Bidirectional Influence of Epinephrine on Hippocampal LTP via β-Adrenergic Receptors

The formation and storage of memories within the brain remains a subject that is not well understood. The hippocampus has been identified by many studies as a likely center for memory formation (Lynch, 2004), and further research into this subject has begun to suggest that synaptic plasticity in the hippocampus could be partly responsible for the physical changes in the brain, which underlie memory formation. Long Term Potentiation is a form of synaptic plasticity, and is considered to be a physical increase in the strength of connection between neurons or groups of neurons. Much like memories, the duration of a given LTP can last anywhere from minutes to years, depending upon the conditions under which the LTP was induced. Stress, in particular, has been found to either enhance or impair LTP formation, under different conditions. The brain’s response to stress, or any kind of emotional arousal, is in part mediated by the release of the hormone epinephrine. This type of “stress memory”, or epinephrine-mediated memory formation, is important because it could explain the pathological memory formation that is commonly seen in phenomena such as Post Traumatic Stress Disorder (Korol and Gold, 2008). Epinephrine release in the periphery has been seen to influence LTP in the hippocampus, however epinephrine itself cannot enter the brain. These experiments served to explore the mechanisms by which epinephrine can act to bidirectionally influence hippocampal LTP through activation of β-adrenergic receptors

The α-Tubulin gene TUBA1A in Brain Development: A Key Ingredient in the Neuronal Isotype Blend

Microtubules are dynamic cytoskeletal polymers that mediate numerous, essential functions such as axon and dendrite growth and neuron migration throughout brain development. In recent years, sequencing has revealed dominant mutations that disrupt the tubulin protein building blocks of microtubules. These tubulin mutations lead to a spectrum of devastating brain malformations, complex neurological and physical phenotypes, and even fatality. The most common tubulin gene mutated is the α-tubulin gene TUBA1A, which is the most prevalent α-tubulin gene expressed in post-mitotic neurons. The normal role of TUBA1A during neuronal maturation, and how mutations alter its function to produce the phenotypes observed in patients, remains unclear. This review synthesizes current knowledge of TUBA1A function and expression during brain development, and the brain malformations caused by mutations in TUBA1A