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Review
. 2007 Sep 12;27(37):9824-5.
doi: 10.1523/JNEUROSCI.2938-07.2007.

A molecular switch for induction of long-term depression of corticostriatal transmission

Mazen A Kheirbek  1
Affiliations
Review

A molecular switch for induction of long-term depression of corticostriatal transmission

Mazen A Kheirbek. J Neurosci. .
No abstract available

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Figures

Figure 1.
Figure 1.
Signaling pathways involved in corticostriatal HFS-LTD and FPL-LTD. A, High-frequency stimulation of cortical afferents with coincident depolarization of the postsynaptic membrane to 0 mV is required for induction of HFS-LTD. In addition, there is a dependence on D2 receptors, either on the MSN itself, promoting retrograde endocannabinoid (ECN) release, or on acetylcholine (ACH)-positive interneurons by reducing ACH tone, thus reducing the M1 muscarinic receptor-mediated inhibition of Cav1.3 channels (Wang et al., 2006; Kreitzer and Malenka, 2007). Influx of calcium through voltage-gated Cav1.3 type channels or by release from intracellular stores by an mGluR-dependent inositol triphosphate mechanism can also promote the retrograde release of ECNs. Activation of presynaptic CB1 receptor induces a depression in glutamate release. B, In FPL-LTD, strong activation of Cav1.3 channels can induce large increases in intracellular calcium, bypassing dopamine- and mGluR-dependent mechanisms, promoting the retrograde release of ECNs and depression of glutamate release. DA, Dopamine; AMPA-R, AMPA receptor; ECB, endocannabinoid.
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