1. Response dynamics of primary and secondary muscle spindle endings to small-amplitude sinusoidal stretches were found to be unaltered by tonic repetitive stimulation of fusistatic or fusidynamic fibers. 2. Overall sensitivity of these receptors is decreased by fusistatic stimulation and either unchanged, increased, or decreased by fusidynamic stimulation at rates of 75/s or greater. 3. In the case of primary endings, the results obtained with small-amplitude sinusoidal stretches are not compatible with the response of these receptors to large-amplitude ramp stretches. The difference is explained by dependence of receptor dynamics on stretch amplitude. Fusistatic stimulation tends to prevent those changes in dynamics, whereas fusidynamic stimulation tends to enhance them. 4. In the case of secondary endings, the results obtained with small- and large-amplitude stretches appear to be compatible with a linear model for this receptor (i.e., one with dynamics independent of input parameters). 5. By modulating the frequency of stimulation applied to fusimotor fibers and comparing the resulting afferent response to the receptor response to stretch dynamic characteristics of intrafusal muscle contraction can be deduced. The results suggest that the dynamics of fusiastatic and fusidynamic contraction are the same and, furthermore, that they are the same as those of extrafusal muscle. We note that the result is incompatible with measurements of the time course of twitch and tetanus development and suggest, therefore, that muscle dynamics are a function of contractile state.

Neural migration is regarded as a key step for cortical development and cortical lamination. While classical theory holds that immature neurons migrate to their destinations along radial glia, there is some preliminary evidence showing that vasculature is probably involved in that process as well. In this study, we compared vascular development with that of radial glia and the migration of neurons, so that the relationships among them could be elucidated. We found that the radial glial cells and vasculature were highly similar in their distribution and development. For instance, in the external granular layer (EGL, the putative molecular layer), the processes of radial glial cells were arranged in an orderly radial pattern, whereas in the deep areas of the cerebellum, their arrangements were in relative disorder. On the other hand, the vasculatures in EGL were usually orientated radially, which paralleled the projections of radial glia; however, the distribution of vasculature in the internal granular layer (IGL, the putative granular layer) and white matter was in relative disorder as well, similar to the pattern exhibited by radial glial processes. This high harmonization between vasculature and radial glia suggests their interconnected biological relationships during cerebellar development and neural migration. We also observed that a large number of newborn neurons were migrating along blood vessels, suggesting that the vasculature could serve as a scaffold for cell migration. In conclusion, cerebellar vasculature could guide neural migration not only as a platform for biological interaction with radial glia, but also serve scaffolding functions for neural migration.

This study involves the research progress in pathophysiological mechanism of dyskinesia in Parkinson's disease. Levodopa-induced dyskinesia is a complication characterized by involuntary movements in Parkinson's patients after long-term treatment with levodopa. Dyskinesia is a kind of abnormal movement involving the face, neck, arm, leg and axial muscles. It often occurs on the serious side of the disease. It may be manifested as variety of phenomenologies, such as choreiform, dystonia, ballism, myoclonus and other forms of abnormal movements can manifest as well. At present, the research on the mechanisms of levodopa-induced dyskinesia is not yet fully understood. Nigrostriatal degeneration and levodopa administration are considered to be the basis of levodopa-induced dyskinesia. There appears to be variety mechanisms involved, such as abnormal dopaminergic transmission in presynaptic and postsynaptic membrane as well as non-dopaminergic systems. Nigrostriatal degeneration is considered to be the basis and premise of levodopa-induced dyskinesia. With the deepening of the research, non-dopaminergic systems such as glutamate, serotonin, adenosine, cholinergic and epinephrine have been proved to be involved in the occurrence of dyskinesia in animal models and clinical studies. This article is a more detailed review of the possible pathophysiological mechanisms of levodopa-induced dyskinesia, especially non-dopaminergic systems.