raw data for Plasticity, genetics and epigenetics in dystonia: An update

<p>Legend of &nbsp;Fig. 13.2.&nbsp;Striatal ACh/DA interactions in dystonia. (A) Schematic representation of simplified striatal circuit showing the inter- actions between ACh, released by cholinergic interneurons (ChI,&nbsp;blue), and dopamine (DA), released by dopaminergic terminals (green). DA, by acting on D2 receptors inhibits firing activity of interneurons and ACh release at synaptic terminals. Released ACh, activates muscarinic M1 receptors on SPNs, exerting a modulatory effect over bidirectional synaptic plasticity at corticostriatal synapses (inset). Moreover, ACh activates also the nicotinic receptors (nACh) on DA terminals that promote DA release. (B) In DYT1 dystonia animal model, stimulation of D2 receptors induces an abnormal excitatory response that causes an anomalous ACh release at SPNs synaptic terminals. Higher level of ACh disrupts the normal activity of M1 muscarinic receptors resulting in turn to abnormal bidirectional synaptic plasticity at corticostriatal synapses (inset).</p>