How does sunlight help cognition and mood?
Sunlight makes UCA urocanic acid which ASTROCYTES converts into glutamate and then lactate that increases the energy of the neuron via the lactate shuttle.
Urocanic acid is made from L-histidine in the stratium corneum of the skin (sweat) and functions as an endogenous sunscreen, hence it arises from sunlight.
Interestingly, the loss of astrocyte function and structure, damages neurons and is associated with neurodegenerative diseases including depression and dementia. Activated inflammatory astrocytes are named CA-1 and they increase in percentage in the focal areas of disease. For example the basal ganglia in Parkinson's disease.
Astrocytes are the "canaries in the mine" because they produce lactate for neurons. They empty themselves of energy and thereby increase their vulnerability to oxidative stress. Urocanic acid-glutamate-lactate increases neuron function, hence improved mood and cognition derived from sunlight!
In dementia, NMDA inhibitors (namenda) block glutaminergic overdrive which might be viewed as a normal function of astrocytes that converts glutamate into lactate and neuronal energy. Namenda also improves depression but does not save astrocytes. Saving astrocytes is
1. the job of Nrf2 activation which reduces the activation of astrocytes into CA-1. It is also
2. the job of the cholinergic anti-inflammatory pathway that is activated by vagal nerve stimulation. (See DrLiverman. blogspot.com/smokingcessation....)
Sulforaphane is concentrated in astrocytes and provides protection for themselves and their offspring. Save the astrocytes; save the neuron/brain/person. Sulforaphane is the most potent Nrf2 activator known. Sulforaphane is concentrated in broccoli sprouts and broccoli sprout extract.
Highlights
Sunlight exposure is known to affect mood, learning, and cognition. However, the molecular and cellular mechanisms remain elusive. Here, we show that moderate UV exposure elevated blood urocanic acid (UCA), which then crossed the blood-brain barrier. Single-cell mass spectrometry and isotopic labeling revealed a novel intra-neuronal metabolic pathway converting UCA to glutamate (GLU) after UV exposure. This UV-triggered GLU synthesis promoted its packaging into synaptic vesicles and its release at glutamatergic terminals in the motor cortex and hippocampus. Related behaviors, like rotarod learning and object recognition memory, were enhanced after UV exposure. All UV-induced metabolic, electrophysiological, and behavioral effects could be reproduced by the intravenous injection of UCA and diminished by the application of inhibitor or short hairpin RNA (shRNA) against urocanase, an enzyme critical for the conversion of UCA to GLU. These findings reveal a new GLU biosynthetic pathway, which could contribute to some of the sunlight-induced neurobehavioral changes.
Jo
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