Src dependency of the regulation of LTP by alternative splicing of exon 5.

Alternative splicing of exon 5 regulates induction of long-term potentiation (LTP) at Schaffer collateral-CA1 synapses: LTP in mice lacking the GluN1 exon 5-encoded N1 cassette (GluN1a mice) is significantly increased compared with that in mice compulsorily expressing this exon (GluN1b mice). The mechanism underlying this difference is unknown. Here, we report that blocking the non-receptor tyrosine kinase Src prevents induction of LTP in GluN1a mice but not in GluN1b.

Hippocampal hyperphosphorylated tau-induced deficiency is rescued by L-type calcium channel blockade.

Aging and Alzheimer's disease are associated with chronic elevations in neuronal calcium influx L-type calcium channels. The hippocampus, a primary memory encoding structure in the brain, is more vulnerable to calcium dysregulation in Alzheimer's disease. Recent research has suggested a link between L-type calcium channels and tau hyperphosphorylation.

Olfactory threat extinction in the piriform cortex: An age-dependent employment of NMDA receptor-dependent long-term depression.

Extinction of threat memory is a measure of behavioral flexibility. In the absence of additional reinforcement, the extinction of learned behaviors allows animals and humans to adapt to their changing environment. Extinction mechanisms and their therapeutic implications for maladaptive learning have been extensively studied.

Contributions of carotid bodies, retrotrapezoid nucleus neurons and preBötzinger complex astrocytes to the CO -sensitive drive for breathing.

Current models of respiratory CO chemosensitivity are centred around the function of a specific population of neurons residing in the medullary retrotrapezoid nucleus (RTN). However, there is significant evidence suggesting that chemosensitive neurons exist in other brainstem areas, including the rhythm-generating region of the medulla oblongata - the preBötzinger complex (preBötC). There is also evidence that astrocytes, non-neuronal brain cells, contribute to central CO chemosensitivity.

Modulation of L-type calcium channels in Alzheimer's disease: A potential therapeutic target.

Calcium plays a fundamental role in various signaling pathways and cellular processes in the human organism. In the nervous system, voltage-gated calcium channels such as L-type calcium channels (LTCCs) are critical elements in mediating neurotransmitter release, synaptic integration and plasticity. Dysfunction of LTCCs has been implicated in both aging and Alzheimer's Disease (AD), constituting a key component of calcium hypothesis of AD.