Corticothalamic Neurons in Motor Cortex Have a Permissive Role in Motor Execution
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ABSTRACT:
PROVIDER: PRJNA1241835 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32856262_1.fastq.gz | Fastqsanger.gz | |||
| SRR32856262_2.fastq.gz | Fastqsanger.gz | |||
| SRR32856263_1.fastq.gz | Fastqsanger.gz | |||
| SRR32856263_2.fastq.gz | Fastqsanger.gz | |||
| SRR32856264_1.fastq.gz | Fastqsanger.gz |
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Project description:The primary motor cortex (M1) is a central hub for motor learning and execution. M1 is composed of heterogeneous cell types with varying relationships to movement. Here, we tagged active neurons at different stages of motor task performance in mice and characterized cell type composition. We identified corticothalamic neurons (M1CT) as consistently enriched with training progression. Using two-photon calcium imaging, we found that M1CT activity is largely suppressed during movement, and this negative correlation augments with training. Increasing M1CT activity through closed-loop optogenetic manipulations during forelimb movement significantly hinders execution, an effect that became stronger with training. Similar manipulations, however, had little effect on locomotion. In contrast, M1 corticospinal neurons positively correlate with movement, with an increase during training. We uncovered that M1CT neurons suppress corticospinal activity via feedforward inhibition, also scaling with training. These results identify a permissive role of corticothalamic neurons in movement execution through disinhibition of corticospinal neurons.
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Project description:Gene expression analysis of motor cortex after spinal C3 lesion Dorsal column wire knife lesions: Adult female Fischer 344 rats weighing 150-200 gm were used. Animals underwent a laminectomy at spinal level C3. Dorsal funiculus lesions were made in the middle of C3 using a Kopf microwire device (Kopf Instruments, Tujunga, CA). After fixation in a spinal stereotaxic unit, a small dural incision was made. The wire knife was lowered into the spinal cord to a depth of 1.1 mm ventral to the dorsal cord surface and 1.1 mm to the left of the midline. The tip of the wireknife was extruded, forming a 2.25 mm-wide arc that was raised to the dorsal surface of the cord. To ensure complete axotomy of the dorsal funiculus, spinal tissue was compressed against the microwire knife surface using a microaspiration pipette until all visible white matter was transected. Cortical microdissection: The forelimb and hindlimb motor cortex were microdisected from rat cortices: Rostral to Bregma: an area from 2.0 to 4.5 mm mediolateral and from 0 to 2 mm anterior-posterior Caudal to Bregma: an area from 2.0 to 3.5 mediolateral and from 0 to 3 mm caudal to Bregma. Only the inferior half of the cortex containing layer V corticospinal motor neurons was sampled in each region.
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Project description:Molecular mechanisms controlling specification and differentiation of distinct neuron subtypes in the cerebral cortex are not well understood. Corticothalamic projection neurons (CThPN) are a diverse set of neurons, critical for function of the neocortex, but little is known about the molecular mechansims controlling their development. We used microarrays to detail CThPN gene expression at 3 developmental time points. We then compared CThPN gene expression, with the gene expression of other neuron subtypes in the cerebral cortex at the same stages (previously described in Arlotta et a., 2005)
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Project description:Introduction: Male estrogen receptor beta (ERβ) knockout (BERKO) mice display anxiety and aggression linked to, among others, altered serotonergic signaling in the basolateral amygdala and dorsal raphe, impaired cortical radial glia migration and reduced GABAergic signaling. Effects on primary motor cortex (M1 cortex) and locomotor activity as a consequence of ERβ loss have not been investigated. Objective: The aim of this study was to determine whether locomotor activity is altered as a consequence of the changes in the M1 cortex. Methods: Locomotor activity of WT and BERKO male mice was evaluated using the open-field and rotarod tests. Molecular changes in the M1 cortex were analyzed by RNA-sequencing, electron microscopy, electrophysiology, and immunofluorescence techniques. In addition, we established oligodendrocyte cultures from WT and BERKO mouse embryonic stem cells to evaluate oligodendrocyte function. Results: Locomotor profiling revealed that BERKO mice were more active than WT mice but had impaired motor coordination. Analysis of the M1 cortex pointed out differences in synapse function and myelination. There was a reduction in GABAergic signaling resulting in imbalanced excitatory and inhibitory neurotransmission, as well as a defective oligodendrocyte differentiation accompanied by myelin defects. The effects of loss of ERβ on oligodendrocyte differentiation was confirmed in vitro. Conclusion: ERβ is an important regulator of GABAergic interneurons and oligodendrocyte differentiation, which impacts on adult M1 cortex function, and may be linked to increased locomotor activity and decreased motor coordination in BERKO mice.
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