391 research outputs found
Moral Courage in Organizations: Doing the Right Thing at Work by Debra R. Comer and Gina Vega (Eds.)
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A Direct Projection from Mouse Primary Visual Cortex to Dorsomedial Striatum
The mammalian striatum receives inputs from many cortical areas, but the existence of a direct axonal projection from the primary visual cortex (V1) is controversial. In this study we use anterograde and retrograde tracing techniques to demonstrate that V1 directly innervates a topographically defined longitudinal strip of dorsomedial striatum in mice. We find that this projection forms functional excitatory synapses with direct and indirect pathway striatal projection neurons (SPNs) and engages feed-forward inhibition onto these cells. Importantly, stimulation of V1 afferents is sufficient to evoke phasic firing in SPNs. These findings therefore identify a striatal region that is functionally innervated by V1 and suggest that early visual processing may play an important role in striatal-based behaviors
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Dopaminergic neurons inhibit striatal output via non-canonical release of GABA
The substantia nigra pars compacta (SNc) and ventral tegmental area (VTA) contain the two largest populations of dopamine (DA)-releasing neurons in the mammalian brain. These neurons extend elaborate projections in striatum, a large subcortical structure implicated in motor planning and reward-based learning. Phasic activation of dopaminergic neurons in response to salient or reward-predicting stimuli is thought to modulate striatal output via the release of DA to promote and reinforce motor action1–4. Here we show that activation of DA neurons in striatal slices rapidly inhibits action potential firing in both direct-and indirect-pathway striatal projection neurons (SPNs) through vesicular release of the inhibitory transmitter γ-aminobutyric acid (GABA). GABA is released directly from dopaminergic axons but in a manner that is independent of the vesicular GABA transporter VGAT. Instead GABA release requires activity of the vesicular monoamine transporter VMAT2, which is the vesicular transporter for DA. Furthermore, VMAT2 expression in GABAergic neurons lacking VGAT is sufficient to sustain GABA release. Thus, these findings expand the repertoire of synaptic mechanisms employed by DA neurons to influence basal ganglia circuits, reveal a novel substrate whose transport is dependent on VMAT2, and demonstrate that GABA can function as a bona fide co-transmitter in monoaminergic neurons
Evaluating Success Factors and Challenges Among Small-Scale Agricultural Producers: A Texas Case Study
Literature on small farms in the U.S. is limited though they are the most numerous farm type, generate over twenty percent of agricultural production, and are more likely to be operated by historically underserved (i.e., beginning, minority, veteran, women, young) farmers than large-scale farms. This article details an online survey study of small-scale agricultural producers using a purposive sample from Texas. We used cross tabulations to evaluate qualitative operational and demographic (e.g., age, gender) factors of success, finding several significant variables with moderate effect sizes. Generally, producers regarded quality of life as more important to success than profitability. Producers’ top challenges were capital, production, marketing, legal, financial, informational, and social, in that order. While results may not be representative of all small producers, in Texas or otherwise, they provide an important look at an understudied population who contribute meaningfully to sustainable production, local and regional food systems, and overall agricultural structure
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Midbrain dopamine neurons sustain inhibitory transmission using plasma membrane uptake of GABA, not synthesis
Synaptic transmission between midbrain dopamine neurons and target neurons in the striatum is essential for the selection and reinforcement of movements. Recent evidence indicates that nigrostriatal dopamine neurons inhibit striatal projection neurons by releasing a neurotransmitter that activates GABAA receptors. Here, we demonstrate that this phenomenon extends to mesolimbic afferents, and confirm that the released neurotransmitter is GABA. However, the GABA synthetic enzymes GAD65 and GAD67 are not detected in midbrain dopamine neurons. Instead, these cells express the membrane GABA transporters mGAT1 (Slc6a1) and mGAT4 (Slc6a11) and inhibition of these transporters prevents GABA co-release. These findings therefore indicate that GABA co-release is a general feature of midbrain dopaminergic neurons that relies on GABA uptake from the extracellular milieu as opposed to de novo synthesis. This atypical mechanism may confer dopaminergic neurons the flexibility to differentially control GABAergic transmission in a target-dependent manner across their extensive axonal arbors. DOI: http://dx.doi.org/10.7554/eLife.01936.00
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