Striatal plasticity and basal ganglia circuit function

By A. Kreitzer, R. Malenka. 2008

992 citations recorded by the source corpus.

The dorsal striatum, which consists of the caudate and putamen, is the gateway to the basal ganglia. It receives convergent excitatory afferents from cortex and thalamus and forms the origin of the direct and indirect pathways—distinct basal ganglia circuits involved in motor control. It is also a major site of activity-dependent synaptic plasticity. Striatal plasticity alters the transfer of information throughout basal ganglia circuits and may represent a key neural substrate for adaptive motor control and procedural memory. Here, we review current understanding of synaptic plasticity in the striatum and its role in the physiology and pathophysiology of basal ganglia function.

Subfields: Cellular and Molecular Neuroscience, Neurology

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Citations in the corpus

Coordinated and Compartmentalized Neuromodulation Shapes Sensory Processing in Drosophila (2015, positive): “…for example, different temporal patterns of dopamine release are thought to select the relevant circuit configurations that control inherently motivated behaviors as well as reinforcement learning (Graybiel et al., 1994; Grillner et al., 2005; Kreitzer and Malenka, 2008; Yin and Knowlton, 2006).”
Amygdala inhibitory circuits and the control of fear memory. (2009, background): “In the striatum, a network of GABAergic projection neurons with local axon collaterals, in concert with distinct subgroups of local, inhibitory interneurons generates activity patterns that shape basal ganglia output and motor control (Kreitzer and Malenka, 2008; Tepper and Bolam, 2004).”
Distinct coincidence detectors govern the corticostriatal spike timing‐dependent plasticity (2010, background): “The dopaminergic control on corticostriatal plasticity induced by either HFS or MFS has been established, but the effects remain debated (reviewed in Kreitzer & Malenka, 2008; Kano et al. 2009).”
Convergent evidence for abnormal striatal synaptic plasticity in dystonia (2009, neutral): “…2001; Bar-Gad et al., 2003; Barnes et al., 2005; Berns and Sejnowski, 1998; Frank et al., 2004; Graybiel, 2008; Horvitz, 2009; Krebs et al., 2001; Kreitzer and Malenka, 2008; Messier et al., 2007; Packard and Knowlton, 2002; Pisani et al., 2005; Williams and Eskandar, 2006; Yin and Knowlton,…”
Backpropamine: training self-modifying neural networks with differentiable neuromodulated plasticity (2018, background): “…neuromodulation of plasticity, which involves several chemicals (particularly dopamine; Calabresi et al. 2007; He et al. 2015; Li et al. 2003; Yagishita et al. 2014), plays an important role in learning and adaptation (Molina-Luna et al., 2009; Smith-Roe & Kelley, 2000; Kreitzer & Malenka, 2008).”
Absence of CNTNAP2 leads to epilepsy, neuronal migration abnormalities and core autism-related deficits (2011, positive): “At the neuronal level, the ultimate firing output to the direct and indirect pathways is determined by excitatory inputs from cortex and thalamus and inhibitory inputs from local interneurons within the striatum (Kreitzer and Malenka, 2008).”
Drug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling (2011, background): “In the dorsal striatum, there is growing evidence that these two subpopulations of MSNs exhibit different physiological and synaptic properties, including different forms of synaptic plasticity (Kreitzer and Malenka, 2008; Shen et al., 2008).”