Researchers discuss how psychedelics can affect the brain and provide therapeutic benefits for those suffering from a range of psychiatric disorders.
A new neuro-optics technique can manipulate memory consolidation in mouse models by hindering long-term potentiation. Researchers say eliminating local LTP in the hippocampus erased memories. The method could be used to isolate memory formation at the cellular level.
Hard wired neural circuits in mice that govern aggression are strengthened following victories in aggressive encounters. Synapses in the hypothalamus show signs of LTP following aggression training.
Researchers have made an important discovery about the mechanisms behind learning and memory. Depending on the number of synapses, and their proximity, information is processed and stored differently.
Repeatedly administered tactile simulation over a sustained period of time alters neural processing of the hand area in the brain. The observable changes over time illustrate neuroplasticity and shed new light on the process of learning.
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.
Visceral fat impairs memory via proinflammatory interleukin-1 beta mediated microglia activation in the hippocampus.
New memories are laid down via different mechanisms in older mice compared to younger mice. Additionally, synaptic changes linked to new memory formation were harder to modify in older mice.
A lack of oxygen as a result of preterm birth does not cause hippocampal neurons to die but does impair hippocampal development. Hypoxia causes hippocampal cells to fail to mature normally, causing a reduction in long-term potentiation and impaired learning.
Mouse study reveals a clear correlation between cognitive ability in aging and presynaptic calcium levels.
A pairing of presynaptic and postsynaptic activity in a population of hippocampal neurons can reduce the required number of synaptic plasticity evoking events. When spikes occur within ten milliseconds of each other, synapses strengthen for up to four hours.
Researchers report estrogen may play a significant role in synaptic plasticity and memory formation. The study reports mice whose neurons did not produce estrogen have impairments in spatial reference memories, recognition and contextual fear memories. Restoring estrogen levels assisted in reversing the memory impairments, the study revealed.
