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Abstract Biomass and composition of the phytoplankton community were investigated in the deep-water Gulf of Mexico (GoM) at the edges of Loop Current anticyclonic eddies during May 2017 and May 2018. Using flow cytometry, high-performance liquid chromatography pigments and microscopy, we found euphotic zone integrated chlorophyll a of ~10 mg m−2 and autotrophic carbon ranging from 463 to 1268 mg m−2, dominated by picoplankton (<2 μm cells). Phytoplankton assemblages were similar to the mean composition at the Bermuda Atlantic Time-series Study site, but differed from the Hawaii Ocean Times-series site. GoM phytoplankton biomass was ~2-fold higher at the deep chlorophyll maximum (DCM) relative to the mixed layer (ML). Prochlorococcus and prymnesiophytes were the dominant taxa throughout the euphotic zone; however, other eukaryotic taxa had significant biomass in the DCM. Shallower DCMs were correlated with more prymnesiophytes and prasinophytes (Type 3) and reduced Prochlorococcus. These trends in ML and DCM taxonomic composition likely reflect relative nutrient supply—with ML populations relying on remineralized ammonium as a nitrogen source, and the taxonomically diverse DCM populations using more nitrate. These spatially separated phytoplankton communities represent different pathways for primary production, with a dominance of picoplankton in the ML and more nano- and microplankton at the DCM. 

There is an ongoing debate on the contribution of the neuronal glutamate transporter EAAC1 to the onset of compulsive behaviors. Here, we used behavioral, electrophysiological, molecular, and viral approaches in male and female mice to identify the molecular and cellular mechanisms by which EAAC1 controls the execution of repeated motor behaviors. Our findings show that, in the striatum, a brain region implicated with movement execution, EAAC1 limits group I metabotropic glutamate receptor (mGluRI) activation, facilitates D1 dopamine receptor (D1R) expression, and ensures long-term synaptic plasticity. Blocking mGluRI in slices from mice lacking EAAC1 restores D1R expression and synaptic plasticity. Conversely, activation of intracellular signaling pathways coupled to mGluRI in D1R-containing striatal neurons of mice expressing EAAC1 leads to reduced D1R protein level and increased stereotyped movement execution. These findings identify new molecular mechanisms by which EAAC1 can shape glutamatergic and dopaminergic signals and control repeated movement execution.