brain plasticity: underlying mechanisms (Introduction)

by David Turell , Friday, November 20, 2015, 15:55 (3292 days ago) @ David Turell

There are complex enzymatic and chemical changes at the synaptic level which change connections and networks in response to the mental tasks we begin or use:-http://www.sciencedaily.com/releases/2015/11/151118155301.htm-"When the brain forms memories or learns a new task, it encodes the new information by tuning connections between neurons. MIT neuroscientists have discovered a novel mechanism that contributes to the strengthening of these connections, also called synapses.-"At each synapse, a presynaptic neuron sends chemical signals to one or more postsynaptic receiving cells. In most previous studies of how these connections evolve, scientists have focused on the role of the postsynaptic neurons. However, the MIT team has found that presynaptic neurons also influence connection strength.-***-"Over the past 30 years, scientists have found that strong input to a postsynaptic cell causes it to traffic more receptors for neurotransmitters to its surface, amplifying the signal it receives from the presynaptic cell. This phenomenon, known as long-term potentiation (LTP), occurs following persistent, high-frequency stimulation of the synapse.-***-"His lab has spent several years working out the mechanism for how presynaptic cells release neurotransmitter in response to spikes of electrical activity known as action potentials. When the presynaptic neuron registers an influx of calcium ions, carrying the electrical surge of the action potential, vesicles that store neurotransmitters fuse to the cell's membrane and spill their contents outside the cell, where they bind to receptors on the postsynaptic neuron.-"The presynaptic neuron also releases neurotransmitter in the absence of action potentials, in a process called spontaneous release. These 'minis' have previously been thought to represent noise occurring in the brain. However, Littleton and Cho found that minis could be regulated to drive synaptic structural plasticity.-***-"The enhancement of minis appears to provoke the postsynaptic neuron to release a signaling factor, still unidentified, that goes back to the presynaptic cell and activates an enzyme called PKA. This enzyme interacts with a vesicle protein called complexin, which normally acts as a brake, clamping vesicles to prevent release neurotransmitter until it's needed. Stimulation by PKA modifies complexin so that it releases its grip on the neurotransmitter vesicles, producing mini events. (my bold)-"When these small packets of neurotransmitter are released at elevated rates, they help stimulate growth of new connections, known as boutons, between the presynaptic and postsynaptic neurons. This makes the postsynaptic neuron even more responsive to any future communication from the presynaptic neuron."-Comment: this is a complex interplay between biochemicals which are produced to respond to specific uses of the brain. No wonder one of them is called 'complexin'. Somehow, the brain 'knows' how it is being used and responds to help the process at play. The enzymes mentioned are also very complex, giant molecules. How did evolution discover them from the vast array of potential molecules that can be manufactured? This is why the only possible way this developed is through intelligent planning. This is specified complexity, the concept of 'too complex to happen by chance'.