Light in our biology, in our head.
Are there anything in the biology that possibly could explain this light to us? The light gives euphoria, joy, love, strength, wisdom. It is a psychedelic drug. In biology we know of endorphins giving pleasure, phenethylamine PEA is addicting in love, sex stimulates the release of vasopressin and oxytocin, DMT makes you see God, and so on.
So, I read an interesting paper. Coordination involves a subtle kind of ballet in the brain, and like dancers, cortical areas are capable of coming together as an ensemble (integration) while still exhibiting a tendency to do their own thing (segregation). What? Quantum biology in working?
Because of the fourth dimension afforded by this colorimetric method, it is possible to observe and interpret oscillatory activity of the entire brain as it evolves in time, millisecond by millisecond, and show how to tell apart real and false episodes of synchronization. For the first time, true episodes of brain coordination can be spotted directly in EEG records and carefully analyzed.
The brain areas active in love are different from the areas activated in other emotional states, such as fear and anger. Parts of the brain that are in love include the one responsible for gut feelings, and the ones which generate the euphoria induced by drugs such as cocaine. So the brains deeply in love do not look like those experiencing strong emotions, but instead like those of people snorting coke. Love, in other words, uses the neural mechanisms that are activated during the process of addiction.
Strong social bonds depends on the receptors for vasopressin and oxytocin. Evolution acts on the distribution of these receptors to generate social behavior. The more receptors located in regions associated with reward, the more rewarding social interactions become. There are variations between individuals. But once romantic love begins, it is one of the strongest drives on Earth. This power is enough to warp judgment in otherwise sensible people. Althruism is also a social bond, or a freeing from the singular I.
Some suggest this mental state might share neurochemical characteristics with the manic phase of manic depression. Means love can be "treated" pharmacologically (serotonin-inhibitors)? It might even to be possible to create a more sociable human? And what about a more loving one? A few people even think that “paradise-engineering” is possible?
The experience of romantic attraction activates those sites in the brain with a high concentration of receptors for dopamine, closely tied to states of euphoria, craving and addiction. "The brain activity pattern is markedly different from when they looked at a picture of a close friend," reported neurobiologists Andreas Bartels and Semir Zeki. They linked high levels of dopamine and norepinephrine to heightened attention and short-term memory, hyperactivity, sleeplessness and goal-oriented behavior. Bartels and Zeki compared brain scans taken from people in different emotional states, including sexual arousal, feelings of happiness and cocaine-induced euphoria. The pattern for romantic love was unique. But there was some overlap with and close proximity to other positive states. "It's this combination of friendship, affection and lust, that makes it so powerful."
And where in the brain is this light?
Let us look at some conditions. There are many parameters that make up the control levels. Not one frequence or amplitude, nor one molecule, but a parameter space of multidimensional character (a 4-D brain as Matti Pitkänen says, with time as one parameter?).
The brain’s reward circuit are located along the medial forebrain bundle (MFB). The ventral tegmental area (VTA) and the nucleus accumbens are the two major centres in this circuit, but it also includes several others, such as the septum, the amygdala, the prefrontal cortex, and certain parts of the thalamus. All of these centres are interconnected and innervate the hypothalamus (red arrows), informing it of the presence of rewards.
1. Love and addiction areas. The vasopressin and oxytocin receptors were equally distributed in the brains of male and female voles, according to Dr. Young, coupled with the close proximity of the nucleus accumbens and ventral pallidum - two regions with heavily interconnected structures - suggest that a common neural circuit in male and female voles regulates pair bond formation. The dopamine system of the nucleus accumbens produces the rewarding and sometimes addictive effects of sex, food and drugs of abuse. The receptors are closely located to the nerve fibers that release oxytocin and vasopressin.
Using fMRI to view the brains of easily orgasmic women as they climaxed, either with visual stimuli or by self-stimulation, Whipple found that the body's pain-killing center in the midbrain is activated during peak arousal. Signals from this part of the brain instruct the body to release endorphins and corticosteroids, and is also coupled to anxiety.
