dropping out of dopaminergic cells in deep-brain nuclei, primarily the melanin-pigmented neurons in the substantia nigra but secondarily the noradrenergic neurons of the locus coeruleus. Treatments potentiating the effect of dopamine precursors have been proposed and effected, with moderate success.{{cn|date=January 2025}}

• Cocaine, for example, blocks the reuptake of dopamine, leaving these neurotransmitters in the synaptic gap for longer.
• AMPT prevents the conversion of tyrosine to L-DOPA, the precursor to dopamine; reserpine prevents dopamine storage within vesicles; and deprenyl inhibits monoamine oxidase (MAO)-B and thus increases dopamine levels.

{{Further|Serotonin#Gross anatomy}}

File:Serotonin-2D-skeletal.svg

The serotonin created by the brain comprises around 10% of total body serotonin. The majority (80-90%) is found in the gastrointestinal (GI) tract.{{cite web| vauthors = McIntosh J |title=What is serotonin? What does serotonin do?|url=http://www.medicalnewstoday.com/articles/232248.php#where_does_serotonin_come_from|website=Medical News Today|access-date=12 April 2015}}{{cite journal | vauthors = Berger M, Gray JA, Roth BL | title = The expanded biology of serotonin | journal = Annual Review of Medicine | volume = 60 | pages = 355–366 | date = 2009 | pmid = 19630576 | pmc = 5864293 | doi = 10.1146/annurev.med.60.042307.110802 | author3-link = Bryan Roth }} It travels around the brain along the medial forebrain bundle and acts on serotonin receptors. In the peripheral nervous system (such as in the gut wall) serotonin regulates vascular tone.{{cn|date=January 2025}}

• Selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine are widely used antidepressants that specifically block the reuptake of serotonin with less effect on other transmitters.{{cite book|title=Principles of Neural Science| vauthors = Kandel ER |publisher=Appleton & Lang|year=1991|isbn=978-0-8385-8034-9|location=East Norwalk, Connecticut|pages=[https://archive.org/details/principlesofneur00kan/page/872 872–873]|url-access=registration|url=https://archive.org/details/principlesofneur00kan/page/872}}{{Cite web|url=http://emedicine.medscape.com/article/286759-medication#2|title=Depression Medication: Antidepressants, SSRIs, Antidepressants, SNRIs, Antidepressants, TCAs, Antidepressants, MAO Inhibitors, Augmenting Agents, Serotonin-Dopamine Activity Modulators, Antidepressants, Other, Stimulants, Thyroid Products, Neurology & Psychiatry, Herbals|website=emedicine.medscape.com|access-date=7 November 2016}}{{Cite book|chapter-url=http://www.merckmanuals.com/professional/psychiatric-disorders/mood-disorders/drug-treatment-of-depression#v27413108|title=The Merck Manual| vauthors = Coryell W |publisher=Merck|year=2016|isbn=978-0-911910-19-3| veditors = Porter RS |edition=19th |location=Whitehouse Station, N.J.|language=en|chapter=Drug Treatment of Depression}}
• Tricyclic antidepressants also block reuptake of biogenic amines from the synapse, but may primarily affect serotonin or norepinephrine or both. They typically take four to six weeks to alleviate any symptoms of depression. They are considered to have immediate and long-term effects.{{Cite news|url=http://www.merckmanuals.com/professional/psychiatric-disorders/mood-disorders/drug-treatment-of-depression#v27413108|title=Drug Treatment of Depression|newspaper=Merck Manuals Professional Edition|access-date=7 November 2016}}
• Monoamine oxidase inhibitors allow reuptake of biogenic amine neurotransmitters from the synapse, but inhibit an enzyme which normally destroys (metabolizes) some of the transmitters after their reuptake. More of the neurotransmitters (especially serotonin, noradrenaline and dopamine) are available for release into synapses. MAOIs take several weeks to alleviate the symptoms of depression.{{cite journal |last1=Shulman |first1=Kenneth I. |last2=Walker |first2=Scott E. |title=Irreversible monoamine oxidase inhibitors revisited |journal=Psychiatric Times |date=October 2012 |volume=29 |issue=10 |pages=27 |id={{Gale|A332893508}} |url=https://www.psychiatrictimes.com/view/irreversible-monoamine-oxidase-inhibitors-revisited }}{{cite journal | vauthors = Wimbiscus M, Kostenko O, Malone D | title = MAO inhibitors: risks, benefits, and lore | journal = Cleveland Clinic Journal of Medicine | volume = 77 | issue = 12 | pages = 859–882 | date = December 2010 | pmid = 21147941 | doi = 10.3949/ccjm.77a.09103 | doi-access = free }}

