Motor Thalamic Nuclei Size
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The thalamus is a neural structure found in all vertebrates, located at the dorsal end (top) of the brain stem. It consists of 30 to 40 “nuclei”, or interconnected groups of neurons. “Motor” thalamic nuclei receive inputs from motor-related structures (including primary motor cortex, the cerebellum, globus pallidus, and substantia nigra) and sends its strongest outputs to the primary motor cortex (Armstrong & Armstrong, 1980). “Motor” thalamic nuclei include the ventrolateral complex (VL), which is thought to be involved in adjustments to posture during voluntary movements.
The human VL had about one-and-a-half times as many neurons as did those of the great apes. The numbers of neurons in the VL appeared to increase at a faster rate than changes in the pyramidal tract (a set of fibers connecting motor information from brain to the spinal cord), but at a slower rate than expansion of the primary motor cortex and cerebellum. This may reflect greater associations of motor programs in cortex, in order to construct more complex or skilled motor programs (Armstrong & Armstrong, 1980).
The human VL complex shows asymmetric function, with the left VL complex being involved in language function such as word repetition, naming, verbal memory, and speech articulation (Johnson and Ojemann, 2000), while the right VL complex show involvement in visual function such as perceptual matching (Vilkki, 1978). These associations mirror associations in function in the cortex. Specializations in cortical function may cause, or be caused by, asymmetric specialization of the VL thalamus.
The cerebellar, pallidial, and nigral circuits are anatomically independent in the VL (Percheron et al, 1996). The separation between pallidial and nigral pathways seems to be a specialization of the primate thalamus; it has not been found in rats nor cats. The nigral portion of the motor thalamus is increased in humans compared to what would be predicted from the great apes, and does not correspond to any known difference in the substantia nigra itself. This might be explained by connectivity to the frontal cortex or the amygdala (Percheron et al, 1996). Note also that only the pallidial circuit, and not the nigral circuit, is implicated in Parkinson's disease, a degenerative neurological disease found only in humans (Rosenbaum, 2006).
The cerebellar, pallidial, and nigral circuits are anatomically independent in the VL (Percheron et al, 1996). The separation between pallidial and nigral pathways seems to be a specialization to the primate thalamus; it has not been found in rats nor cats. There are also local circuit differences compared to rats and cats, including the presence of extremely small neurons ("microneurons") and connections between the input parts of neurons (dendro-dendritic connections) in the primate thalamus (Percheron et al, 1996).
Unknown, but it is notable that the increased number of neurons in human VL was similar to the increase in neuron number in the somatosensory (VL) sensory nucleus, but greater than those of the auditory (MGN) and visual (LGN) sensory nuclei, and less than those of the limbic and association nuclei.
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