Gamma wave

From Wikipedia, the free encyclopedia
Jump to navigation Jump to search
Gamma waves

A gamma wave is a pattern of neural oscillation in humans with a frequency between 25 and 140 Hz, the 40-Hz point being of particular interest.[1] Gamma rhythms are correlated with large scale brain network activity and cognitive phenomena such as working memory, attention, and perceptual grouping, and can be increased in amplitude via meditation[2] or neurostimulation.[1][3] Altered gamma activity has been observed in many mood and cognitive disorders such as Alzheimer's disease,[4] epilepsy,[5] and schizophrenia.[6]

Discovery[edit]

Gamma waves can be detected by electroencephalography or magnetoencephalography. One of the earliest reports of gamma wave activity was recorded from the visual cortex of awake monkeys.[7] Subsequently, significant research activity has concentrated on gamma activity in visual cortex.[8][9][10][11]

Gamma activity has also been detected and studied across premotor, parietal, temporal, and frontal cortical regions[12] Gamma waves constitute a common class of oscillatory activity in neurons belonging to the cortico-basal ganglia-thalamo-cortical loop.[13] Typically, this activity is understood to reflect feedforward connections between distinct brain regions, in contrast to alpha wave feedback across the same regions.[14] Gamma oscillations have also been shown to correlate with the firing of single neurons, mostly inhibitory neurons, during all states of the wake-sleep cycle.[15] Gamma wave activity is most prominent during alert, attentive wakefulness.[13] However, the mechanisms and substrates by which gamma activity may help to generate different states of consciousness remain unknown.

Controversy[edit]

Some researchers contest the validity or meaningfulness of gamma wave activity detected by scalp EEG, because the frequency band of gamma waves overlaps with the electromyographic frequency band. Thus, gamma signal recordings could be contaminated by muscle activity.[16] Studies utilizing local muscle paralysis techniques have confirmed that EEG recordings do contain EMG signal,[17][18] and these signals can be traced to local motor dynamics such as saccade rate[19] or other motor actions involving the head. Advances in signal processing and separation, such as the application of independent component analysis or other techniques based on spatial filtering, have been proposed to reduce the presence of EMG artifacts.[16]

Function[edit]

Conscious perception[edit]

Electrocorticographic movie showing changes in high-frequency broadband gamma activity in specific cortical regions when visual stimuli are presented during a face-/place-naming task.

Gamma waves may participate in the formation of coherent, unified perception, also known as the problem of combination in the binding problem, due to their apparent synchronization of neural firing rates across distinct brain regions.[20][21][22] 40-Hz gamma waves were first suggested to participate in visual consciousness in 1988[23] that two neurons oscillate synchronously (though they are not directly connected) when a single external object stimulates their respective receptive fields. Subsequent experiments by many others demonstrated this phenomenon in a wide range of visual cognition. In particular, Francis Crick and Christof Koch in 1990[24] argued that there is a significant relation between the binding problem and the problem of visual consciousness and, as a result, that synchronous 40 Hz oscillations may be causally implicated in visual awareness as well as in visual binding. Later the same authors expressed skepticism over the idea that 40-Hz oscillations are a sufficient condition for visual awareness.[25]

A number of experiments conducted by Rodolfo Llinás supports a hypothesis that the basis for consciousness in awake states and dreaming is 40-Hz oscillations throughout the cortical mantle in the form of thalamocortical iterative recurrent activity. In two papers entitled "Coherent 40-Hz oscillation characterizes dream state in humans” (Rodolfo Llinás and Urs Ribary, Proc Natl Acad Sci USA 90:2078-2081, 1993) and "Of dreaming and wakefulness” (Llinas & Pare, 1991), Llinás proposes that the conjunction into a single cognitive event could come about by the concurrent summation of specific and nonspecific 40-Hz activity along the radial dendritic axis of given cortical elements, and that the resonance is modulated by the brainstem and is given content by sensory input in the awake state and intrinsic activity during dreaming. According to Llinás’ hypothesis, known as the thalamocortical dialogue hypothesis for consciousness, the 40-Hz oscillation seen in wakefulness and in dreaming is proposed to be a correlate of cognition, resultant from coherent 40-Hz resonance between thalamocortical-specific and nonspecific loops. In Llinás & Ribary (1993), the authors propose that the specific loops give the content of cognition, and that a nonspecific loop gives the temporal binding required for the unity of cognitive experience.