Although changes in neurochemistry are found immediately after taking these antidepressants, symptoms may not begin to improve until several weeks after administration. Increased transmitter levels in the synapse alone does not relieve the depression or anxiety.

The cholinergic system consists of projection neurons from the pedunculopontine nucleus, laterodorsal tegmental nucleus, and basal forebrain and interneurons from the striatum and nucleus accumbens. It is not yet clear whether acetylcholine as a neuromodulator acts through volume transmission or classical synaptic transmission, as there is evidence to support both theories. Acetylcholine binds to both metabotropic muscarinic receptors (mAChR) and the ionotropic nicotinic receptors (nAChR). The cholinergic system has been found to be involved in responding to cues related to the reward pathway, enhancing signal detection and sensory attention, regulating homeostasis, mediating the stress response, and encoding the formation of memories.{{cite journal | vauthors = Picciotto MR, Higley MJ, Mineur YS | title = Acetylcholine as a neuromodulator: cholinergic signaling shapes nervous system function and behavior | journal = Neuron | volume = 76 | issue = 1 | pages = 116–129 | date = October 2012 | pmid = 23040810 | pmc = 3466476 | doi = 10.1016/j.neuron.2012.08.036 }}{{cite journal | vauthors = Hasselmo ME, Sarter M | title = Modes and models of forebrain cholinergic neuromodulation of cognition | journal = Neuropsychopharmacology | volume = 36 | issue = 1 | pages = 52–73 | date = January 2011 | pmid = 20668433 | pmc = 2992803 | doi = 10.1038/npp.2010.104 }}

File:GABA Nomenclature Example1 V.1.svg

Gamma-aminobutyric acid (GABA) has an inhibitory effect on brain and spinal cord activity. GABA is an amino acid that is the primary inhibitory neurotransmitter for the central nervous system (CNS). It reduces neuronal excitability by inhibiting nerve transmission. GABA has a multitude of different functions during development and influences the migration, proliferation, and proper morphological development of neurons. It also influences the timing of critical periods and potentially primes the earliest neuronal networks. There are two main types of GABA receptors: GABAa and GABAb. GABAa receptors inhibit neurotransmitter release and/or neuronal excitability and are a ligand-gated chloride channel. GABAb receptors are slower to react due to a GCPR that acts to inhibit neurons. GABA can be the culprit for many disorders ranging from schizophrenia to major depressive disorder because of its inhibitory characteristics being dampened.{{cite book | vauthors = Allen MJ, Sabir S, Sharma S | chapter = GABA Receptor |date=2024 | title = StatPearls | chapter-url = http://www.ncbi.nlm.nih.gov/books/NBK526124/ |access-date=2024-06-27 |place=Treasure Island (FL) |publisher=StatPearls Publishing |pmid=30252380 }}{{cite journal | vauthors = Sigel E, Steinmann ME | title = Structure, function, and modulation of GABA(A) receptors | journal = The Journal of Biological Chemistry | volume = 287 | issue = 48 | pages = 40224–40231 | date = November 2012 | pmid = 23038269 | pmc = 3504738 | doi = 10.1074/jbc.R112.386664 | doi-access = free }}{{Cite book | vauthors = Sorge R |title=Dynamics of Pain |date=2020 |publisher=Great River | isbn = 978-1-64496-496-5 }}