2. Feel good, feel bad. The pleasure system includes the septal area and part of the almond-shaped amygdala; the other half of the amygdala, the hippocampus, the thalamus, and the tegmentum (in the midbrain) constitute the punishment system (rage, anxiety, pain). The flip side of joy is pain. Whenever a mental patient flew into a violent rage or turned into a catatonic zombie, the EEG was almost certain to display the telltale sawtooth pattern. If the patient got well, the spike disappeared. ...
3. Schizophrenia. "The primary symptom of schizophrenia isn't hallucinations or delusions," says Heath. "It's a defect in the pleasure response. Schizophrenics (negative symptoms?) have a predominance of painful emotions. They function in an almost continuous state of fear or rage, fight or flight, because they don't have the pleasure to neutralize it." ... It turned out that electrical stimulation of the pleasure center automatically turned off the punishment system. The cerebellum, Heath learned, is a better entryway to the brain's emotional circuitry. Stimulating a precise half-inch of its cauliflowerlike surface automatically fires the pleasure area and inhibits the rage centers.
[From a patient story:] "There -- see the big delta wave appearing in the septal region. Sure enough, large, languorous waves are now coming from the lead to the septal electrode. There's almost an exact correlation. When he gets a rush of good feeling, the record shows large-amplitude waves in the pleasure system."" ...
Along with depth electrodes, Heath's team would often surgically implant a sort of tube, a canula, through which they could deliver precise amounts of a chemical directly into the brain. Oriental sacred texts (and Aldous Huxley's Brave New World) mention a legendary bliss drug called "soma", the food of the Himalayan gods. The real life version might be acetylcholine. When acetylcholine was injected into a patient's septal area, "vigorous activity" showed up on the septal EEG, and the patient usually reported intense pleasure - including multiple sexual orgasms lasting as long as thirty minutes. An ominous-looking scrawl on the EEG looks almost like the spoke-and-dome pattern of epileptic seizure. It's a very explosive activity. (Afrodisiaca is often acetylcholinic).
4. Psychosis. Nucleus accumbens is the key structure of the brain responsible for reward, motivation and addiction. Addiction, motivation and impulsivity has much in common, also learning. Amphetamine-like drugs (which increase dopamine levels by blocking its re-uptake) are the main drug treatment for Attention Deficit/Hyperactivity disorder of which impulsivity is a component.
Psychosis refers to a subset of the symptoms associated with schizophrenia - symptoms which include hallucinations and delusional thoughts. It is rather striking that although there is no cure for all of the symptoms of schizophrenia, there is a single pharmacological treatment for the psychotic symptoms - blockade of dopamine receptors. Nobody knows why an excess of dopamine might lead to delusional thoughts or hallucinations, but it seems rather remarkable that the control of a single type of molecule in the brain is capable of influencing a person's thought processes in such a selective fashion.
Dopamine is a neuromodulator released by dopaminergic cells that originate in the midbrain (Ventral Tegmental Area (VTA) and Substantia Nigra) and which project to a number of brain regions including the Prefrontal Cortex (PFC), the amygdala, the hippocampus and the striatum (Caudate nucleus). All of these brain regions have been implicated in schizophrenia, although perhaps the most interesting region of all is the nucleus accumbens. The nucleus accumbens is connected to all of these other important regions, and is known to contain a large proportion of D2 receptors. The importance of the D2 receptor in particular is suggested by the striking correlation between the ability of an antipsychotic drug to block this receptor and the ability of that drug to mitigate the symptoms of psychosis. What does the nucleus accumbens do in the brain? What does the D2 receptor do? When and why is dopamine released? What is the functional role of dopamine?
5. Migraine and epilepsy. In certain syndromes the two conditions epilepsy and migraine are associated, characterized by visual symptoms followed by a partial seizure and postictal migraine. The EEG reveals occipital spikes (visual?). The visual symptoms are often followed by seizures. After the seizure, approximately 25–40% of the patients develop migrainelike headaches with a migrainous aura.
Another epilepsy-syndrome is characterized by unilateral somatosensory or motor seizures and centrotemporal spikes. Clinical and electrographic features can shift from side to side. Speech arrest, pooling of saliva, and usually preservation of consciousness are also typical, although spread and generalization do occur. Epileptic seizures are predominantly multi-coloured with circular or spherical patterns as opposed to the predominantly black and white linear patterns of migraine. Also those of epileptic patients are predominantly centrally localized, whereas those of migraine patients are predominantly peripherally localized.
