| || Models ||Description|
Deconstruction of cortical evoked potentials generated by subthalamic DBS (Kumaravelu et al 2018)
High frequency deep brain stimulation (DBS) of the
subthalamic nucleus (STN) suppresses parkinsonian motor symptoms and
modulates cortical activity.
Cortical evoked potentials (cEP) generated by STN DBS reflect
the response of cortex to subcortical stimulation, and the goal was to
determine the neural origin of cEP using a two-step approach.
we recorded cEP over ipsilateral primary motor cortex during different
frequencies of STN DBS in awake healthy and unilateral 6-OHDA lesioned
Second, we used a biophysically-based model of the
thalamocortical network to deconstruct the neural origin of the
cEP. The in vivo cEP included short (R1), intermediate (R2) and
long-latency (R3) responses. Model-based cortical responses to
simulated STN DBS matched remarkably well the in vivo responses.
was generated by antidromic activation of layer 5 pyramidal neurons,
while recurrent activation of layer 5 pyramidal neurons via excitatory
axon collaterals reproduced R2. R3 was generated by polysynaptic
activation of layer 2/3 pyramidal neurons via the
Antidromic activation of the
hyperdirect pathway and subsequent intracortical and
cortico-thalamo-cortical synaptic interactions were sufficient to
generate cEP by STN DBS, and orthodromic activation through basal
ganglia-thalamus-cortex pathways was not required. These results
demonstrate the utility of cEP to determine the neural elements
activated by STN DBS that might modulate cortical activity and
contribute to the suppression of parkinsonian symptoms."
Engaging distinct oscillatory neocortical circuits (Vierling-Claassen et al. 2010)
||"Selective optogenetic drive of fast-spiking (FS) interneurons (INs) leads to enhanced local field potential (LFP) power across the traditional “gamma” frequency band (20–80 Hz; Cardin et al., 2009).
In contrast, drive to regular-spiking (RS) pyramidal cells enhances power at lower frequencies, with a peak at 8 Hz.
The first result is consistent with previous computational studies emphasizing the role of FS and the time constant of GABAA synaptic inhibition in gamma rhythmicity.
However, the same theoretical models do not typically predict low-frequency LFP enhancement with RS drive.
To develop hypotheses as to how the same network can support these contrasting behaviors, we constructed a biophysically principled network model of primary somatosensory neocortex containing FS, RS, and low-threshold spiking (LTS) INs. ..."
LFP signature of monosynaptic thalamocortical connection (Hagen et al 2017)
||"A resurgence has taken place in recent years in the use of the
extracellularly recorded local field potential (LFP) to investigate
neural network activity. To probe monosynaptic thalamic activation of
cortical postsynaptic target cells, so called spike-trigger-averaged
LFP (stLFP) signatures have been measured. In these experiments, the
cortical LFP is measured by multielectrodes covering several cortical
lamina and averaged on spontaneous spikes of thalamocortical (TC)
cells. Using a well established forward-modeling scheme, we
investigated the biophysical origin of this stLFP signature with
simultaneous synaptic activation of cortical layer-4 neurons,
mimicking the effect of a single afferent spike from a single TC
Simulations of oscillations in piriform cortex (Wilson & Bower 1992)
||"1. A large-scale computer model of the piriform cortex was
constructed on the basis of the known anatomic and physiological
organization of this region.
2. The oscillatory field potential and electroencephalographic
(EEG) activity generated by the model was compared with actual
physiological results. The model was able to produce patterns of
activity similar to those recorded physiologically in response to
both weak and strong electrical shocks to the afferent input. The
model also generated activity patterns similar to EEGs recorded in