A lead article by Andreas K. Engel et al. in the journal Consciousness and Cognition (1999) that argues for temporal synchrony as the basis for consciousness, defines the gamma wave hypothesis thus: [26]

The hypothesis is that synchronization of neuronal discharges can serve for the integration of distributed neurons into cell assemblies and that this process may underlie the selection of perceptually and behaviorally relevant information.

Attention[edit]

The suggested mechanism is that gamma waves relate to neural consciousness via the mechanism for conscious attention:

The proposed answer lies in a wave that, originating in the thalamus, sweeps the brain from front to back, 40 times per second, drawing different neuronal circuits into synch with the precept [sic], and thereby bringing the precept [sic] into the attentional foreground. If the thalamus is damaged even a little bit, this wave stops, conscious awarenesses do not form, and the patient slips into profound coma.[21]

Thus the claim is that when all these neuronal clusters oscillate together during these transient periods of synchronized firing, they help bring up memories and associations from the visual percept to other notions. This brings a distributed matrix of cognitive processes together to generate a coherent, concerted cognitive act, such as perception. This has led to theories that gamma waves are associated with solving the binding problem.[20]

Gamma waves are observed as neural synchrony from visual cues in both conscious and subliminal stimuli.[27][28][29] [30] This research also sheds light on how neural synchrony may explain stochastic resonance in the nervous system.[31]

Clinical relevance[edit]

Mood disorders[edit]

Altered gamma wave activity is associated with mood disorders such as major depression or bipolar disorder and may be a potential biomarker to differentiate between unipolar and bipolar disorders. For example, human subjects with high depression scores exhibit differential gamma signaling when performing emotional, spatial, or arithmetic tasks. Increased gamma signaling is also observed in brain regions that participate in the default mode network, which is normally suppressed during tasks requiring significant attention. Rodent models of depression-like behaviors also exhibit deficient gamma rhythms.[32]

Schizophrenia[edit]

Decreased gamma-wave activity is observed in schizophrenia. Specifically, the amplitude of gamma oscillations is reduced, as is the synchrony of different brain regions involved in tasks such as visual oddball and Gestalt perception. People with schizophrenia perform worse on these behavioral tasks, which relate to perception and continuous recognition memory.[33] The neurobiological basis of gamma dysfunction in schizophrenia is thought to lie with GABAergic interneurons involved in known brain wave rhythm-generating networks.[34] Antipsychotic treatment, which diminishes some behavioral symptoms of schizophrenia, does not restore gamma synchrony to normal levels.[33]

Epilepsy[edit]

Gamma oscillations are observed in the majority of seizures[5] and may contribute to their onset in epilepsy. Visual stimuli such as large, high-contrast gratings that are known to trigger seizures in photosensitive epilepsy also drive gamma oscillations in visual cortex.[35] During a focal seizure event, maximal gamma rhythm synchrony of interneurons is always observed in the seizure onset zone, and synchrony propagates from the onset zone over the whole epileptogenic zone.[36]

Alzheimer's disease[edit]

Enhanced gamma band power and lagged gamma responses have been observed in patients with Alzheimer's disease (AD).[4][37] Interestingly, the tg APP-PS1 mouse model of AD exhibits decreased gamma oscillation power in the lateral entorhinal cortex, which transmits various sensory inputs to the hippocampus and thus participates in memory processes analogous to those affected by human AD.[38] Decreased hippocampal slow gamma power has also been observed in the 3xTg mouse model of AD.[39]

