Topic: dopamine transmission

Deficits in reward processing are a characteristic symptomatic dimension of psychiatric diseases such as major depression, bipolar disorder and schizophrenia. These deficits have been linked to the dysfunction of the mesocorticolimbic dopamine transmission suggesting the existence of common underlying pathophysiological mechanisms. Numerous clinical studies have described a decrease in n-3 polyunsaturated fatty acids (PUFAs) in subpopulations of patients suffering from psychiatric disorders (Conklin et al., 2010; Messamore and McNamara, 2016). Moreover, preclinical results from our laboratory

Dopamine transmission is involved in reward processing and motor control, and its impairment plays a central role in numerous neurological disorders. Despite its strong pathophysiological relevance, the molecular and structural organization of the dopaminergic synapse remains to be established. We used targeted labeling and fluorescence-activated sorting to purify striatal dopaminergic synaptosomes. Our data reveal the adhesion of dopaminergic varicosities to glutamatergic, GABAergic, or cholinergic synapses in tripartite structures we named “dopamine hub synapses.” We provide the proteome of

We previously reported that pregestational chronic unpredictable stress (CUS) and prenatal treatment with the antidepressant mirtazapine alter offspring anxiety and spatial memory (Viñas-Noguera et al. PLoS One 17: e0255546, 2022). The present study was designed to investigate the potential involvement of dopamine transmission in these behavioral changes. Maternal CUS and mirtazapine were administered as previously described. Adult offspring were anesthetized with chloral hydrate and electrodes were placed in the ventral tegmental area. Dopamine neurons were detected and recorded. We found no