During non-REM sleep, visual areas of the brain exhibit an excitation/inhibition balance indicative of increased plasticity. REM sleep appears to be essential for people to reap the benefits of the increased plasticity that occurs during NREM sleep.
Oxytocin, the so-called "love hormone," could help to treat cognitive disorders, including Alzheimer's disease. Researchers demonstrated oxytocin reversed the effects of amyloid-beta on hippocampal LTP in mice. The findings suggest oxytocin could be used as a therapeutic for the treatment of Alzheimer's disease and other dementias.
Dropping the level of the IL-33 immune molecule increased the number of synapses in the brain. In older mice, ramping up IL-33 helped push the number of new synapses toward a more youthful state.
Adult born neurons are essential for synaptic structural remodeling and memory consolidation during REM sleep, a new mouse study found.
Study reveals a self-corrective mechanism within synapses that is activated by neurodegeneration and slows disease progression in animal models of ALS.
Learning produces changes in connectivity via multiple synaptic mechanisms that are consistent with observed behavioral changes.
Neurons in the caudal pedunculopontine nucleus, an area of the brain that regulates motor coordination, switch neurotransmitters from acetylcholine to GABA as a result of exercise. The switch appears to provide feedback control that regulates motor coordination and skill learning.
Brain connections strengthened with treatment from fast-acting antidepressants, such as ketamine, are consolidated during deep sleep. Researchers propose rapid antidepressant treatments share the ability to regulate both synaptic potentiation and homeostatic mechanisms, which may contribute to how the brain reorganizes its activity to defeat depression.
Mice deficient in the NFIA gene presented astrocytes with defective shapes and altered functions in the hippocampus.
Following a meal, astrocytes associated with POMC neurons in the hypothalamus alter their shape. After eating, glucose levels increase temporarily. Astrocytes detect the signal and react within one hour, causing POMC neurons to activate and promote the feeling of satiety.
When autoantibodies are able to enter the bran and act on NMDA receptors, people experience relief from symptoms of anxiety, depression, and stress.
Study explains how an overexpression of the RCAN1 gene may cause intellectual disabilities in people with Down syndrome.
