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. 1. Striatum: An Overview The striatum plays a vital role in the coordination of movement (primary motor control), emotions, and cognition [1–3]. In humans, the striatum is divided into two nuclei, the caudate and the putamen, by the internal capsule, whereas in mice it is one structure. This is shown in Figure 1. The complexity and importance of the striatum is best highlighted when it is impaired. There are a number of diseases that may produce striatal damage, including acquired conditions such as a stroke and genetically inherited conditions such as Huntington’s disease (HD). HD is a condition that is characterised by neuronal dysfunction and neuronal loss that principally affects the medium spiny neurons (MSNs) of the striatum. MSNs are the major projection neuron and constitute the vast majority of neurons in this structure. HD results in progressive deterioration of movement and cognition and, in many cases, additional behavioural deficits over a period of 15–30 years, and eventually renders an individual unable to care for themselves. To date there is little in the way of symptomatic treatment and no disease-modifying agents available. A better understanding of striatal development is likely to accelerate our understanding of the pathogenic processes
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