|Ph.D Student||Rapoport Sophia|
|Subject||Active Dendritic Properties of Layer 4 Spiny Stellate|
Neurons in the Rat Somatosensory Cortex
|Department||Department of Medicine||Supervisor||Professor Jackie Schiller|
|Full Thesis text|
Layer 4 neurons are the first station of the cortex that receives sensory information from the thalamus. The major excitatory recipients of sensory input are the spiny stellate neurons. Despite the critical role of these cells in sensory information processing, the basic properties of their dendrites and especially the role of active dendritic processing in shaping sensory responses are still unknown.
We used whole cell recordings combined with dendritic calcium imaging and glutamate uncaging in the thalamocortical slice preparation to investigate the active dendritic properties of layer 4 spiny stellate neurons of the rodent barrel cortex.
Our findings show that activation of cortico-cortical synapses on a single branch can generate local spikes on the activated branch. Moreover, using glutamate uncaging in combination with specific pharmacological blockers we revealed that these spikes are mediated by the NMDA-R channels with almost no contribution of voltage gated calcium or sodium channels. Thus we concluded that NMDA spikes are the main regenerative event in the dendrites of spiny stellate cells. Similar to cortical pyramidal neurons, NMDA spikes evoked large calcium influx which was localized to the activated dendritic segments.
In addition to local spikes, the data demonstrate a novel form of active dendritic mechanism in layer 4 neurons - global multi-branch NMDA spikes. These spikes are evoked by coactivation of distributed cortico - cortical and thalamocortical inputs and are accompanied by calcium hot spots at multiple dendritic branches indicating a multi-focal generation mechanism.
Our findings suggest that local and global NMDA spikes can amplify convergent thalamo-cortical and cortico-cortical inputs to spiny stellate neurons and, thus, can play a critical role in shaping the sensory signal relayed by the thalamus.
Additionally, we investigated the role of NMDA spikes in plasticity of spiny stellate synapses. We find that indeed NMDA spikes are very efficient post synaptic signal for LTP. Pairing the activated synapses with NMDA spikes can cause a long lasting 200 % increase in the amplitude of the EPSP. Thus, local NMDA spike may constitute a synaptic mechanism responsible for experience-dependent plasticity in layer 4.