I was wondering why REM sleep is so skewed in depression. where REM onset hits abnormally fast instead of a delay and gets overactive, similar to narcolepsy. where both conditions come with daytime exhaustion.
why would this be happening
During REM sleep myelin repair goes up (oligodendrocyte precursor cell proliferation doubles)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874087/
In major recurrant depression there's a loss of neurons in the hippocampus The possibility of neurotoxicity in the hippocampus in major depression: a primer on neuron death - PubMed
From things like 1. chronic stress inducing death of neurons by heightened cortisol
or 2. consistently high serotonin being neurotoxic
or 3. damaged mitochondria or mao breakdown of excess serotonin/dopamine induced h2o2 damage/lack of adequate glutathione protection
or 4. floods of continuous extreme levels of dopamine through drugs porn videogames addictions,
etc
Why are neurotransmitters neurotoxic? An evolutionary perspective
1 main reason why REM sleep is so skewed in depression is this is a response to myelin breakdown by whatever is causing brain damage
Myelination of the brain in Major Depressive Disorder: An in vivo quantitative magnetic resonance imaging study
Some of the antidepressants (if they work) fix this REM skew back to normal
lithium for example also plays a role in myelin formation
Neuroglialpharmacology: Myelination As A Shared Mechanism of Action of Psychotropic Treatments
why would this be happening
During REM sleep myelin repair goes up (oligodendrocyte precursor cell proliferation doubles)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3874087/
https://www.ncbi.nlm.nih.gov/pmc/ar...nt,learning or increased neuronal activation.oligodendrocyte precursor cells (OPCs) are responsible for the formation of new myelin in both the injured and the normal adult brain.
We then confirmed through BrdU and other experiments that OPC proliferation doubles during sleep and positively correlates with time spent in REM sleep, whereas OPC differentiation is higher during wake.
In major recurrant depression there's a loss of neurons in the hippocampus The possibility of neurotoxicity in the hippocampus in major depression: a primer on neuron death - PubMed
From things like 1. chronic stress inducing death of neurons by heightened cortisol
or 2. consistently high serotonin being neurotoxic
or 3. damaged mitochondria or mao breakdown of excess serotonin/dopamine induced h2o2 damage/lack of adequate glutathione protection
or 4. floods of continuous extreme levels of dopamine through drugs porn videogames addictions,
etc
Why are neurotransmitters neurotoxic? An evolutionary perspective
1 main reason why REM sleep is so skewed in depression is this is a response to myelin breakdown by whatever is causing brain damage
Myelination of the brain in Major Depressive Disorder: An in vivo quantitative magnetic resonance imaging study
ironically this REM skew worsens depression with acute effect from lack of restorative sleepIn this study we used qMRI to measure R1 in 40 MDD and 40 healthy control (CTL) participants. We found that the MDD participants had lower levels of myelin than did the CTL participants at the whole-brain level and in the NAcc, and that myelin in the LPFC was reduced in MDD participants who had experienced a greater number of depressive episodes.
Some of the antidepressants (if they work) fix this REM skew back to normal
lithium for example also plays a role in myelin formation
The brain is classically divided into gray matter (defined as the regions containing neuronal cell bodies and almost all synaptic connections) and white matter (composed primarily of the very long neuronal appendage (axon) that acts as a “wire” connecting widely dispersed neurons, plus the oligodendrocytes that produce the axon’s “insulating” myelin sheaths).
The roughly 100 billion neurons in the human brain are actually a small minority of brain cells (10%) while glia, which are present in both gray and white matter, account for the rest: astrocytes (45%), oligodendrocytes (35%), microglia (5%), and progenitor (NG2) cells (5%, the vast majority of which differentiate into oligodendrocytes).
The human brain consumes 20% of our total energy expenditure compared to 13% in monkeys and 2-8% in other vertebrates. This striking shift in resource use was made possible by important evolutionary adaptations in lipid and energy metabolism. Compared to other species, these adaptations made it possible to devote a greater proportion (approximately 25%) of our brain’s mass to myelin and thus achieve the information processing capacity that defines the human species
Human brain myelination has a quadratic-like (inverted “U”) trajectory across the lifespan with increasing myelin content that peaks in middle–age (Figure 1). The “connectivity” provided by myelination consists of increased action potential transmission speed (over 100-fold) and decreased refractory time (34-fold) which increases the number of action potentials that can be transmitted per unit time (in Internet terminology this would represent expanded “bandwidth”).
Myelination thus potentially increases the information processing capacity of our brain’s “Internet” by over 3,000 fold, making human myelination indispensable for developing our species’ elaborate cognitive functions
From the perspective of the exceptionally myelinated human species, the development and maintenance/repair of myelin’s functional integrity may be the single most important and vulnerable element for acquiring and maintaining optimal cognitive and behavioral function.
Neuroglialpharmacology: Myelination As A Shared Mechanism of Action of Psychotropic Treatments
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