Gamma stimulation may have therapeutic potential for AD and other neurodegenerative diseases. Optogenetic stimulation of fast-spiking interneurons in the gamma wave frequency range was first demonstrated in mice in 2009. [40] Entrainment or synchronization of hippocampal gamma oscillations and spiking to 40 Hz via non-invasive stimuli in the gamma frequency band, such as flashing lights or pulses of sound,[3] reduces amyloid beta load and activates microglia in the well-established 5XFAD mouse model of AD.[41] Subsequent human clinical trials of gamma band stimulation have shown mild cognitive improvements in AD patients who have been exposed to light, sound, or tactile stimuli in the 40 Hz range.[1] However, the precise molecular and cellular mechanisms by which gamma band stimulation ameliorates AD pathology is unknown.

Fragile X syndrome[edit]

Hypersensitivity and memory deficits in Fragile X syndrome may be linked to gamma rhythm abnormalities in sensory cortex and hippocampus. For example, decreased synchrony of gamma oscillations has been observed in auditory cortex of FXS patients. The FMR1 knockout rat model of FXS exhibits an increased ratio of slow (~25-50 Hz)to fast (~55-100 Hz) gamma waves.[39]

Meditation and mindfulness[edit]

High-amplitude gamma wave synchrony can be self-induced via meditation. Long-term practitioners of meditation such as Tibetan Buddhist monks exhibit both increased gamma-band activity at baseline as well as significant increases in gamma synchrony during meditation, as determined by scalp EEG.[2] fMRI on the same monks revealed greater activation of right insular cortex and caudate nucleus during meditation.[42] The neurobiological mechanisms of gamma synchrony induction are thus highly plastic.[43] This evidence may support the hypothesis that one's sense of consciousness, stress management ability, and focus, often said to be enhanced after meditation, are all underpinned by gamma activity. At the 2005 annual meeting of the Society for Neuroscience, the current Dalai Lama commented that if neuroscience could propose a way to induce the psychological and biological benefits of meditation without intensive practice, he "would be an enthusiastic volunteer."[44]

See also[edit]

Brain waves[edit]

External links[edit]

References[edit]

