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Abstract Sleep deprivation is known to cause memory impairment and is associated with inflammation and cell damage linked to neurodegenerative diseases

The obtained data may be of advantage when comparing: (i) exact glutamate and GABA homeostasis and proposed neurotransmission, (ii) glutamine reserves as neurotransmitter precursors and metabolic substrate, or also for glutamine-dependent glia activation, as well as (iii) relative metabolic aspects of the brain in situ ammonia transfer within glutamate/GABA/glutamine cycle within the brain substructures

A modification of receptor theory