Neuroscience 3 - Plasticity

Transient or permanent changes in neural structure and function

Non-neuronal cells that play a support role Do not have synapses

Oligodendrocyte Microglia Astrocytes Ependyma

Myelinate neuron axons

immune defense

They are active in the repair following a injury

Involved in the production of cerebrospinal fluid (CSF)

Proliferation Migration Apoptosis Differentiation Network formation and function Synaptogenesis

Stem cells divide, axonal and dendritic growth They divide and become more specific to where they go: progenitor

Go to different areas

Selective, programmed cell death

Neurons get specialized for certain functions A result of differential gene expression: turning some genes on and others off.

Different neuron types are put together to carry out a higher-level function The brain can start to create networks

creation of synapses Allows for new healthy cells

The selective elimination of synapses and their connections to refine neural circuits

It is not sequential; the processes overlap

Each processes is associated with a neurodevelopmental disorder Ex. Neural migration is associated with Autism

Cells that fire together, wire together Weights of neuronal connections can change over time as a consequence of joint excitation

The strength with which a response will be connected with a situation increases with the number of times the response has occurred in that situation

The change in weight between (j) and (i) will increase as a function of the learning rate (L) and as a function of their coincident firing wij = L x xj x xi L = learning rate xj = activity of the pre-synaptic neuron xi = activity of the post-synaptic neuron

Procedures: Record neural activity in the hippocampus based on the electrode stimulation experimenters provide (rabbit brain) to neuron A, to then stimulate neuron B. They give a weak stimulation to get a baseline, which leads to minimal activity in the post-synaptic. They then give a tetanus shot (brief high-frequency stimulation), which leads to the post-synaptic neuron having post-tetanus potentiation (responds strongly). It will taper off but not fully. This leads to long-term potentiation that lasts for about an hour. In the LTP, we have the post-synaptic neuron responding more than before tetanus. Implications: Shows what Hebb claimed, that neurons that are firing together lead to their connection strengthening

There are many different ways LTP can be expressed. One way is that there is an increase in the number of neurotransmitters released by the presynaptic neuron. Another way is that there is an increase in receptors of the postsynaptic neuron, leading to more opportunities for binding. Lastly, there is the possibility that both the number of neurotransmitters and the number of receptors increase.

It is the principle that the strength in potentiation depends on timing. So, the closer the presynaptic and the postsynaptic fire, the stronger the long-term potentiation is.

When the pre-synaptic neuron fires after the post-synaptic which shows that the pre-synaptic neuron didn’t lead to the firing of the post-synaptic neuron. This leads to it weakening the connection between the pre and post-synaptic neurons.