  1. ^ a b c McDermott B, Porter E, Hughes D, McGinley B, Lang M, O'Halloran M, Jones M. (2018). "Gamma Band Neural Stimulation in Humans and the Promise of a New Modality to Prevent and Treat Alzheimer's Disease". J Alzheimers Dis. 65 (2): 363–392. doi:10.3233/JAD-180391. PMC 6130417. PMID 30040729.CS1 maint: multiple names: authors list (link)
  2. ^ a b Lutz A, Greischar LL, Rawlings NB, Ricard M, Davidson RJ (2004). "Long-term meditators self-induce high-amplitude gamma synchrony during mental practice". Proc Natl Acad Sci U S A. 101 (46): 16369–73. doi:10.1073/pnas.0407401101. PMC 526201. PMID 15534199.CS1 maint: multiple names: authors list (link)
  3. ^ a b Thomson H (2018). "How flashing lights and pink noise might banish Alzheimer's, improve memory and more". Nature. 555 (7694): 20–22. doi:10.1038/d41586-018-02391-6. PMID 29493598.
  4. ^ a b van Deursen JA, Vuurman EF, Verhey FR, van Kranen-Mastenbroek VH, Riedel WJ (2008). "Increased EEG gamma band activity in Alzheimer's disease and mild cognitive impairment". J Neural Transm (Vienna). 115 (9): 1301–11. doi:10.1007/s00702-008-0083-y. PMC 2525849. PMID 18607528.CS1 maint: multiple names: authors list (link)
  5. ^ a b Hughes JR (July 2008). "Gamma, fast, and ultrafast waves of the brain: their relationships with epilepsy and behavior". Epilepsy Behav. 13 (1): 25–31. doi:10.1016/j.yebeh.2008.01.011. PMID 18439878.
  6. ^ Jia X, Kohn A (2011). "Gamma rhythms in the brain". PLOS Biol. 9 (4): e1001045. doi:10.1371/journal.pbio.1001045. PMC 3084194. PMID 21556334.
  7. ^ HUGHES JR (1964). "Responses from the Visual Cortex of Unanesthetized Monkeys". Int Rev Neurobiol. International Review of Neurobiology. 6: 99–152. doi:10.1016/s0074-7742(08)60266-4. ISBN 9780123668073. PMID 14282370.
  8. ^ Adjamian, P; Holliday, IE; Barnes, GR; Hillebrand, A; Hadjipapas, A; Singh, KD (2004). "Induced stimulus-dependent Gamma oscillations in visual stress". European Journal of Neuroscience. 20 (2): 587–592. doi:10.1111/j.1460-9568.2004.03495.x. PMID 15233769.
  9. ^ Hadjipapas A.; Adjamian P; Swettenham J.B.; Holliday I.E.; Barnes G.R. (2007). "Stimuli of varying spatial scale induce gamma activity with distinct temporal characteristics in human visual cortex". NeuroImage. 35 (2): 518–30. doi:10.1016/j.neuroimage.2007.01.002. PMID 17306988.
  10. ^ Muthukumaraswamy SD, Singh KD (2008). "Spatiotemporal frequency tuning of BOLD and gamma band MEG responses compared in primary visual cortex". NeuroImage. 40 (4): 1552–1560. doi:10.1016/j.neuroimage.2008.01.052. PMID 18337125.
  11. ^ Swettenham JB, Muthukumaraswamy SD, Singh KD (2009). "Spectral properties of induced and evoked gamma oscillations in human early visual cortex to moving and stationary stimuli". Journal of Neurophysiology. 102 (2): 1241–1253. doi:10.1152/jn.91044.2008. PMID 19515947.
  12. ^ Kort, N; Cuesta, P; Houde, JF; Nagarajan, SS (2016). "Bihemispheric network dynamics coordinating vocal feedback control". Human Brain Mapping. 37 (4): 1474–1485. doi:10.1002/hbm.23114. PMID 26917046.
  13. ^ a b McCormick DA, McGinley MJ, Salkoff DB (2015). "Brain state dependent activity in the cortex and thalamus". Curr Opin Neurobiol. 31: 133–40. doi:10.1016/j.conb.2014.10.003. PMC 4375098. PMID 25460069.CS1 maint: multiple names: authors list (link)
