Glutamate Controls Growth Rate and Branching of Dopaminergic Axons

• DOI: 10.1523/jneurosci.2927-09.2009
• Publication Date: 2009-09-23T17:30:28Z
• Authors: Yvonne Schmitz; James Luccarelli; Minji Kim; Mi Wang; David Sulzer
• Keywords: Kainate receptor; Long-term depression

Dopamine-releasing neurons of the substantia nigra pars compacta produce an extraordinarily dense and expansive plexus innervation in striatum converging with glutamatergic corticostriatal thalamostriatal axon terminals at dendritic spines medium spiny neurons. Here, we investigated whether signaling promotes arborization growth dopaminergic axons. In postnatal ventral midbrain cultures, axons rapidly responded to glutamate stimulation accelerated cone splitting when NMDA AMPA/kainate receptors were activated. contrast, selectively activated, rate was decreased. To address this switch axonal response mediated by distinct calcium signals, used imaging. Combined receptor activation elicited signals cones that influx through L-type voltage-gated channels ryanodine receptor-induced release from intracellular stores. alone solely attributable channels. We found inhibitors calcium/calmodulin-dependent protein kinases prevented receptor-dependent acceleration, whereas AMPA/kainate-induced decrease blocked calcineurin increased cAMP levels. Our data suggest balance between regulates pattern dopamine competing calcium-dependent pathways. Understanding mechanisms is essential development treatments aim restore Parkinson's disease.