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This review deals with recent studies on the lungs of fossil and extant coelacanths with classical techniques (dissections, photonic histology) and modern techniques (SEM, X-ray tomography). This recent knowledge allows to attest the homology between: i) the large bony plates of the calcified organ of extinct coelacanths and the small plates that surround the lung of the extant coelacanth Latimeria; ii) the (supposed functional) lung covered with bony plates of extinct coelacanths and the vestigial (non-functional) lung of the extant coelacanth Latimeria. These results point the fatty organ of Latimeria as probably a mesenteric specialization, questioning its previous attribution to its pulmonary origin.

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Three subtypes of vesicular transporters accumulate glutamate into synaptic vesicles to promote its vesicular release. One of the subtypes, VGLUT3, is expressed in neurons, including cholinergic striatal interneurons, that are known to release other classical transmitters. Here we showed that disruption of the Slc17a8 gene (also known as Vglut3) caused an unexpected hypocholinergic striatal phenotype. Vglut3–/– mice were more responsive to cocaine and less prone to haloperidol-induced catalepsy than wild-type littermates, and acetylcholine release was decreased in striatum slices lacking VGLUT3. These phenotypes were associated with a colocalization of VGLUT3 and the vesicular acetylcholine transporter (VAChT) in striatal synaptic vesicles and the loss of a synergistic effect of glutamate on vesicular acetylcholine uptake. We propose that this vesicular synergy between two transmitters is the result of the unbalanced bioenergetics of VAChT, which requires anion co-entry for continuing vesicular filling. Our study reveals a previously unknown effect of glutamate on cholinergic synapses with potential functional and pharmacological implications.