Molecular Regulation of Striatal Development: A Review

Abstract

The central nervous system is composed of the brain and the spinal cord. The brain is a complex organ that processes and coordinates activities of the body in bilaterian, higher-order animals. The development of the brain mirrors its complex function as it requires intricate genetic signalling at specific times, and deviations from this can lead to brain malformations such as anencephaly. Research into how the CNS is specified and patterned has been studied extensively in chick, fish, frog, and mice, but findings from the latter will be emphasised here as higher-order mammals show most similarity to the human brain. Specifically, we will focus on the embryonic development of an important forebrain structure, the striatum (also known as the dorsal striatum or neostriatum). Over the past decade, research on striatal development in mice has led to an influx of new information about the genes involved, but the precise orchestration between the genes, signalling molecules, and transcription factors remains unanswered. We aim to summarise what is known to date about the tightly controlled network of interacting genes that control striatal development. This paper will discuss early telencephalon patterning and dorsal ventral patterning with specific reference to the genes involved in striatal development.

Vessel maturation schedule determines vulnerability to neuronal injuries of prematurity

“…Likewise, differences in gestational out-migrating timing of periventricular-born neurons as well as differences in their periventricular subregions of origin are likely to determine which neuronal subset will be affected. For example, because the murine GE is essential for proper development of all telencephalic structures, it was not surprising that neuronal apoptosis in subpallial regions inflicted by vascular loss at E13.5 culminated in severe reduction of the striatum known to develop from these neurons (32). In human PVL, on the other hand, more lesions in the thalamus and fewer in the striatum are the common feature (33).…”

Transplantation in HD: Are We Transplanting the Right Cells?

“…However, studies of rodent-torodent grafts show similar behavioural improvement in both LGE-and WGE-derived grafts, although the overall striatal graft volumes and mean numbers of striatal-like neurons were greater in the WGE-derived grafts. Thus, contrary to expectation, it is suggested that the presence of interneurons from the MGE may facilitate graft survival and integration, thus favouring a WGE-derived cell population for transplantation [29][30][31]. Studies of human foetal brain samples show DARPP-32-positive MSNs beginning to appear in the LGE from 7-weeks postconception with the number increasing over the following 2 weeks [32,33], but to date there have been no systematic studies using human foetal donor tissue in animal models to address the issue of 'optimal dissection', largely due to the scarcity of tissue.…”

Melatonin Reduces Projection Neuronal Injury Induced by 3-Nitropropionic Acid in the Rat Striatum

“…Meanwhile, the striatum is one of the vulnerable areas of the brain in a pathological state. Studies have confirmed that a number of diseases may produce striatal damage as well as abnormal behavior related to the function of the striatum, including acquired conditions such as a stroke [29] and genetically inherited conditions such as PD and HD [30,31]. As a model of HD, our previous data are in agreement with several other studies, since our 3NP injections caused motor impairments on balance beam and grip strength, as well as cognitive impairments in the Morris water maze.…”