Brain cells communicate with one another by passing chemical messengers at functional contacts called synapses. Neurobiological studies have demonstrated that synapses play an important role in learning, memory, aging, stress and addiction.
What is a synapse?[i]
The word synapse stems from the Greek words “syn” (together) and “haptein” (to clasp). It is a critical element to neurotransmission. The synapse is made up of two brain cells as well as the small pocket of extracellular space between them.
Your average neuron is made up of three basic parts: the soma, or cell body; the axon, a nerve fiber extending from the soma; and dendrites, branching pathways that may extend outward from cell. The synaptic junction is not one of these parts but rather the minute gap between two or more neurons through which neurotransmitters and other neuroactive molecules pass. A single neuron may have thousands of synapses, with chemical signals being passed from axon to dendrite (axodendritic), axon to soma (axosomatic), or axon to axon (axoaxonic). One type of neuron called the Purkinje cell, found in the cerebellum, may have as many as one hundred thousand synapses.
How big is a synapse? [ii]
Synapses are very small. This narrow gap of extracellular space is approximately 20-40 nanometers (nm) wide. For an idea of scale, one inch is about 25.4 million nm long. The thickness of a single sheet of paper is about 100,000 nm.[iii]
How many synapses are in the human brain?[iv][v]
Current studies estimate that the average adult male human brain contains approximately 86 billion neurons. As a single neuron has hundreds to thousands of synapses, the estimated number of these functional contacts is much higher, in the trillions (estimated at 0.15 quadrillion).
What is synaptic transmission?
Synaptic transmission occurs when neurons pass various molecules between them at the synapse. One neuron, called the pre-synaptic cell, releases a chemical or chemicals from synaptic vesicles, or pouches, clustered near the cell membrane. These chemicals are then taken up by membrane receptors on the post-synaptic cell, which results in the excitation, inhibition, or modulation of that receiving cell’s behavior. Synapses can also work in the reverse direction: post-synaptic cells may release molecules that work on pre-synaptic cells, altering how much or how often a neurotransmitter is released.
What is the difference between a Type I and Type II synapse?
Some neurobiologists distinguish synapses as Type I and Type II. These synapses vary in size, structure and shape. Type I synapses are found mainly on dendrites and result in an excitatory response in the post-synaptic cell. Type II synapses, in contrast, are found on the soma and inhibit the receiving cell’s activity.
What is the difference between a chemical synapse and an electrical synapse?[vi]
Most synapses are chemical in nature, releasing neurotransmitters or other neuroactive proteins and chemicals to be taken up by receiving cells. Electrical synapses, also known as gap junctions, are smaller, approximately 1-4 nm in width, and conduct impulses in neural circuits that require quick and immediate responses. Additionally, most electrical synapses are bi-directional. Though overlooked for a long time, some now hypothesize that electrical synapses play an equally important role in the creation, maintenance, and strengthening of neural circuits as their chemical brethren.
What is synaptic plasticity?[vii]
Synaptic plasticity refers to changes in strength of a given synapse. Though it was once believed that synapses were fixed—they were simple way stations transferring information from cell to cell—it is now known that the strength of a synapse, or ability to influence the behavior of receiving cells, can be altered through its own activity or as part of a larger network of neurons. The more a synapse is used, the stronger it become and the more influence it wields over post-synaptic neurons.
What is long-term potentiation? [viii]
One type of synaptic plasticity of great interest to neuroscientists is called long term potential (LTP). Repetitive chemical communication between two cells over time strengthens the synapse, resulting in an amplified response in the post-synaptic cell. Simply stated, LTP enhances cell communication by allowing the pre-synaptic and post-synaptic cells to communicate faster and more efficiently. This synaptic strengthening is long-lasting and thought to underlie learning and memory in an area of the brain called the hippocampus. Researchers are working to better understand the cellular mechanisms of LTP and how it results in learning and memory at the behavioral level.
How is synaptic plasticity involved in addiction?[ix]
Today, synaptic plasticity is an active line of research in addiction. Researchers hypothesize that drugs of abuse may make actual physical changes to the synapses, similar to what you’d see in natural plasticity like long-term potentiation. As such, repetitive use of these drugs may result in the artificial strengthening of synapses in brain areas fueled by the neurotransmitter dopamine like the nucleus accumbens; reorganization of neural circuits; and, ultimately, addictive behavior.
What can we expect in the future from the study of synapses?
Synapses, particularly their plasticity, remain an important avenue of study in the neuroscience community. Many researchers are actively trying to connect the molecular activity observed at the synapse with cognitive and behavioral outcomes involved with learning, memory, and addiction. In addition, the study of the shape, size and density of synapses are also offering new insights into the aging brain[x], as well as its response to stress.[xi]
[i] Dowling JE. Neurons and Networks: An Introduction to Behavioral Neuroscience. 2001. The Belknap Press of Harvard University Press, Cambridge, Massachusetts.
[iv] Azevedo FAC, Carvalho LRB, Grinberg LT, Farfel JM, Ferretti REL, Leite REP, Filho WJ, Lent R and Herculano-Houzel S. Equal numbers of neuronal and nonneuronal cells make the human brain an isometrically scaled-up primate brain. The Journal of Comparative Neurology. 2009, 513(5): 532-541.
[v] Pakkenberg B, Pelvig D, Marner L, Bundgaard MJ, Gundersen HJ, Nyengaard JR and Regeur L. Aging and the human neocortex. Experimental Gerontology. 2003, 38(1-2):95-9.
[vi] Hormuzdi SG, Filippov MA, Mitropoulou G, Monyer H and Bruzzone R. Electrical synapses: a dynamic signaling system that shapes the activity of neural networks. Biochimica et Biophysica Acta. 23 March 2004, 1662(1-2): 113-137.
[viii] Whitlock JR, Heynen AJ, Shuler MG and Bear MF. Learning induces long-term potentiation in the hippocampus. Science. 25 August 2006, 313(5790): 1093-1097.
[ix] Lüscher C and Malenka RC. Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling. Neuron. 24 February 2011, 69(4): 650-663.
[x]Dumitriu D, Hao J, Hara Y, Kaufmann J, Janssen WGM, Lou W, Rapp PR and Morrison JH. Selective changes in thin spine density and morphology in monkey prefrontal cortex correlate with aging-related cognitive impairment. The Journal of Neurosicence. 2 June 2010, 30(22): 7507-7515.
[xi] Radly JJ, Rocher AB, Janssen WGM, Hof PR, McEwen BS and Morrison JH. Reversibility of apical dendritic retraction in the rat medial prefrontal cortex following repeated stress. Experimental Neurology. 2005, 196: 199-203.