{{Main|Neuropeptide}}

Neuropeptides are small proteins used for communication in the nervous system. Neuropeptides represent the most diverse class of signaling molecules, and vary considerably between animals. There are 90 known genes that encode human neuropeptide precursors. In the fruit fly Drosophila there are ~50 known genes encoding precursors,{{cite journal | vauthors = Nässel DR, Zandawala M | title = Recent advances in neuropeptide signaling in Drosophila, from genes to physiology and behavior | journal = Progress in Neurobiology | volume = 179 | pages = 101607 | date = August 2019 | pmid = 30905728 | doi = 10.1016/j.pneurobio.2019.02.003 }} and in the worm C. elegans 120 genes specify more than 250 neuropeptides.{{cite journal |last1=Alcedo |first1=Joy |last2=Prahlad |first2=Veena |title=Neuromodulators: an essential part of survival |journal=Journal of Neurogenetics |date=October 2020 |volume=34 |issue=3–4 |pages=475–481 |doi=10.1080/01677063.2020.1839066 |pmid=33170042 |pmc=7811185 }} Most neuropeptides bind to G-protein coupled receptors, however some neuropeptides directly gate ion channels{{cite journal |last1=Cottrell |first1=Glen A. |title=The First Peptide-Gated Ion Channel |journal=Journal of Experimental Biology |date=15 September 1997 |volume=200 |issue=18 |pages=2377–2386 |doi=10.1242/jeb.200.18.2377 |pmid=9343851 |bibcode=1997JExpB.200.2377C }} or act through kinase receptors.{{cite journal |last1=Rozengurt |first1=Enrique |title=Signal transduction pathways in the mitogenic response to G protein-coupled neuropeptide receptor agonists |journal=Journal of Cellular Physiology |date=December 1998 |volume=177 |issue=4 |pages=507–517 |doi=10.1002/(SICI)1097-4652(199812)177:4<507::AID-JCP2>3.0.CO;2-K |pmid=10092204 }}

• Opioid peptides – a large family of endogenous neuropeptides that are widely distributed throughout the central and peripheral nervous system. Opiate drugs such as heroin and morphine act at the receptors of these neurotransmitters.{{cite book|title=Principles of Neural Science| vauthors = Kandel ER |publisher=Appleton & Lang|year=1991|isbn=978-0-8385-8034-9|location=East Norwalk, Connecticut|pages=[https://archive.org/details/principlesofneur00kan/page/872 872–873]|url-access=registration|url=https://archive.org/details/principlesofneur00kan/page/872}} {{verify source |date=September 2019 |reason=This ref was deleted Special:Diff/912795686 by a bug in VisualEditor and later restored by a bot from the original cite located at Special:Permalink/907671901 cite #14 - verify the cite is accurate and delete this template. User:GreenC bot/Job 18}}{{cite journal | vauthors = Froehlich JC | title = Opioid peptides | journal = Alcohol Health and Research World | volume = 21 | issue = 2 | pages = 132–136 | date = 1 January 1997 | pmid = 15704349 | pmc = 6826828 | url = http://pubs.niaaa.nih.gov/publications/arh21-2/132.pdf }} {{verify source |date=September 2019 |reason=This ref was deleted Special:Diff/912795686 by a bug in VisualEditor and later restored by a bot from the original cite located at Special:Permalink/907671901 cite #22 - verify the cite is accurate and delete this template. User:GreenC bot/Job 18}}

1. Endorphins
2. Enkephalins
3. Dynorphins

• Vasopressin
• Oxytocin
• Gastrin
• Cholecystokinins
• Somatostatin
• Cortistatins
• RF-amides
• Neuropeptide FF
• Neuropeptide Y -
• Pancreatic Polypeptide
• Peptide YY
• Prolactin-releasing peptide
• Calcitonin
• Adrenomedullin
• Natriuretic
• Bombesin-like peptides
• Endothelin
• Glucagon
• Secretin
• Vasoactive Intestinal Peptide
• Growth Hormone Releasing Hormone
• Gastric Inhibitory Peptide
• Corticotropin Releasing Hormone
• Urocortin
• Urotensin
• Substance P
• Neuromedins
• Tensin
• Kinin
• Granin
• Nerve Growth Factor
• Motilin
• Ghrelin
• Galanin
• Neuropeptide B/W
• Neurexophilin
• Insulin
• Relaxin
• Agouti-related protein homolog gene
• Prolactin
• Apelin
• Metastasis-suppressor
• Diazepam-binding inhibitor
• Cerebellins
• Leptin
• Adiponectin
• Visfatin
• Resistin
• Nucleibindin
• Ubiquitin

