Not sure if this has been analyzed in the Nexus but represents important figures and processes that involve form constants and their role with specific receptors. Quite interesting, safe, reliable and professional data. Helpful for those interested about learning more in depth about the development, changes and plasticity of brain functions during particular visual states including low doses, loops, mapping, oscillators, networks, circuits, disinhibition, phosphenes and visual markings.
http://en.wikipedia.org/wiki/Form_constants[/url]
By James Kent: May 23, 2008, Beta Review
Abstract/Summary Quote:The most potent tryptamine hallucinogens – such as DMT, psilocybin, and LSD – are all active at the 5-HT2A receptor subtype and all produce similar visual perceptual results that are immediately recognizable as uniquely psychedelic. Although it is widely accepted that selective serotonin receptor subtype 2A agonism is directly responsible for producing the distinct hallucinations seen on a psychedelic trip, no single theory has yet explained why this is so. Utilizing what we know about psychedelic tryptamine receptor interaction, sensory processing circuits in the neocortex, and EEG scans of psychedelics in action, this review will propose a novel multi-state theory of psychedelic action which invokes a variety of neural processing mechanisms, including phase-coupled neural oscillators; network excitation, disinhibition, and destabilization; recurrent feedback excitation; and neural circuit spike synchrony and brainwave cohesion to close the knowledge gap between the pharmaceutical interactions of selective 5-HT2A hallucinogens, their direct effects on perception and consciousness at varying dose ranges, and their potential long-term adverse effects.
http://www.tripzine.com/pit/html/multi-state-theory.htmReferences
1. G. Aghajanian, G. Marek; Seratonin and Hallucinogens; Neuropsychopharmacology 21-2-1 (1999) 162-23S.
2 P.W.J. Burnet, S.L. Eastwooda, K. Laceya, P.J. Harrison; The distribution of 5-HT1A and 5-HT2A receptor mRNA in human brain; Brain Research 676-1 (1995) 157-168.
3. F. Forutan et al.; Distribution of 5-HT2A receptors in the human brain; Nuklearmedizin 41 (2002) 197-201.
4. M.W. Spratling; Cortical region interactions and the functional role of apical dendrites; Behavioral and Cognitive Neuroscience Reviews, 1-3 (2002) 219-228.
5. E. Lumer, G. Edelman, G. Tononi et al.; Neural dynamics in a model of the thalamocortical system. II. The role of neural synchrony tested through perturbations of spike timing; Cerebral Cortex, Vol 7 (1997) 228-236.
6. E. Jones; Thalamic circuitry and thalamocortical synchrony; Phil.Trans. R. Soc. Lond. B (2002) 357, 1659–1673.
7. G.B. Ermentrout, J.D. Cowan, A mathematical theory of visual hallucinations, Kybernetic 34 (1979) 137–150.
8. P.C. Bressloff, J.D. Cowan, M. Golubitsky, P.J. Thomas, M. Wiener, Geometric visual hallucinations, Euclidean symmetry, and the functional architecture of striate cortex, Philos.T Roy. Soc.B 356 (2001) 299–330.
9. P.C Bressloff et al.; What Geometric Visuals Tell Us about the Visual Cortex; Neural Computation 14 (2002) 473-491.
10. B. Gutkin, D. Pinto, B. Ermentrout; Mathematical neuroscience: from neurons to circuits to systems; J. Physiology, Paris 97 (2003) 209-219.
11. G. Aghajanian, G. Marek; Serotonin, via 5-HT2A receptors, increases ESPCs in layer V pyramid cells of prefrontal cortex by an asynchronous mode of glutamate release; Brain Research 825 (1999) 161-171.
12. J.M. Hupé et al.; Cortical feedback improves discrimination between figure and background by V1, V2 and V3 neurons; Nature 394 (199
784-787.
13. L. Kass, P. Hartline, A. Adolf; Presynaptic Uptake Blockade Hypothesis for LSD Action at the Lateral Inhibitory Synapse in Limulus. J. Gen. Physiol 82 (1983) 245-267.
14. Stuckey DE, Lawson R, Luna LE.; EEG gamma coherence and other correlates of subjective reports during ayahuasca experiences. J Psychoactive Drugs. 2005 Jun;37(2):163-78.
15. D. Contreras, et al; Propagating Waves in Visual Cortex. Neuron, 55-1 (2007) 3-5.
16. H.D. Abraham, F. Hopkins Duffy; EEG coherence in post-LSD visual hallucinations. Psychiatry Research: Neuroimaging 107 (2001) 151-163.
17. J. Riba, et al; Topographic pharmaco-EEG mapping of the effects of the South American psychoactive beverage ayahuasca in healthy volunteers. J. Clinical Pharmacology 53 (2002) 613-628.
18. Erik Hoffmann, Effects of a Psychedelic, Tropical Tea, Ayahuasca, on the Electroencephalographic (EEG) Activity of the Human Brain during a Shamanistic Ritual. MAPS Spring (2001) 25-30.
19. Jordi Riba, et al. Increased frontal and paralimbic activation following ayahuasca, the pan-amazonian inebriant. Psychopharmacology (2006) 186: 93Р98.
20. Abraham HD, Duffy FH., Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: evidence for disinhibition. Psychiatry Res. 1996 Oct 7;67(3):173-87.
21. ZHENGWEI SHAO AND ANDREAS BURKHALTER, Role of GABAB Receptor-Mediated Inhibition in Reciprocal Interareal Pathways of Rat Visual Cortex, J Neurophysiol 81:1014-1024, 1999.
22. Backus, B. T. & Oruç, I. (2005). Illusory motion from change over time in the response to contrast and luminance. Journal of Vision, 5(11):10, 1055-1069,
http://journalofvision.org/5/11/10/, doi:10.1167/5.11.10.
Perhaps there is more updated information regarding functional changes in neuronal networks? MAPS is doing some new work with this kind of research. I found this paper through an online image and thought it could have some reference for those interested.
'What's going to happen?' 'Something wonderful.'
Skip the manual, now, where's the master switch?
We are interstellar stardust, the re-dox co-factors of existence. Serve the sacred laws of the universe before your time comes to an end. Oh yes, you shall be rewarded.