Regulation of gene transcription by neuronal activity

<p><strong>Background</strong></p> <p>Synaptic activity can trigger gene expression programs that are required for the stable change of neuronal properties, a process that is essential for learning and memory. Currently, it is still unclear how the stimulation of dendritic synapses can be coupled to transcription in the nucleus in a timely way given that large distances can separate these two cellular compartments. Although several mechanisms have been proposed to explain long distance communication between synapses and the nucleus, the possible co-existence of these models and their relevance in physiological conditions remain elusive. In a review published on <em><strong>F1000Research</strong></em>, I provide a critical overview of the suggested mechanisms for coupling synaptic stimulation to transcription, the underlying assumptions behind them and their plausible physiological significance.</p> <p><strong>Image description</strong></p> <p>Confocal image of a mouse piriform cortex section stained with P-ERK1/2 antibodies. A 16 pseudo-color palette highlights the intensity of P-ERK1/2 fluorescence (blue is low; red is high). High P-ERK1/2 immunoreactivity is present in the nucleus of neurons in response to synaptic activity. Nuclear P-ERK1/2 participates in the regulation of gene transcription.</p

Differential nuclear architecture of striatal neuron populations

<p><strong>Background:</strong></p> <p>The striatum is composed by five different neuronal populations of which the MSNs constitute the major cell type (~95%). The remaining ~5% of the striatal neurons comprise aspiny interneurons, which have been classified on the basis of their morphology, protein content and electrophysiological properties as large cholinergic interneurons and somatostatin-, parvalbumin- and calretinin-expressing GABAergic interneurons. In addition to these discriminative features, we showed that nuclear morphology is also particular for each striatal cell type (Matamales/Bertran-Gonzalez et al., 2009). Indeed, the characteristic nuclear architecture of striatal populations is evident on DNA staining with TO-PRO-3, which reveals differences regarding the nuclear diameter, the nuclear shape and the pattern of heterochromatin distribution. Thus, nuclear staining with TO-PRO-3 provides a simple means for the identification of MSNs in the absence of other markers. In addition, the other striatal neurons also have distinct nuclear staining patterns, which allow a good prediction of their nature. This method may be useful to identify striatal neurons in tissue sections and potentially in living tissue, using vital DNA fluorescent dyes. With this simple method we carefully quantified striatal neuronal populations and we clearly showed that all MSNs express either D1R or D2R or both. It will be worth to test whether nuclear architecture in striatal neurons is linked to differences in rates of transcriptional activity. In addition, it will be interesting to analyze whether a correlation between the organization of the nucleus of striatal neurons and their characteristic neuronal activity exists.</p> <p> </p> <p><strong>Figure Legend: </strong></p> <p>(A-E) Schematic view of striatal neurons nuclear morphology: (A), MSNs; (B), Parvalbumin interneurons; (C), Calretinin interneurons; (D), Somatostatin interneurons; (E), Cholinergic interneurons. The three different features that allow the identification of striatal neuronal populations based on their nuclear architecture are represented: blue line designates nuclear shape; dashed green line and numbers indicate average nuclear diameter (μm); red dots are DNA chromocenters; red line represents heterochromatin rim. For details, see Matamales/Bertran-Gonzalez et al., 2009.</p

Code for Manuscript "Adaptation of sequential action benefits from timing variability related to lateral basal ganglia circuitry"

Code used to generate and visualise the data for manuscript "Adaptation of sequential action benefits from timing variability related to lateral basal ganglia circuitry".</p