Attention-deficit hyperactivity disorder (ADHD) is also much more common in epileptics (20%) as compared to normal children (3-7%). Several mechanisms may account for the high prevalence, such as a common genetic propensity, noradrenergic system dysregulation, subclinical epileptiform discharges, or even seizures, antiepileptic drug effects. Children with attention-deficit hyperactivity disorder have a higher than normal rate of EEG abnormalities. The noise or the input level is much higher, and so the attention fades. Also memory can be halted.
The clinical diagnosis of visual seizures is easy if individual elements of duration, colour, shape, size, location, movement, speed of development and progress are identified. They are markedly different from visual aura of migraine, although they often trigger migrainous headache, probably by activating trigemino vascular or brain stem mechanisms.
6. Pain on/off. The trigeminothalamic tract and periaqueductal grey (PAG). Also indicates that the thalamocortical tract is an important component of migraine pathophysiology. The central sensitization observed in migraineurs is most probably related to an abnormal activity of the trigeminal sensory pathway. A possible dysfunction of the periaqueductal grey in migraineurs without aura, which could result in a lowering of the threshold for initiation of migraine attack through a lack of inhibition of the trigeminal sensory activation.
As a critical pain neuromodulating structure, the periaqueductal grey matter has been implicated with the activation of the nervous system in migraine. The ventrolateral periaqueductal grey is part of a descending paininhibiting system from the hypothalamus and frontal cortex projecting to the medullary and spinal dorsal horns. Periaqueductal grey matter activation inhibits contralateral trigeminovascular nociception. PAG was hyperactive during migraine. The exact neurotransmitters behind the aura are unknown, ev. NO. PAG is also involved in narcotic abuse.
The PAG has a large influence on the nociceptive pathways (pain treshold)(perception of pain = treshold value for pain) with extensive networks from thalamus, hypothalamus and autonomic nervous system. It is full of opiate receptors (endorphins and others) according to Pert, and is a control area for pain, and also for most of other peptides/receptors. Pain is a highly complex and with subjective experience that is not linearly related to the nociceptive input. It is well known that pain perception for patients and normal subjects can be modulated by psychological factors, such as attention, stress, and arousal. Activation in the periaqueductal gray was significantly increased when pain was inhibited. In many sensory modalities, afferent processing is dynamically modulated by attention and this modulation produces altered sensory experiences.
An increase in flow of the middle meningeal artery (MMA) also occured. Pert says that pain can be altered by expectanses, faith and it can even be altered into pleasure. What is the role of consciousness in this, asks Pert.
Trigeminus input to the brain has also a profound impact on the consciousness level according to Damasio. Pain is a conscious experience, an interpretation of the nociceptive input influenced by memories, emotional, pathological, genetic, and cognitive factors. Is consciousness dependent on perception (of pain = disturbance or noise?)? Or attention? PAG is also our first body map in the nervous system. And pain and serotonin is dependent on each other. Paininhibition means serotonin excreation with urine. Adrenaline and noradrenaline is the counterpart. Noradrenaline is happiness, says Pert. Is our consciousness dependent on a disturbance, or arousal? Sounds a simple question, but it isn't. These painmodulations can be initiated reflexively or by contextual manipulations of the pain experience including cognitive and emotional factors. This provides a necessary survival function since it allows the pain experience to be altered according to the situation. Plasticity, sensitization and other amplification processes might occur along the pain neuraxis for an individual and one can relate this to their specific pain experience or measure of pain. Individuals can gain voluntary control over activation in a specific brain region given appropriate training (biofeedback as ex.), that voluntary control (over behavior and cognition) over activation in the rostral anterior cingulate cortex (rACC), leads to control over pain perception, and that these effects are powerful enough to impact severe, chronic clinical pain. Pert also points out that breeding is a control of pain. Forced breeding make more peptides and of a different kind in the brain stem. They are then expressed in PAG.
