Altered distribution of striatal activity-dependent synaptic plasticity in the 3-nitropropionic acid model of Huntington's disease

Decreased Striatal Dopamine Release Underlies Increased Expression of Long-Term Synaptic Potentiation at Corticostriatal Synapses 24 h after 3-Nitropropionic-Acid-Induced Chemical Hypoxia

“…Dalbem et al (2005) found multiple, high-dose systemic injections of 3-NP increased LTP at corticostriatal synapses for 48–60 hours in Wistar rats. By contrast, Picconi et al (2006) reported a 4-day cycle of multiple 3-NP injections did not change Mg 2+ -free saline-dependent LTP.…”

“…However, their use of Mg 2+ -free saline may have masked the 3-NP-mediated increase in corticostriatal LTP observed under normal Mg 2+ and Ca 2+ conditions (Fig. 1)(Dalbem et al, 2005). Our study also differed in using a single injection of 3-NP, that did not create striatal lesions, and we recorded from the less vulnerable dorsomedial striatum.…”

“…Dalbem et al (2005) reported systemic 3-NP caused a reduction in LTD of corticostriatal field potentials for 48–60 hours after a four-day regime of 3-NP injections. In this study, we examined the potential mechanisms underlying changes in corticostriatal function created by systemic 3-NP and discovered 3-NP created unique conditions for enhancing corticostriatal LTP expression produced by a change in dopamine modulation of corticostriatal synapses.…”

Alterations of corticostriatal plasticity by ammonium and rescue by green tea polyphenols

“…Corticostriatal LTP is induced by calcium entry via NMDA receptors (NMDAR) and requires co-activation of D1 dopamine receptors and M1 cholinoceptors, while LTD is initiated by calcium entry via Ltype calcium channels and requires co-activation of D2 dopamine receptors, group I metabotropic glutamate receptors (mGluR I) [14,19] and CB1 receptors for endocannabinoids [20]. Changes in the expression and direction of synaptic plasticity in a corticostriatal pathway were reported for pathological conditions modelling Parkinson's disease at different stages and L-DOPA-induced dyskinesia [21-23], Huntington's disease [24,25], and dystonia [26]. Impairment of corticostriatal synaptic plasticity was found to accompany alcoholism [27,28] and brain aging [29].…”

Forskolin Enhances Synaptic Transmission in Rat Dorsal Striatum through NMDA Receptors and PKA in Different Phases

“…LTP is evoked rather than long-term depression (LTD) or LTD expression is suppressed (Dalbem et al, 2005;Picconi et al, 2005). Our results may contribute to better understanding of the enhancement of synaptic transmission in the dorsal striatum and may provide an additional model for pathological studies of the striatal diseases.…”