Ebf Activates Expression of a Cholinergic Locus in a Multipolar Motor Ganglion Interneuron Subtype in Ciona

Conserved transcription factors termed “terminal selectors” regulate neuronal sub-type specification and differentiation through combinatorial transcriptional regulation of terminal differentiation genes. The unique combinations of terminal differentiation gene products in turn contribute to the functional identities of each neuron. One well-characterized terminal selector is COE (Collier/Olf/Ebf), which has been shown to activate cholinergic gene batteries in C. elegans motor neurons. However, its functions in other metazoans, particularly chordates, is less clear. Here we show that the sole COE ortholog in the non-vertebrate chordate Ciona robusta, Ebf, controls the expression of the cholinergic locus VAChT/ChAT in a single dorsal interneuron of the larval Motor Ganglion, which is presumed to be homologous to the vertebrate spinal cord. We propose that, while the function of Ebf as a regulator of cholinergic neuron identity conserved across bilaterians, its exact role may have diverged in different cholinergic neuron subtypes (e.g., interneurons vs. motor neurons) in chordate-specific motor circuits.

Cholinergic stimulation improves electrophysiological rate adaptation during pressure overload-induced heart failure in rats

Analysis of electrophysiology from optical mapping of failing left ventricular myocardium provided insight into the possible therapeutic outcomes of cholinergic stimulation within the left ventricle. Chronic hypothalamic oxytocin neuron activation for downstream cardiac cholinergic neuron stimulation blunted onset of failing electrophysiology induced by pressure overload-induced heart failure in rats.

From Neuroinflammation to Neuroprotection: Focus on Potential New Therapeutic Targets in Cognitive Impairment

Neurodegeneration is closely linked to neuroinflammation. It is often associated with oxidative stress and meaningful changes in cell energy metabolism. Neuroinflammation is due to non-neuronal cell activation (microglia, astrocytes, mast cells) activation and proliferation. Also, it is associated with pro-inflammatory substances release, able to modify synaptic plasticity. Microglia and astrocytes activation lead to toxic agent’s release (reactive oxygen species, inflammatory cytokines); however, the final target of this process is the cholinergic neuron. A number of substances can promote neuroprotection; recent scientific evidence focuses on the role of sirtuins. In particular, SIRT1 is activated by caloric restriction, NAD biosynthesis and different activators, called STACs (Sirtuin Activating Compounds). Citicoline is one of the most powerful STACs. It has been widely shown to possess neuroprotective action, and lots of studies strengthened its possible role.