7. Gender, developement, morphology, cognition and mood; the Dentate gyrus in hippocampus. In the late 1980s, the finding that the dentate gyrus contains more granule cells in the male than in the female of certain mouse strains provided the first indication that the dentate gyrus is a significant target for the effects of sex steroids during development. Gonadal hormones also play a crucial role in shaping the function and morphology of the adult brain. Besides reproduction-related processes, sex steroids participate in higher brain operations such as cognition and mood, in which the hippocampus is a critical mediator. Sex steroids modulate the function of dentate neurons under normal conditions. In addition, recent research suggests that hormone-induced cellular plasticity may play a larger role than previously thought, particularly in the dentate gyrus. Specifically, the regulation of dentate gyrus neurogenesis and synaptic remodeling by sex steroids, and gonadal hormones have neuroprotective potential. Gonadal hormones could also influence the dentate gyrus indirectly, by subcortical hormone-sensitive structures such as the cholinergic septohippocampal pleasure system.
Serotonin has also been linked to the effect of estradiol on dentate neurogenesis. Indeed, several studies indicate that estrogen influences the dentate serotonergic system, f.ex. estradiol treatment reduces serotonin gene expression in the dentate gyrus. That's perhaps the reason why menopause has been linked to kundalini-experience.
8. The secondary sexual behavior is also related to the anterior cingulate gyrus (in the roof of the limbic area), as a response of vasopressin and oxytocin receptors. Care for the offspring belongs here, as well as aggressive behavior (male). Large bilateral leisons abolish voluntary movement, but not awareness. "Nothing matters", and "I had nothing to say", said a patient. Smaller leisons gave severe depression and anxiety. Or loss of voluntary control of a hand (alien-hand syndrome), that has a will of its own. (Brain-wise by Churchland).
Selfcontrol over sexual arousal belongs here. Limbic areas can be controlled by free will. Autistic people have disturbances in cingulate gyrus (small cells, high density), hypothalamus, amygdala, mammillary bodies and cerebellum.
Motivation and decision-making belongs here too, orchestrated by serotonin and dopamine, norepinephrine and acetylcholine, as well as various hormones, estrogen and testosterone. Judgement and impulse control can fail due to too much estrogen or testosterone.
Control by suppressing emotions, feelings and inclinations is often believed to be rational (and virtue). But reason can never be a motive, or make decisions. Reason can't make free will, can't give aversion against something or a drawing to something. Reason can tell lies, storytellings and fantasies. Feelings is against or for, a common sense. Emotions is a good thing, but too much emotions and too much reason, virtue and moral can be fatal. As a rule strong passion can't be controlled, too much reason and you go astray.
9. The pineal gland is unique in its solitary status within the brain. All other brain sites are paired, meaning that they have left and right counterparts; for example, there are left and right frontal lobes and left and right temporal lobes. As the only unpaired organ deep within the brain, the pineal gland remained an anatomical curiosity.
The pineal gland of evolutionarily older animals, such as lizards and amphibians, is also called the "third" eye. Just like the two seeing eyes, the third eye possesses a lens, cornea, and retina. It is light-sensitive and helps regulate body temperature and skin coloration—two basic survival functions intimately related to environmental light (and emotions).
What have transcerebral, weak (1 microT) complex magnetic fields and mystical experiences in common? Are they generated by field-induced dimethyltryptamine (DMT) release from the pineal organ? Structurally, DMT is analogous to the neurotransmitter serotonin and other psychedelic tryptamines. Some believe it plays a role in mediating the visual effects of natural dreaming, and also near-death experiences, religious visions and other mystical states. In addition to being involved in altered states of consciousness, endogenous DMT may be involved in the creation of normal waking states of consciousness. Dimethyltryptamine dose dependently elevated blood pressure (tonus), heart rate, pupil diameter, and rectal temperature, in addition to elevating blood concentrations of beta-endorphin, corticotropin, cortisol, and prolactin. Growth hormone blood levels rose equally in response to all doses of DMT, and melatonin levels were unaffected. DMT and other endogenous hallucinogens mediate their neurological abilities by acting as neurotransmitters at a sub class of the trace amine receptors?
