This study describes the extrinsic connections of the dorsal telencephalon (pallium) of gymnotiform fish. We show that the afferents to the dorsolateral and dorsomedial pallial subdivisions of gymnotiform fish arise from the preglomerular complex. The preglomerular complex receives input from four clearly distinct regions: (1) descending input from the pallium itself (dorsomedial and dorsocentral subdivisions and nucleus taenia); (2) other diencephalic nuclei (centroposterior, glomerular, and anterior tuberal nuclei and nucleus of the posterior tuberculum); (3) mesencephalic sensory structures (optic tectum, dorsal and ventral torus semicircularis); and (4) basal forebrain, preoptic area, and hypothalamic nuclei. Previous studies have implicated the majority of the diencephalic and mesencephalic nuclei in electrosensory, visual, and acousticolateral functions. Here we discuss the implications of preglomerular/pallial electrosensory-associated afferents with respect to a major functional dichotomy of the electric sense. The results allow us to hypothesize that a functional distinction between electrocommunication vs. electrolocation is maintained within the input and output pathways of the gymnotiform pallium. Electrocommunication information is conveyed to the pallium through complex indirect pathways that originate in the nucleus electrosensorius, whereas electrolocation processing follows a conservative pathway inherent to all vertebrates, through the optic tectum. We hypothesize that cells responsive to communication signals do not converge onto the same targets in the preglomerular complex as cells responsive to moving objects. We also hypothesize that efferents from the dorsocentral (DC) telencephalon project to the dorsal torus semicircularis to regulate processing of electrocommunication signals, whereas DC efferents to the tectum modulate sensory control of movement.

Mature messenger RNAs (mRNAs) consist of coding sequence (CDS) and 5' and 3' UTRs, typically expected to show similar abundance within a given neuron. Examining mRNA from defined neurons, we unexpectedly show extremely common unbalanced expression of cognate 3' UTR and CDS sequences; many genes show high 3' UTR relative to CDS, others show high CDS to 3' UTR. In situ hybridization (19 of 19 genes) shows a broad range of 3' UTR-to-CDS expression ratios across neurons and tissues. Ratios may be spatially graded or change with developmental age but are consistent across animals. Further, for two genes examined, a 3' UTR-to-CDS ratio above a particular threshold in any given neuron correlated with reduced or undetectable protein expression. Our findings raise questions about the role of isolated 3' UTR sequences in regulation of protein expression and highlight the importance of separately examining 3' UTR and CDS sequences in gene expression analyses.

In Parkinson's disease (PD), L-DOPA therapy leads to the emergence of motor complications including L-DOPA-induced dyskinesia (LID). LID relies on a sequence of pre-and postsynaptic neuronal events, leading to abnormal corticostriatal neurotransmission and maladaptive changes in striatal projection neurons. In recent years, additional non-neuronal mechanisms have been proposed to contribute to LID. Among these mechanisms, considerable attention has been focused on L-DOPA-induced inflammatory responses. Microglia and astrocytes are the main actors in neuroinflammatory responses, and their double role at the interface between immune and neurophysiological responses is starting to be elucidated. Both microglia and astrocytes express a multitude of neurotransmitter receptors and via the release of several soluble molecules modulate synaptic function in neuronal networks. Here we review preclinical and clinical evidence of glial overactivation by L-DOPA, supporting a role of microglia and astrocytes in the development of LID. We propose that in PD, chronically and abnormally activated microglia and astrocytes lead to an aberrant neuron-glia communication, which affect synaptic activity and neuroplasticity contributing to the development of LID.

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