Neuroscience
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The history of brain science is dominated by the study of neurons. However, there are as many glial cells as neurons in the human brain, their complexity increases during evolution, and glial cells play important roles in brain function, behavior, and neurological disorders. Although neurons and glial cells were first described at the same time in the early 19th century, why did the physiological study of glial cells only begin in the 1950s? What are the scientific breakthroughs and conceptual shifts that determined the history of glial cells in relation to that of neurons? What is the impact of the history of glia on the evolution of neuroscience? In order to answer these questions, we reconstructed the history of glial cells, from their first description until the mid-20th century, by examining the relative role of technical developments and scientific interpretations.
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For the past two decades, we have advanced in our understanding of the mechanisms implicated in the formation of brain circuits. The connection between the cortex and thalamus has deserved much attention, as thalamocortical connectivity is crucial for sensory processing and motor learning. ⋯ In this review, I will summarize the most relevant discoveries that have been made in this field, from development to early plasticity processes covering three major aspects: axon guidance, thalamic influence on sensory cortical specification, and the role of spontaneous thalamic activity. I will emphasize how the implementation of new tools has helped the field to progress and what I consider to be open questions and the perspective for the future.
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Ras homolog enriched in striatum (Rhes) is predominantly expressed in the corpus striatum. Rhes mRNA is localized in virtually all dopamine D1 and D2 receptor-bearing medium-sized spiny neurons (MSNs), and cholinergic interneurons of striatum. Early studies in rodents showed that Rhes is developmentally regulated by thyroid hormone, as well as by dopamine innervation in adult rat, monkey and human brains. ⋯ Accordingly, lack of Rhes attenuated such motor disturbances in 6-OHDA-lesioned Rhes knockout mice. In support of its role in MSN-dependent functions, several studies documented that mutant animals displayed alterations in striatum-related phenotypes reminiscent of psychiatric illness in humans, including deficits in prepulse inhibition of startle reflex and, most interestingly, a striking enhancement of behavioral responses elicited by caffeine, phencyclidine or amphetamine. Overall, these data suggest that Rhes modulates molecular and biochemical events underlying striatal functioning, both in physiological and pathological conditions.