Decreased sensitivity to the serotonergic hallucinogens psilocybin and LSD is induced by drugs with effects on serotonergic neurotransmission, allopurinol and fluoxetine?
Hallucinogens' effects in humans are mediated by serotonergic receptors?In this way waking consciousness can be thought of as a controlled psychedelic experience, or stress induced by environment and giving rise to muscle work? It is when the control of these systems becomes loosened and their behavior no longer correlates with the external world that the altered states arise. A theory was also that a massive release of DMT from the pineal gland prior to death or near death was the cause of the near death experience (NDE) phenomenon. Several test subjects reported NDE-like audio or visual hallucinations. The explanation for this experience was the possible lack of panic/pain.
Attention and concentration is also an effect of serotonin, as well as violence and suicide can be that. In fact serotonin is very central to our human being charachters. This is something I have called "the serotonine wheel" for my own purposes. Are there also a "dopamine wheel", an endorphine wheel" etc.?
One of the most obvious physiologic manifestations of seasonality is the phenomenon of seasonal breeding. The pineal gland hormone, melatonin,mediates the antireproductive effects of decreased light exposure during winter months. Annual rhythms in humans have also been established, including, for example, seasonal variations in suicides, general mortality, a need for electroconvulsive therapy and the incidence of episodes of depression and mania. Melatonin is made from serotonin.
Pineal gland is very sensitive to magnetism. How is it with normal visual perception and magnetism? Pineal gland can easily be calcified with "brain sand" (fluor) and so can be hypofunctional.
Was Descartes right after all?
We shall continue with the God-concept. See also http://zone-reflex.blogspot.com/2009/07/chakras-and-colors-i.html
See also links.
Dynamical Theory and Novel 4D Colorimetric Method Reveal the Essential Modus Operandi of the Intact Living Brain--Study shows how areas in the brain integrate and segregate at the same time. Newswise. See also Tognoli, E., Kelso, J.A.S., Brain coordination dynamics: True and false faces of phase synchrony and metastability. Prog. Neurobiol. (2008), doi:10.1016/j.pneurobio.2008.09.014
Sheena K Aurora. Pathophysiology of Migraine. NeuroScience 2007 - Supplement to EU/US Neurological Disease 2007 Issue 1 (BTG). http://www.touchneurology.com/files/article_pdfs/neuro_7463
Knight Y.E., Goadsby P.J. The periaqueductal grey matter modulates trigeminovascular input: a role in migraine? Neuroscience, Volume 106, Number 4, 31 October 2001, 793-800(8).
Afridi and Goadsby. New onset migraine with a brain stem cavernous angioma
J Neurol Neurosurg Psychiatry.2003; 74: 680-681 http://brain.oxfordjournals.org/cgi/content/abstract/125/6/1392 - The selective low efficacy adenosine A1 receptor agonist, GR190178 (30–1000 µg/kg i.v.), also inhibited SSS-evoked neuronal activity in a dose-dependent fashion. In this model of trigeminovascular nociception, adenosine A1 receptor activation leads to neuronal inhibition without concomitant vasoconstriction,
C P Panayiotopoulos: Elementary visual hallucinations in migraine and epilepsy. J Neurol Neurosurg Psychiatry. 1994 November; 57(11): 1371–1374. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1073189
Michael A. Rogawski 2008: Common Pathophysiologic Mechanisms in Migraine and Epilepsy. Arch Neurol. 2008;65(6):709-714. http://archneur.ama-assn.org/cgi/content/abstract/65/6/709
Tibor Hajszan, Teresa A Milner,and Csaba Leranth, Sex Steroids and the Dentate Gyrus. Prog Brain Res. 2007; 163C: 399–816. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1964752.
Sculthorpe L, Persinger MA. Does phase-modulation of applied 40-Hz transcerebral magnetic fields affect subjective experiences and hypnotic induction? http://www.ncbi.nlm.nih.gov/pubmed/15002842?dopt=Abstract
Patricia Smith Churchland, 2002: Brain-Wise: Studies in Neurophilosophy. Cambridge. MIT Press.
Revisiting the deflated ego problem
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