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  • January 31, 2022
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M1.1 H2 Zelfstudie opdracht – Neuroplasticity

1. 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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