scholarly journals Anterolateral Motor Cortex Connects with a Medial Subdivision of Ventromedial Thalamus through Cell Type-Specific Circuits, Forming an Excitatory Thalamo-Cortico-Thalamic Loop via Layer 1 Apical Tuft Dendrites of Layer 5B Pyramidal Tract Type Neurons

2018 ◽  
Vol 38 (41) ◽  
pp. 8787-8797 ◽  
Author(s):  
KuangHua Guo ◽  
Naoki Yamawaki ◽  
Karel Svoboda ◽  
Gordon M.G. Shepherd
2020 ◽  
Author(s):  
Benjamin D. Harris ◽  
Megan Crow ◽  
Stephan Fischer ◽  
Jesse Gillis

ABSTRACTSingle-cell RNA-sequencing (scRNAseq) data can reveal co-regulatory relationships between genes that may be hidden in bulk RNAseq due to cell type confounding. Using the primary motor cortex data from the Brain Initiative Cell Census Network (BICCN), we study cell type specific co-expression across 500,000 cells. Surprisingly, we find that the same gene-gene relationships that differentiate cell types are evident at finer and broader scales, suggesting a consistent multiscale regulatory landscape.


Neuron ◽  
2020 ◽  
Vol 107 (5) ◽  
pp. 954-971.e9 ◽  
Author(s):  
Shahar Levy ◽  
Maria Lavzin ◽  
Hadas Benisty ◽  
Amir Ghanayim ◽  
Uri Dubin ◽  
...  

2020 ◽  
Author(s):  
Liqiang Chen ◽  
Yerim Kim ◽  
Hong-Yuan Chu

AbstractThe hypokinetic motor symptoms of Parkinson’s disease (PD) are closely linked with a decreased motor cortical output as a consequence of elevated basal ganglia inhibition. However, whether and how the loss of dopamine alters the cellular properties of motor cortical neurons in PD remains undefined. We induced experimental parkinsonism in adult C57BL6 mice of both sexes by injecting neurotoxin, 6-hydroxydopamine, into the medial forebrain bundle. By using ex vivo patch-clamp recording and retrograde tracing approach, we found that the intrinsic excitability of pyramidal tract neurons (PTNs) in the motor cortical layer 5b was greatly decreased following the degeneration of midbrain dopaminergic neurons; but the intratelencephalic neurons (ITNs) were not affected. The cell-type-specific intrinsic adaptations were associated with a significant broadening of the action potentials in PTNs but not in ITNs. Moreover, the loss of midbrain dopaminergic neurons impaired the capability of M1 PTNs to sustain high-frequency firing, which could underlie their abnormal pattern of activity in the parkinsonian state. We also showed that the decreased excitability and broadened action potentials were largely caused by a disrupted function of the large conductance, Ca2+-activated K+ channels. The restoration of dopaminergic neuromodulation failed to rescue the impaired intrinsic excitability of M1 PTNs in parkinsonian mice. Altogether, our data show cell-type-specific decreases of the excitability of M1 pyramidal neurons following the loss of midbrain dopaminergic neurons. Thus, intrinsic adaptations in the motor cortex, together with pathological basal ganglia inhibition, underlie the decreased motor cortical output in parkinsonian state and exacerbate parkinsonian motor deficits.Significance statementThe degeneration of midbrain dopaminergic neurons in Parkinson’s disease remodels the connectivity and function of cortico–basal ganglia–thalamocortical network. However, whether and how the loss of dopamine and aberrant basal ganglia activity alter motor cortical circuitry remain undefined. We found that pyramidal neurons in the layer 5b of the primary motor cortex (M1) exhibit distinct adaptations in response to the loss of midbrain dopaminergic neurons, depending on their long-range projections. Besides the decreased thalamocortical synaptic excitation as proposed by the classical model of Parkinson’s pathophysiology, these results, for the first time, show novel cellular and molecular mechanisms underlying the abnormal motor cortical output in parkinsonian state.


2021 ◽  
Author(s):  
Candice Lee ◽  
Emerson Harkin ◽  
Richard Naud ◽  
Simon Chen

The primary motor cortex (M1) is known to be a critical site for movement initiation and motor learning. Surprisingly, it has also been shown to possess reward-related activity, presumably to facilitate reward-based learning of new movements. However, whether reward-related signals are represented among different cell types in M1, and whether their response properties change after cue-reward conditioning remains unclear. Here, we performed longitudinal in vivo two-photon Ca2+ imaging to monitor the activity of different neuronal cell types in M1 while mice engaged in a classical conditioning task. Our results demonstrate that most of the major neuronal cell types in M1 showed robust but differential responses to both cue and reward stimuli, and their response properties undergo cell-type specific modifications after associative learning. PV-INs' responses became more reliable to the cue stimulus, while VIP-INs' responses became more reliable to the reward stimulus. PNs only showed robust response to the novel reward stimulus, and they habituated to it after associative learning. Lastly, SOM-IN responses emerged and became more reliable to both conditioned cue and reward stimuli after conditioning. These observations suggest that cue- and reward-related signals are represented among different neuronal cell types in M1, and the distinct modifications they undergo during associative learning could be essential in triggering different aspects of local circuit reorganization in M1 during reward-based motor skill learning.


2017 ◽  
Vol 55 (05) ◽  
pp. e28-e56
Author(s):  
S Macheiner ◽  
R Gerner ◽  
A Pfister ◽  
A Moschen ◽  
H Tilg

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 2430-PUB
Author(s):  
FRANKIE D. HEYWARD ◽  
EVAN ROSEN

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