TY - CHAP
T1 - Regulation of Corticostriatal Synaptic Plasticity in Physiological and Pathological Conditions
AU - Di Filippo, M.
AU - Calabresi, P.
PY - 2017
Y1 - 2017
N2 - In this chapter we describe the basic characteristics of corticostriatal synaptic plasticity in both physiological and pathological conditions. In particular, we analyze the general features of the most important forms of activity-dependent plasticity of striatal glutamatergic transmission such as long-term depression (LTD), long-term potentiation (LTP), and depotentiation (reversal of previously induced LTP) in medium spiny projection neurons. We also report on the role of distinct ionotropic and metabotropic glutamate receptors as well as the modulatory function of dopaminergic, cholinergic, and endocannabinoid systems in the expression of these forms of striatal plasticity. Moreover, we describe some forms of synaptic plasticity induced by repetitive glutamatergic stimulation in striatal interneurons. Finally, we analyze the alterations of synaptic plasticity in toxic and genetic models of the most important neurological disorders involving the striatum such as Parkinson's disease, L-DOPA-induced dyskinesia, Huntington's disease, dystonia, and brain ischemia.
AB - In this chapter we describe the basic characteristics of corticostriatal synaptic plasticity in both physiological and pathological conditions. In particular, we analyze the general features of the most important forms of activity-dependent plasticity of striatal glutamatergic transmission such as long-term depression (LTD), long-term potentiation (LTP), and depotentiation (reversal of previously induced LTP) in medium spiny projection neurons. We also report on the role of distinct ionotropic and metabotropic glutamate receptors as well as the modulatory function of dopaminergic, cholinergic, and endocannabinoid systems in the expression of these forms of striatal plasticity. Moreover, we describe some forms of synaptic plasticity induced by repetitive glutamatergic stimulation in striatal interneurons. Finally, we analyze the alterations of synaptic plasticity in toxic and genetic models of the most important neurological disorders involving the striatum such as Parkinson's disease, L-DOPA-induced dyskinesia, Huntington's disease, dystonia, and brain ischemia.
KW - corticostriatal
KW - dopamine
KW - long-term depression
KW - Long-term potentiation
KW - Parkinson's disease
KW - striatum
KW - synaptic plasticity
UR - http://www.scopus.com/inward/record.url?scp=84999027740&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84999027740&partnerID=8YFLogxK
U2 - 10.1016/B978-0-12-802206-1.00023-4
DO - 10.1016/B978-0-12-802206-1.00023-4
M3 - Chapter
VL - 24
T3 - Handbook of Behavioral Neuroscience
SP - 459
EP - 476
BT - Handbook of Behavioral Neuroscience
PB - Elsevier B.V.
ER -