Brain self-activation

Now the emphasis on the power of the formal approach to the study of dreaming should become clear even to those who still long for the mystique of fortune-cookie dream interpretation. We can see that, when the brain self-activates in sleep, it changes its chemical self-instructions. The mind has no choice but to go along with the programme. It sees, it moves, and it feels things intensely but it does not think, remember, or focus attention very well. This, in turn, shows clearly that our so-called minds are functional states of our brains. The mind is not something else - it is not a spirit, it is not an independent entity. It is the self-activated brain whose capacity for subjectivity remains to be explained but whose form of subjectivity can now be understood. 

We have already given our answer to the question of why we dream based on physiological mechanisms because the brain self-activates in sleep. We have already hinted that dreaming itself may be an epiphenomenon of brain self-activation, so dreaming may occur for reasons that are quite different from those that we would infer from the psychological study of REM sleep dreaming. 

The reason for this is twofold first the input-output gates are closed by active inhibition second, the central representations of sensation and movement in the cortical and subcortical brain are self-activated. 

In 1954, experiments by Olds and Milner revealed that the brain has specialized centers for reward functions. In these studies electrical stimulation of certain brain sites was found to be highly rewarding in the sense that rats operantly respond for electrical stimulation of these brain sites, often to the exclusion of any other activity. A neurotransmitter system that is particularly sensitive to electrical self-stimulation is the mesolimbic dopamine projection that originates in the ventral tegmental area and projects to structures closely... 

In addition to their inherent self-sustaining properties, brain tumor stem cells may be more resistant to chemotherapy and radiation therapy than other tumor cells. Bao et al. (2006) found glioma stem cells (CD133+) were relatively radioresistant compared to CD133- tumor cells and preferentially activated the DNA damage checkpoint response. This relative resistance to standard treatment approaches of tumor stem cells compared to the majority of other cells within a tumor may underlie our current inability to cure patients with aggressive brain tumors such as glioblastoma. 

Corrigall, W.A., Coen, K.M., Adamson, K.L. Self-administered nicotine activates the mesolimbic dopamine system through the ventral tegmental area. Brain Res. 653 278, 1994. 

Leccese, A.R, Lyness, W.H. The effects of putative 5-hydroxytryptamine receptor active agents on D-amphetamine self-administration in controls and rats with 5,7-dihydroxytryptamine median forebrain bundle lesions. Brain Res. 303 153, 1984. 

In many cells, the capacity for de novo synthesis to supply purines and pyrimidines is insufficient, and the salvage pathway is essential for adequate nucleotide synthesis. In patients with Lesch-Nyhan disease, an enzyme for purine salvage (hypoxanthine guanine phosphoribosyl pyrophosphate transferase, HPRT) is absent. People with this genetic deficiency have CNS deterioration, mental retardation, and spastic cerebral palsy associated with compulsive self-mutilation, Cells in the basal ganglia of the brain (fine motor control) normally have very high HPRT activity. These patients also all have hyperuricemia because purines cannot be salvaged. 

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