  14. ^ van Kerkoerle T, Self MW, Dagnino B, Gariel-Mathis MA, Poort J, van der Togt C, Roelfsema PR (2014). "Alpha and gamma oscillations characterize feedback and feedforward processing in monkey visual cortex". Proc Natl Acad Sci U S A. 111 (40): 14332–41. doi:10.1073/pnas.1402773111. PMC 4210002. PMID 25205811.CS1 maint: multiple names: authors list (link)
  15. ^ Le Van Quyen M.; Muller L.E.; Telenczuk B.; Halgren E.; Cash S.; Hatsopoulos N.; Dehghani N.; Destexhe A. (2016). "High-frequency oscillations in human and monkey neocortex during the wake-sleep cycle". Proceedings of the National Academy of Sciences USA. 113 (33): 9363–8. doi:10.1073/pnas.1523583113. PMC 4995938. PMID 27482084.
  16. ^ a b Muthukumaraswamy SD (2013). "High-frequency brain activity and muscle artifacts in MEG/EEG: a review and recommendations". Front Hum Neurosci. 7: 138. doi:10.3389/fnhum.2013.00138. PMC 3625857. PMID 23596409.
  17. ^ Whitham EM, Pope KJ, Fitzgibbon SP, et al. (Aug 2007). "Scalp electrical recording during paralysis: quantitative evidence that EEG frequencies above 20 Hz are contaminated by EMG". Clin Neurophysiol. 118 (8): 1877–88. doi:10.1016/j.clinph.2007.04.027. PMID 17574912.
  18. ^ Whitham EM, Lewis T, Pope KJ, et al. (May 2008). "Thinking activates EMG in scalp electrical recordings". Clin Neurophysiol. 119 (5): 1166–75. doi:10.1016/j.clinph.2008.01.024. PMID 18329954.
  19. ^ Yuval-Greenberg S, Tomer O, Keren AS, Nelken I, Deouell LY (May 2008). "Transient induced gamma-band response in EEG as a manifestation of miniature saccades". Neuron. 58 (3): 429–41. doi:10.1016/j.neuron.2008.03.027. PMID 18466752.
  20. ^ a b Buzsaki, György (2006). "Cycle 9, The Gamma Buzz". Rhythms of the brain. Oxford. ISBN 978-0195301069.
  21. ^ a b Robert Pollack, The Missing Moment, 1999
  22. ^ Singer, W.; Gray, C.M. (1995). "Visual feature integration and the temporal correlation hypothesis". Annu. Rev. Neurosci. 18: 555–586. CiteSeerX 10.1.1.308.6735. doi:10.1146/annurev.ne.18.030195.003011. PMID 7605074.
  23. ^ Ian Gold (1999). "Does 40-Hz oscillation play a role in visual consciousness?". Consciousness and Cognition. 8 (2): 186–195. doi:10.1006/ccog.1999.0399. PMID 10448001.
  24. ^ Crick, F., & Koch, C. (1990b). Towards a neurobiological theory of consciousness. Seminars in the Neurosciences v.2, 263-275.
  25. ^ Crick, F., Koch, C. (2003). "Framework for consciousness". Nature Neuroscience. 6 (2): 119–26. doi:10.1038/nn0203-119. PMID 12555104.CS1 maint: multiple names: authors list (link)
  26. ^ Andreas K. Engel; Pascal Fries; Peter Koenig; Michael Brecht; Wolf Singer (1999). "Temporal Binding, Binocular Rivalry, and Consciousness". Consciousness and Cognition. 8 (2): 128–151. CiteSeerX 10.1.1.207.8191. doi:10.1006/ccog.1999.0389. PMID 10447995.
  27. ^ Melloni L, Molina C, Pena M, Torres D, Singer W, Rodriguez E (Mar 2007). "Synchronization of neural activity across cortical areas correlates with conscious perception". J Neurosci. 27 (11): 2858–65. doi:10.1523/JNEUROSCI.4623-06.2007. PMC 6672558. PMID 17360907.
  28. ^ Siegel M, Donner TH, Oostenveld R, Fries P, Engel AK (Mar 2008). "Neuronal synchronization along the dorsal visual pathway reflects the focus of spatial attention". Neuron. 60 (4): 709–719. doi:10.1016/j.neuron.2008.09.010. PMID 19038226.
  29. ^ Gregoriou GG, Gotts SJ, Zhou H, Desimone R (Mar 2009). "High-frequency, long-range coupling between prefrontal and visual cortex during attention". Science. 324 (5931): 1207–1210. Bibcode:2009Sci...324.1207G. doi:10.1126/science.1171402. PMC 2849291. PMID 19478185.