Neuromodulators may alter the output of a physiological system by acting on the associated inputs (for instance, central pattern generators). However, modeling work suggests that this alone is insufficient,{{cite journal | vauthors = Stern E, Fort TJ, Miller MW, Peskin CS, Brezina V | title = Decoding modulation of the neuromuscular transform | journal = Neurocomputing | volume = 70 | issue = 10 | pages = 1753–1758 | date = June 2007 | pmid = 19763188 | pmc = 2745187 | doi = 10.1016/j.neucom.2006.10.117 }} because the neuromuscular transformation from neural input to muscular output may be tuned for particular ranges of input. Stern et al. (2007) suggest that neuromodulators must act not only on the input system but must change the transformation itself to produce the proper contractions of muscles as output.

Neurotransmitter systems are systems of neurons in the brain expressing certain types of neurotransmitters, and thus form distinct systems. Activation of the system causes effects in large volumes of the brain, called volume transmission.{{cite journal | vauthors = Taber KH, Hurley RA | title = Volume transmission in the brain: beyond the synapse | journal = The Journal of Neuropsychiatry and Clinical Neurosciences | volume = 26 | issue = 1 | pages = iv, 1-iv, 4 | date = January 2014 | pmid = 24515717 | doi = 10.1176/appi.neuropsych.13110351 | doi-access = free }} Volume transmission is the diffusion of neurotransmitters through the brain extracellular fluid released at points that may be remote from the target cells with the resulting activation of extra-synaptic receptors, and with a longer time course than for transmission at a single synapse.{{cite journal | vauthors = Castañeda-Hernández GC, Bach-y-Rita P | title = Volume transmission and pain perception | journal = TheScientificWorldJournal | volume = 3 | pages = 677–683 | date = August 2003 | pmid = 12920309 | pmc = 5974734 | doi = 10.1100/tsw.2003.53 | doi-access = free }} Such prolonged transmitter action is called tonic transmission, in contrast to the phasic transmission that occurs rapidly at single synapses.{{cite journal | vauthors = Dreyer JK, Herrik KF, Berg RW, Hounsgaard JD | title = Influence of phasic and tonic dopamine release on receptor activation | journal = The Journal of Neuroscience | volume = 30 | issue = 42 | pages = 14273–14283 | date = October 2010 | pmid = 20962248 | pmc = 6634758 | doi = 10.1523/JNEUROSCI.1894-10.2010 }}{{cite journal | vauthors = Goto Y, Otani S, Grace AA | title = The Yin and Yang of dopamine release: a new perspective | journal = Neuropharmacology | volume = 53 | issue = 5 | pages = 583–587 | date = October 2007 | pmid = 17709119 | pmc = 2078202 | doi = 10.1016/j.neuropharm.2007.07.007 }}

There are three main components of tonic transmission: Continued release, sustained release, and baseline regulation. In the context of neuromodulation, continuous release is responsible for releasing neurotransmitters/neuromodulators at a constant low level from glial cells and tonic active neurons. Sustained Influence provides long-term stability to the entire process, and baseline regulation ensures that the neurons are in a continued state of readiness to respond to any signals. Acetylcholine, noradrenaline, dopamine, norepinephrine, and serotonin are some of the main components in tonic transmission to mediate arousal and attention.{{cite journal |last1=Peña-Ortega |first1=Fernando |title=Tonic Neuromodulation of the Inspiratory Rhythm Generator |journal=Frontiers in Physiology |date=2012 |volume=3 |page=253 |doi=10.3389/fphys.2012.00253 |doi-access=free |pmid=22934010 |pmc=3429030 }}

