Anatomical analysis of ventrolateral thalamic input to primate motor cortex

1976 ◽  
Vol 39 (5) ◽  
pp. 1020-1031 ◽  
Author(s):  
P. L. Strick

1. The origin and topographical organization of input to the arm area of the primate motor cortex from the ventrolateral thalamus were examined using the method of retrograde transport of horseradish peroxidase (HRP). 2. A thin, continuous slab of labeled neurons was found in the ventrolateral thalamus followingmultiple injections of HRP into the arm area of the motor cortex. The slab of labeled neurons was flanked, medially and laterally, by groups of unlabeled neurons. 3. The origin of ventrolateral thalamic input was more extensive than previously thought. Labeled neurons were found from A10.0 to A6.0 and occurred in three ventolateral thalamic subdivisions: ventralis lateralis pars oralis (VLo), ventralis lateralis pars caudalis (VLc), and ventralis posterior lateralis pars oralis (VPLo). For simplicity this region containing labeled neurons has been termed the ventrolateral thalamic (VL) arm area. 4. Injections of HRP into the somatic sensory cortex indicated that the thalamic regions which project to the somatic sensory cortex are separate from the VL arm area. 5. The distribution of labeled neurons following single injections of HRP into different regions of the motor cortex arm area indicated that the VL arm area is topographically organized, particularly its caudal part. Ventral regions of the VL arm area were labeled following HRP injections into motor cortex regions adjacent to the central sulcus where the representation of largely distal musculature is localized. Dorsal regions of the VL arm area were labeled following HRP injections into motor cortex regions more rostral to the central sulcus where the representation of more proximal musculature is localized. 6. A larger region of the VL arm area was labeled following HRP injections adjacent to the central sulcus than following the more rostral motor cortex injections. This suggests that, like the arm area of the motor cortex, more of the VL arm area is allotted to the representation of distal than proximal musculature. 7. Following very small cortical HRP injections, isolated labeled thalamic neurons were diffusely scattered throughout a 3-mm rostrocaudal extent of the VL arm area. In addition, a small focal cluster of labeled thalamic neurons was also seen. The labeled cluster was limited to 0.5 mm rostrocaudally and 300 mum in width. The focal distribution of labeled thalamic neurons suggests that aspects of a point to point organization may exist in the connection between VL and the motor cortex arm area.

1992 ◽  
Vol 72 (6) ◽  
pp. 2238-2243 ◽  
Author(s):  
J. C. LaManna ◽  
L. M. Vendel ◽  
R. M. Farrell

Rats were exposed to hypobaric hypoxia (0.5 atm) for up to 3 wk. Hypoxic rats failed to gain weight but maintained normal brain water and ion content. Blood hematocrit was increased by 48% to a level of 71% after 3 wk of hypoxia compared with littermate controls. Brain blood flow was increased by an average of 38% in rats exposed to 15 min of 10% normobaric oxygen and by 23% after 3 h but was not different from normobaric normoxic rats after 3 wk of hypoxia. Sucrose space, as a measure of brain plasma volume, was not changed under any hypoxic conditions. The mean brain microvessel density was increased by 76% in the frontopolar cerebral cortex, 46% in the frontal motor cortex, 54% in the frontal sensory cortex, 65% in the parietal motor cortex, 68% in the parietal sensory cortex, 68% in the hippocampal CA1 region, 57% in the hippocampal CA3 region, 26% in the striatum, and 56% in the cerebellum. The results indicate that hypoxia elicits three main responses that affect brain oxygen availability. The acute effect of hypoxia is an increase in regional blood flow, which returns to control levels on continued hypoxic exposure. Longer-term effects of continued moderate hypoxic exposure are erythropoiesis and a decrease in intercapillary distance as a result of angiogenesis. The rise in hematocrit and the increase in microvessel density together increase oxygen availability to the brain to within normal limits, although this does not imply that tissue PO2 is restored to normal.


2000 ◽  
Vol 40 (8) ◽  
pp. 393-403 ◽  
Author(s):  
Toshihiro KUMABE ◽  
Nobukazu NAKASATO ◽  
Takashi INOUE ◽  
Takashi YOSHIMOTO

1996 ◽  
Vol 213 (2) ◽  
pp. 132-136 ◽  
Author(s):  
Ali Suha Calikoglu ◽  
Gabriel Gutierrez-Ospina ◽  
A. Joseph D'Ercole

2019 ◽  
Author(s):  
Steffen B. E. Wolff ◽  
Raymond Ko ◽  
Bence P. Ölveczky

AbstractThe acquisition and execution of learned motor sequences are mediated by a distributed motor network, spanning cortical and subcortical brain areas. The sensorimotor striatum is an important cog in this network, yet how its two main inputs, from motor cortex and thalamus respectively, contribute to its role in motor learning and execution remains largely unknown. To address this, we trained rats in a task that produces highly stereotyped and idiosyncratic motor sequences. We found that motor cortical input to the sensorimotor striatum is critical for the learning process, but after the behaviors were consolidated, this corticostriatal pathway became dispensable. Functional silencing of striatal-projecting thalamic neurons, however, disrupted the execution of the learned motor sequences, causing rats to revert to behaviors produced early in learning and preventing them from re-learning the task. These results show that the sensorimotor striatum is a conduit through which motor cortical inputs can drive experience-dependent changes in subcortical motor circuits, likely at thalamostriatal synapses.


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