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M1.1 H2 Zelfstudie opdracht – Neuroplasticity1. Study Material
Presentation slides- Hearing college
Books
● Lundy-Ekman, L. (2018). Neuroscience-E-Book: Fundamentals for Rehabilitation. Elsevier
Health Sciences.= Chapter 7
● Shumway-Cook, A., & Woollacott, M. H. (2007). Motor control: translating research into
clinical practice. Lippincott Williams & Wilkins= Chapter 4 (Pages 90-105)
Journal papers
Winstein, C. J., & Kay, D. B. (2015). Translating the science into practice: shaping
rehabilitation practice to enhance recovery after brain damage. In Progress in brain
research (Vol. 218, pp. 331-360). Elsevier.
2. Questions:
For all questions refer to presentation slides of hearing college and also the
suggested literature. In every question there is also referral to the different pages of
the books
a. Define neuroplasticity? Refer to Lundy-Ekman page 137 – introduction
Is the ability of neurons to change their function, chemical profile and/or
structure.
b. What are the mechanisms related to neuroplasticity? Refer to Lundy-Ekman page
137 – introduction
Habituation
Expiernce-dependent plasticity: learning and memory
Recovery or maladaption after injury
c. What is habituation? Refer to Shumway-Cook page 83-84, Lundy-Ekman page 137
subtitle Habituation
Neuroscience: one of the simplest forms of neuroplasticity, is a decrease in
response to a repeated, benign stimulus. After a period of rest in which the
1
, stimulus is no longer present or are partially resolved, and behavior can again
be elicited in response to the same sensory stimulus.
Motor control: is the simplest form of implicit learning, habituation is related to
a decrease in synaptic activity between sensory neurons and their connection
to interneurons and motor neurons.
d. Can you describe the steps of long-term potentiation/depression? Refer to Lundy-
Ekman page 138 and fig 7.1 page 139
Long term potential (LTP)
o LTP is the conversion of silent synapses to active synapses (figuur)
Silent synapses lack functional AMPA receptors are inactive
under normal conditions
Silent synapses can be converted to active synapses by highly
correlated presynaptic and post synaptic firing
Silent synapses become active when mobile AMPA
receptors are inserted into the synaptic membrane
because glutamate in the synaptic cleft can bind to th
exposed receptors.
o The postsynaptic membrane changes with LTP
o 1ste
Ca enters the postsynaptic cell trough channels associated with
NMDA (N-methyl-D-aspartate) glutamate receptors, resulting in
phosphorylation of AMPA receptors and insertion of AMPA
receptors into the membrane
Subsequently, the postsynaptic membrane remodels,
generating a new dendritic spine.
o For an neuron to structurally change, genetic alterations must occur in
the cell during the learning process.
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