There are three main components of phasic transmission: burst release, transient effects, and stimulus-driven effects. As the name suggests, burst release is in charge of releasing neurotransmitters/neuromodulators in intense, acute bursts. Transient effects create acute momentary adjustments in neural activity. Lastly, as the name suggests, stimulus-driven effects react to sensory input, external stressors, and reward stimuli, which involve dopamine, norepinephrine, and serotonin.{{cite journal |last1=Özçete |first1=Özge D. |last2=Banerjee |first2=Aditi |last3=Kaeser |first3=Pascal S. |title=Mechanisms of neuromodulatory volume transmission |journal=Molecular Psychiatry |date=November 2024 |volume=29 |issue=11 |pages=3680–3693 |doi=10.1038/s41380-024-02608-3 |pmid=38789677 |pmc=11540752 }}

{{Main article|Neurotherapy}}

The term Neuromodulation is also known in medicine as a targeted artificial modification of neuronal activity through the delivery of chemical agents or electroceutical stimulation to specific neurological parts (see more in the wikiarticle Neuromodulation (medicine))."International Neuromodulation Society home page". Retrieved 4 March 2025 from https://www.neuromodulation.com/.

Invasive and non-invasive treatment methods form a field of medicine called neurotherapy. There are two main categories for neuromodulation therapy: chemical and electroceutical. The noninvasive electroceutical neurotherapy consists of five techniques:{{cite journal |last1=Val Danilov |first1=Igor |title=The Origin of Natural Neurostimulation: A Narrative Review of Noninvasive Brain Stimulation Techniques |journal=OBM Neurobiology |date=29 November 2024 |volume=08 |issue=4 |pages=1–23 |doi=10.21926/obm.neurobiol.2404260 |doi-access=free }}

• Photonics neurostimulation through the image-forming vision pathways and skin irradiation. This technique is known as Light therapy, and also known as Phototherapy or Luxtherapy. It refers to the body's exposure to intensive electrical light at managed wavelengths to treat different diseases: Depression, Chronic pain, Post-traumatic stress disorder, and Insomnia.Huang X, Tao Q, Ren C (2024). "A comprehensive overview of the neural mechanisms of light therapy". Neurosci Bull. 2024; 40: 350-362.
• Transcranial laser radiation refers to directional low-power and high-fluence monochromatic or quasimonochromatic light radiation, also known as photobiomodulation (PBM).Fernandes F, Oliveira S, Monteiro F, Gasik M, Silva FS, Sousa N, et al. (2024). "Devices used for photobiomodulation of the brain—A comprehensive and systematic review". J NeuroEng Rehabil. 2024; 21: 53.
• Transcranial electric current and magnetic field stimulations;
• Low-frequency sound stimulations, including vibroacoustic therapy (VAT) and rhythmic auditory stimulation (RAS).Wang X, Xie Z, Du G (2024). "Research on the intervention effect of vibroacoustic therapy in the treatment of patients with depression". Int J Ment Health Promot. 2024; 26: 149-160.Lam HL, Li WT, Laher I, Wong RY. (2020). "Effects of music therapy on patients with dementia—A systematic review". Geriatrics. 2020; 5: 62.
• Acoustic photonic intellectual neurostimulation (APIN). It applies features of natural neurostimulation during pregnancy scaled on specific patients. Three therapeutic agents cause oxygenation of neuronal tissues, release of adenosine-5′-triphosphate proteins, and neuronal plasticity. This method shows significant results in chronic pain management in various conditions.{{cite journal |last1=Mihailova |first1=Sandra |last2=Medne |first2=Dace |last3=Val Danilov |first3=Igor |title=Acoustic photonic intellectual neurostimulation (APIN) in dysmenorrhea management: a case study on an adolescent |journal=Brain Stimulation |date=January 2025 |volume=18 |issue=1 |pages=510 |doi=10.1016/j.brs.2024.12.860 |doi-access=free }}{{cite journal |last1=Medne |first1=Dace |last2=Val Danilov |first2=Igor |last3=Mihailova |first3=Sandra |title=The effect of acoustic and photonic intervention combined with mental load on chronic headaches: a case study |journal=Brain Stimulation |date=January 2025 |volume=18 |issue=1 |pages=542–543 |doi=10.1016/j.brs.2024.12.955 |doi-access=free }}{{cite journal |last1=Val Danilov |first1=Igor |last2=Medne |first2=Dace |last3=Mihailova |first3=Sandra |title=Modulating neuroplasticity with acoustic photonic intellectual neurostimulation (APIN): a case study on neurodegenerative disorder |journal=Brain Stimulation |date=January 2025 |volume=18 |issue=1 |pages=561 |doi=10.1016/j.brs.2024.12.1005 |doi-access=free }}