  30. ^ Baldauf D, Desimone R (Mar 2014). "Neural mechanisms of object-based attention". Science. 344 (6182): 424–427. Bibcode:2014Sci...344..424B. doi:10.1126/science.1247003. PMID 24763592.
  31. ^ Ward LM, Doesburg SM, Kitajo K, MacLean SE, Roggeveen AB (Dec 2006). "Neural synchrony in stochastic resonance, attention, and consciousness". Can J Exp Psychol. 60 (4): 319–26. doi:10.1037/cjep2006029. PMID 17285879.
  32. ^ Fitzgerald PJ, Watson BO (2018). "Gamma oscillations as a biomarker for major depression: an emerging topic". Transl Psychiatry. 8 (1): 177. doi:10.1038/s41398-018-0239-y. PMC 6123432. PMID 30181587.
  33. ^ a b Bruce Bower (2004). "Synchronized thinking. Brain activity linked to schizophrenia, skillful meditation". Science News. 166 (20): 310. doi:10.2307/4015767. JSTOR 4015767.
  34. ^ Uhlhaas PJ, Singer W (2010). "Abnormal neural oscillations and synchrony in schizophrenia". Nat Rev Neurosci. 11 (2): 100–13. doi:10.1038/nrn2774. PMID 20087360.
  35. ^ Hermes D, Kasteleijn-Nolst Trenité DGA, Winawer J (2017). "Gamma oscillations and photosensitive epilepsy". Curr Biol. 27 (9): R336–R338. doi:10.1016/j.cub.2017.03.076. PMC 5438467. PMID 28486114.CS1 maint: multiple names: authors list (link)
  36. ^ Sato Y, Wong SM, Iimura Y, Ochi A, Doesburg SM, Otsubo H (2017). "Spatiotemporal changes in regularity of gamma oscillations contribute to focal ictogenesis". Sci Rep. 7 (1): 9362. doi:10.1038/s41598-017-09931-6. PMC 5570997. PMID 28839247.CS1 maint: multiple names: authors list (link)
  37. ^ Başar E, Emek-Savaş DD, Güntekin B, Yener GG (2016). "Delay of cognitive gamma responses in Alzheimer's disease". Neuroimage Clin. 11: 106–115. doi:10.1016/j.nicl.2016.01.015. PMC 4753813. PMID 26937378.CS1 maint: multiple names: authors list (link)
  38. ^ Klein AS, Donoso JR, Kempter R, Schmitz D, Beed P (2016). "Early Cortical Changes in Gamma Oscillations in Alzheimer's Disease". Front Syst Neurosci. 10: 83. doi:10.3389/fnsys.2016.00083. PMC 5080538. PMID 27833535.CS1 maint: multiple names: authors list (link)
  39. ^ a b Mably AJ, Colgin LL (2018). "Gamma oscillations in cognitive disorders". Curr Opin Neurobiol. 52: 182–187. doi:10.1016/j.conb.2018.07.009. PMC 6139067. PMID 30121451.
  40. ^ <J. Cardin, M. Carle, K. Meletis, U. Knoblich, F. Zhang, K. Deisseroth, Li-Huei Tsai and Christopher Moore (2009) Driving fast-spiking cells induces gamma rhythm and controls sensory responses. Nature, 459: 663-668.>
  41. ^ Iaccarino, Hannah F.; Singer, Annabelle C.; Martorell, Anthony J.; Rudenko, Andrii; Gao, Fan; Gillingham, Tyler Z.; Mathys, Hansruedi; Seo, Jinsoo; Kritskiy, Oleg; Abdurrob, Fatema; Adaikkan, Chinnakkaruppan; Canter, Rebecca G.; Rueda, Richard; Brown, Emery N.; Boyden, Edward S.; Tsai, Li-Huei (7 December 2016). "Gamma frequency entrainment attenuates amyloid load and modifies microglia". Nature. 540 (7632): 230–235. Bibcode:2016Natur.540..230I. doi:10.1038/nature20587. PMC 5656389. PMID 27929004.
  42. ^ Sharon Begley (2007-01-29). "How Thinking Can Change the Brain". The Office of His Holiness the Dalai Lama. Retrieved 2019-12-16.
  43. ^ Kaufman, Marc (January 3, 2005). "Meditation Gives Brain a Charge, Study Finds". The Washington Post. Retrieved May 3, 2010.
  44. ^ Reiner PB (2009-05-26). "Meditation On Demand". Scientific American. Retrieved 2019-12-16.