|M.Sc Student||Dori Bat-Elle|
|Subject||Dendritic Excitability Changes of Layer 5 Pyramidal Neurons|
Following Motor Learning in Primary Motor Cortex
|Department||Department of Medicine||Supervisor||Dr. Jackie Schiller|
|Full Thesis text|
The primary motor cortex (M1) is a crucial cortical region participating in motor control and motor learning. Motor learning is the acquisition of novel motor skills which are believed to involve plasticity changes at the cortical network at various levels including structural and synaptic modifications. M1 receives and integrates convergent inputs from multiple sources, and ultimately, conveys the final output motor commands to lower brainstem and spinal cord execution centers via pyramidal track (PT) layer 5B neurons.
In this study we specifically concentrated on the plasticity changes in dendrites of layer 5B neurons during motor learning, as these neurons are the main output command neurons. Layer 5B pyramidal neurons possess an elaborated dendritic arborization which serves to receive and integrate the vast information terminating on these neurons. Tuft dendrites are the most distal part of the layer 5B apical dendritic tree and they were shown to form a separate computational unit. Tuft dendrites were shown to be the primary site for integrating top-down information with bottom-up. Plasticity changes in tuft dendrites of layer 5 pyramidal neurons in motor cortex were shown to be crucial during learning of a new motor task. They were shown to crucially participate by forming new specific branch spikes and by addition of new spines during learning of new motor tasks.
In this study, we investigated the excitability changes taking place at the post-synaptic sites in tuft dendrites of layer 5B pyramidal neurons in M1 after learning a single-pellet hand reaching task in freely moving mice. After training the mice in a “slit-box” to reach for a food pellet, we examined the plasticity changes in excitability of tuft dendrites of layer 5B pyramidal neurons. We examined the attenuation of back-propagating axo-somatic action potentials (BAP) and the generation and spread of dendritic calcium spikes along the apical dendritic arbor. We used acute brain slice preparation taken from mice immediately after motor training and compared them to control naïve mice. Our findings showed that the BAP and dendritic calcium spike propagation were similar in naïve mice and mice that were trained but did not learn the task. However, for the group of mice that were trained and learned the task, we found a significant increase in both propagation of BAPs and dendritic calcium spikes, indicating an increase in dendritic excitability in this group. Interestingly, in this learners' group, in addition to the neurons that showed increase in dendritic excitability, we found a second group of neurons that showed decrease in dendritic excitability compared to the naïve mice and mice that were trained but did not learn.
In conclusion, our data clearly show significant dendritic plasticity of excitability following motor learning in M1.