Electrical neuromodulation has three subcategories: deep brain, spinal cord, and transcranial, each aiming to treat specific conditions. Deep brain stimulation involves electrodes being surgically implanted into specific sections of the brain that are commonly responsible for movement and motor control deficiencies and disorders like Parkinson's and tremors. Spinal cord stimulation works by being placed near the spinal cord to send electrical signals through the body to treat various forms of chronic pain like lower back pain and CRPS. This form of neuromodulator treatment is considered one of the more high-risk treatments because of its manipulation near the spinal cord. Transcranial magnetic stimulation is slightly different in that it utilizes a magnetic field to generate electrical currents throughout the brain. This treatment is widely used to remedy various mental health conditions like depression, obsessive-compulsive disorder, and other mood disorders.{{cite book |doi=10.1016/B978-0-12-374248-3.00002-1 |quote=Neuroprostheses such as cochlear implants and sacral root stimulators are also commonly included within the definition of neuromodulation. Electrical neuromodulation is electrical stimulation of the brain, spinal cord, peripheral nerves, plexuses of nerves, the autonomic system, and functional electrical stimulation of the muscles, while chemical neuromodulation uses direct placement of chemical agents to neural tissues through utilization of technology of implantation such as epidural or intrathecal delivery systems. |chapter=What is Neuromodulation? |title=Neuromodulation |date=2009 |pages=3–8 |isbn=978-0-12-374248-3 | vauthors = Krames ES, Hunter Peckham P, Rezai A, Aboelsaad F }}

Neuromodulation is often used as a treatment mechanism for moderate to severe migraines by way of nerve stimulation. These treatments work by utilizing the basic ascending pathways. There are three main modes. It works by connecting a device to the body that sends electrical pulses directly to the affected site (Transcutaneous Electrical Nerve Stimulation), directly to the brain (invasive electrical Neurotherapy techniques), or by holding a device close to the neck that works to block pain signals modulation from the PNS to the CNS.{{cite web | url=https://www.barrowneuro.org/treatment/neuromodulation-for-headache/ | title=Neuromodulation for Headache }}{{cite web | url=https://medspaclinics.co.uk/benefits-of-botox-for-wrinkle-reduction/ | title=Benefits of Botox for Wrinkle Reduction }} and sends two of the most notable modes of that treatment, which are electrical and magnetic stimulation. Electrical nerve 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.{{cn|date=January 2025}}

Chemical neuromodulation mostly consists of collaborating natural and artificial chemical substances to treat various conditions. It uses both invasive and non-invasive modes of treatment, including pumps, injections, and oral medications. This mode of treatment can be used to manage immune responses like inflammation, mood, and motor disorders.{{cite web | url=https://neuro.stonybrookmedicine.edu/neuromodulation/disorderstreated | title=Disorders Treated with Neuromodulation Therapies | Stony Brook Neurosciences Institute }}

• Three-factor learning
• 5-HT2c receptor agonist
• Natural neuroactive substance

{{Reflist|30em}}

• North American Neuromodulation Society
• [https://web.archive.org/web/20120204072709/http://serendip.brynmawr.edu/bb/neuro/neuro98/202s98-paper2/Casasanto2.html Neuromodulation and Neural Plasticity]
• [http://www.neuromodulation.com/ International Neuromodulation Society]
• [https://web.archive.org/web/20090210225330/http://www.scholarpedia.org/article/Neuromodulation Scolarpedia article on neuromodulation]

{{Neuromodulation}}

{{Nervous system}}

{{Neuroscience}}

{{Cell signaling}}

{{Telencephalon}}

{{Diencephalon}}

{{Mesencephalon}}

{{Rhombencephalon}}

{{Authority control}}

Category:Neurochemistry

Category:Neurophysiology