Development of Dendritic Spines
Neurons have the capability of forming spiny outgrowths on dendrites that are associated with neuroplasticity. Stimulation, especially during post-natal development can lead to activation in the brain, referred to as Long Term Potentiation (LTP), associated with the growth of spines. These dendritic spines, which can number thousands to a single neuron, can have synaptic heads. Greater than 90 percent of synapses in the brain occur on them (1) . Through experimentation it has been found that a spine's glutamate receptors, calcium concentrations, and actin can affect its shape, length, and even presence on a dendrite. In general terms, how do dendritic spines develop and what do they affect in the brain?
When a neuron is first formed it does not yet have dendrites, and therefore also does not have dendritic spines. Dendritic filopodia are formed from the dendrites first and then convert into spines after being innervated by synaptic fibers. Spines on different types of neurons attain their peak actin density at different times. Fewer spines are present in adults than children and there is a peak growth time during post-natal development. Adult brains show up to 50% fewer spines than developing brains (2) . Brain disorders, such as strokes, epilepsy, and forms of mental retardation like Fragile X, have been connected to deformations of dendritic spines or the total absence of them on certain neurons. Spines are predominantly found at excitatory synapses where inputs from many areas of the brain arrive.
Initially during spine formation N-methyl-D-aspartate (NMDA) is the main growth and development regulator. NMDA is a glutamate receptor found at excitatory synapses in most neurons in the mammalian brain. It contains channels permeable to calcium ions. Ions can accumulate and initiate currents at the head of the spine where the calcium channels are located, separate from the shaft of the dendrite. Weak calcium-induced...