Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we will assume that you are happy to receive all cookies and you will not see this message again. Click 'Find out more' for information on how to change your cookie settings.

<jats:title>Abstract</jats:title><jats:p>Ca<jats:sup>2+</jats:sup> entry to nigrostriatal dopamine (DA) neurons and axons via L-type voltage-gated Ca<jats:sup>2+</jats:sup> channels (LTCCs) contributes to pacemaker activity and DA release, but burdens cells with a metabolic stress promoting their vulnerability to parkinsonian degeneration. The level of LTCC function varies between subtypes of DA neurons, but is not proportional to LTCC expression level, indicating that LTCC function is governed by other factors. We used fast-scan cyclic voltammetry in mouse brain slices to identify mechanisms that govern whether LTCCs contribute to DA release in dorsal and ventral striatum. We find that calbindin-D28K limits LTCC function in a regionally and sexually divergent manner; D2-receptors and DA transporters are negative and positive regulators respectively; and lastly, that targeting α<jats:sub>2</jats:sub>δ subunits with gabapentinoid drugs restricts LTCC function without compromising DA release. These data reveal that LTCC function in DA axons is dynamically and locally regulated, which may prove useful for future neuroprotective strategies.</jats:p>

Original publication




Journal article


Cold Spring Harbor Laboratory

Publication Date