L-(+)-2-Amino-4-phosphonobutyric Acid

Glutamate is an excitatory neurotransmitter found in the synaptic vesicles of glutamatergic synapses. The post-synaptic neurons in these synapses contain ionotropic and metabotropic glutamate receptors. Glutamate binds to AMPA (α-amino-3-hydroxy-5- methylisoxazole-4-propionic acid) subtype glutamate receptors, leading to sodium influx into the post-synaptic cell and resulting in neuronal excitability and synaptic transmission. The NMDA (N-methyl-d-aspartate) subtype glutamate receptors, on the other hand, regulate synaptic plasticity, and can influence learning and memory. The metabotropic g-protein coupled mGluRs modulate downstream calcium signaling pathways and indirectly influence the synapse’s excitability. The synaptic architecture includes intracellular scaffolding proteins (PSD-95, GRIP), intercellular cell adhesion molecules (NCAMs, N-Cadherins), and a variety of signaling proteins (CaMKII/PKA, PP1/PP2B). Processes critical for synaptic transmission and plasticity are influenced by these molecules and their interactions. When the function of these molecules is disrupted, it leads to synaptic dysfunction and degeneration, and can contribute to dementia as seen in Alzheimer’s disease.

"Apoptosis & Autophagy in Cancer: Cell Survival by Eluding Cell Death The ability of tumor cells to elude programmed cell death, also known as apoptosis, is a hallmark of most types of cancer. Similary, autophagy is a highly regulated, homeostatic degradative process where cells destroy their own components via the lysosomal machinery and recycle them for prolonged cell survival. Via extensive crosstalk with pro-apoptotic signaling pathways, autophagy can also contribute to cell death and greatly influence general cell health. Elucidating the correlation between autophagy and apoptotic cell death has become the focus of a great deal of research, particularly in tumor biology. On one hand, autophagy may induce cell death by degrading essential components; on the other hand, it may facilitate survival of cancer cells under unfavorable metabolic conditions."