Cellular communication: Tools to study synapses

Electrical and chemical information is transmitted between neurons at asymmetric intercellular junctions called synapses. The human brain contains 86 billion neurons and within the neocortex each neuron has on average 7000 synapses^1,2. Development and maintenance of synaptic connections are regulated by complex molecular mechanisms and are influenced by experience and learning^3,4. Disruption of synaptic development and function has been linked to a variety of neurological disorders including autism, schizophrenia, addiction, dementia, and Alzheimer’s disease^5,6.

Over the past decade the toolbox to study synapses has greatly expanded. Novel genetic and molecular tools, including optogenetics, CLARITY, array tomography, and Brainbow, are helping researchers better understand how neuronal connections are established. These techniques have expanded our knowledge of memory, hearing, and motor control, as well as shedding light on our understanding of Alzheimer’s disease⁷, depression, stroke⁸ and psychiatric disorders⁹.

NeuroScientistNews is pleased to sponsor the upcoming webinar from The Scientist on October 28, 2014: New Models and Tools for Studying Synaptic Development and Function. The webinar will feature presentations by Dr. Ed Boyden, Dr. Donald Arnold and Dr. Loren Looger. A Q&A session where attendees can interact with the experts will follow the presentations. Join us for this event to learn about emerging technologies for studying synaptic development and function.

References

1. 1. Herculano-Houzel S. The human brain in numbers: a linearly scaled-up primate brain. Front. Hum. Neurosci. 2009; 3(November):31. doi:10.3389/neuro.09.031.2009.
2. 2. Pakkenberg B, Pelvig D, Marner L, et al. Aging and the human neocortex. 2003; 38:95-99.
3. 3. Mayford M, Siegelbaum S a, Kandel ER. Synapses and memory storage. Cold Spring Harb. Perspect. Biol. 2012; 4(6). doi:10.1101/cshperspect.a005751.
4. 4. Chia PH, Li P, Shen K. Cell biology in neuroscience: cellular and molecular mechanisms underlying presynapse formation. J. Cell Biol. 2013; 203(1):11-22. doi:10.1083/jcb.201307020.
5. 5. Williams AJ, Umemori H. The best-laid plans go oft awry: synaptogenic growth factor signaling in neuropsychiatric disease. Front. Synaptic Neurosci. 2014; 6(March):4. doi:10.3389/fnsyn.2014.00004.
6. 6. Pozueta J, Lefort R, Shelanski ML. Synaptic changes in Alzheimer’s disease and its models. Neuroscience 2013; 251:51-65. doi:10.1016/j.neuroscience.2012.05.050.
7. 7. Neuman KM, Molina-Campos E, Musial TF, et al. Evidence for Alzheimer’s disease-linked synapse loss and compensation in mouse and human hippocampal CA1 pyramidal neurons. Brain Structure and Function. 2014.
8. 8. Cheng MY, Wang EH, Steinberg GK. Optogenetic Approaches to Study Stroke Recovery. 2014:5-6. doi:10.1038/nrn2735.(3).
9. 9. Steinberg EE, Christoffel DJ, Deisseroth K, Malenka RC. Illuminating circuitry relevant to psychiatric disorders with optogenetics. Curr. Opin. Neurobiol. 2014; 30C:9-16. doi:10.1016/j.conb.2014.08.004.