repair adaptive Freudian activation-synthesis 16.
the activation-synthesis hypothesis.
Upper Brain Activation and Synthesis
Perhaps a few hundred million years after the first mitochondrion appeared, as the oceanic oxygen content, at least on the surface, increased as a result of oxygenic photosynthesis, those complex cells learned to use oxygen instead of hydrogen. It is difficult to overstate the importance of learning to use oxygen in respiration, called . Before the appearance of aerobic respiration, life generated energy via and . Because oxygen , aerobic respiration generates, on average, about per cycle as fermentation and anaerobic respiration do (although some types of anaerobic respiration can get ). The suite of complex life on Earth today would not have been possible without the energy provided by oxygenic respiration. At minimum, nothing could have flown, and any animal life that might have evolved would have never left the oceans because the atmosphere would not have been breathable. With the advent of aerobic respiration, became possible, as it is several times as efficient as anaerobic respiration and fermentation (about 40% as compared to less than 10%). Today’s food chains of several levels would be constrained to about two in the absence of oxygen. Some scientists have and oxygen and respiration in eukaryote evolution. is controversial.
++++ Zone 9 in figure 7. (Neocortical). Inferior parietal lobe. Brodmann's Area 40. Spatial integration of heteromodal input. Solms refers to this area as the PTO junction (Parietal-Temporal-Occipital) and has shown that it is essential for dreaming, allowing us to imagine inner space and without it, all dreaming ceases. Also, it coordinates heteromodal information of all types. As Hobson writes, it "may generate the perception of a fictive dream space necessary for the global experience of dreaming."
Of interest to left-brain/right-brain theorists, PET studies of this area during REM show that much of the parietal lobe is deactivated, and just this right parietal operculum activated. That is, in some studies, the right is more important than the left in this area during dreaming.
dream: Continual-activation theory
++++ Zone 11 in figure 7. (Neocortical) visual association cortex. Higher visual processing centers that contribute visual information to dreams. We can dream even when this area is damaged, but our dreams will be impacted, as in the loss of face recognition in aphasia when the fusiform gyrus is damaged. At the same time, the primary visual centers (V1 and part of V2) are deactivated. This makes sense as the eyes are closed.
++++ Zone 3, figure 7.(Cortical and subcortical) Limbic and paralimbic structures.
Anterior limbic structures (amygdala, anterior cingulate, parahippocampal cortex, medial frontal areas). Emotional aspects of dreaming, emotional coding, goal directed behavior, movement,. For example, the amygdala when activated is correlated with anxiety and high emotions, and the amygdala activates the anterior cingulate, right parietal operculum. Deactivated are the prefrontal cortex, parietal cortex and precuneus.
the anterior cingulate if related to emotional features in waking and dreaming in integrating emotion with fictive actions.
• the activation-synthesis hypothesis.
++++ Zone 4 in figure 7. (Neocortical- deactivated) Dorsolateral prefrontal cortex, or the executive association cortex. Prominent deactivation in the frontal cortex. This is the executive or reasoning part of the brain and the part that we use to do math, think linearly and calculate. Hobson feels this may contribute to many of the "dream deficiencies" such as memory loss, shifts in scenes, disorientation. It will be interesting to see if this area of the brain is more activated in lucid dreaming or not. Having this part of the brain offline may contribute to better facilitation of emotional and memory consolidation processes.
++++ Zone 6, figure 7. (Subcortical) Thalamaocortical relay centers and thalamic subcortical circuitry. Thalamic nuclei (e.g. lateral geniculate body). Relays sensory and pseudosensory information to cortex.
In NREM sleep, corticothalamic waves suppress perception and mentation, but this process is reversed in REM. In REM, the thalamic nuclei activate sensorimotor parts of the brain and fill these parts of the brain with general activation. Hobson feels this may present basic elements of dream scenes in the form of pseudosensory information.
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The Science Behind Dreaming - Scientific American
Hobson has accepted much of Solms research, particularly on the specific higher brain areas that are activated during dreaming sleep. But Hobson doesn't feel that REM activation can ever be separated from other aspects of dreaming and is still holding out on whether or not upper brain functioning during dreaming is modulated by dopaminergic systems. (A separate dopamine system from the one often related to Parkinsons).
Why Do We Dream? Explore the Top Theories Behind It
Recent brain imaging supports this theory that dreaming involves very specific brain structures. These *activated* structures include anterior and lateral hypothalamic areas, amygdaloid complex, septal-ventral striatal areas, as well as the infralimbic, prelimbic, orbitofrontal, anterior cingulate, entorhinal, insular and occipitotemporal cortical areas. *Deactivated* structures include the primary visual cortex (where waking eye information would go, not the same as the activated higher visual centers) and dorsolateral prefrontal cortex (the calculating part of the brain).
Dreaming, Philosophy of | Internet Encyclopedia of Philosophy
In terms of the process of dreaming at the level of the brain/body, we have learned quite a bit since the discovery of REM 50 years ago by Aserinsky and Kleitmann in the Chicago University sleep labs. REM or Rapid Eye Movement sleep occurs on a regular cycle about 20 minutes every 90 minutes of sleep. (More accurately, we have shorter REM the first part of the night, and longer REM periods, up to two hours, towards the end of the night). People often report dreams if awakened from REM.
Now we look at three different levels brain dreaming, the activation of various sites in the brain, the gating or input/output during Wake/Sleep/ REM stages and the different neurotransmitters that are impacting these stages.
In brief, when the sleeping person enters REM sleep, much of the mind that was quiet "wakes up", the dominate neurotransmitter changes from aminergic to cholinergic washes, and the output from the brain is cut off at the level of the lower brain stem. That is, messages from the activated brain go out to the body as in waking, but never make it there and so we get a kind of REM paralysis. Two areas of the brain that don't wake up are the parts of the pre-frontal cortex that one usually uses to calculate the lunch bill, and the primary visual centers used during waking site. (Higher visual centers are still activated. Its unclear still what brain parts are activated during lucid dreaming).
Energy and the Human Journey: Where We Have Been; …
In Solms theory, dreaming begins in the higher brain when a particular area of the forebrain is activated, the mediobasal frontal cortex. Here the hunting, seeking, desiring, wanting system is deeply networked with the limbic system (emotions, sensory info) and mesocortical dopamine systems. There are deep connections of dopanminergic cells from this ventral tegmental area to the hypothalamus, the septal area, the cingulated gyrus and the frontal cortex, and amygdala. In other words, this frontal cortex area of motivation connects with many other parts of the higher brain, the sensory brain and the emotional brain.
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