Abstract
Salt, commonly known as sodium chloride, is an important ingredient that the body requires in relatively minute quantities. However, consuming too much salt can lead to high blood pressure, heart disease and even disruption of circadian rhythms. The biological process of the circadian rhythm was first studied in Drosophila melanogaster and is well understood. Their locomotor activity gradually increases before the light is switched on and off, a phenomenon called anticipation. In a previous study, we showed that a high-salt diet (HSD) impairs morning anticipation behavior in Drosophila. Here, we found that HSD did not significantly disrupt clock gene oscillation in the heads of flies, nor did it disrupt PERIOD protein oscillation in clock neurons or peripheral tissues. Remarkably, we found that HSD impairs neuronal plasticity in the axonal projections of circadian pacemaker neurons. Interestingly, we showed that increased excitability in PDF neurons mimics HSD, which causes morning anticipation impairment. Moreover, we found that HSD significantly disrupts neurotransmitter-related biological processes in the brain. Taken together, our data show that an HSD affects the multiple functions of neurons and impairs physiological behaviors.
Highlights
Valentini Konstantinidou and Sodium is an essential nutrient that contributes to many physiological processes, including the transmission of nerve impulses and normal cellular function [1]
To test whether an high-salt diet (HSD) affects the expression of core clock genes and contributes to the impairment of morning anticipation, we examined the expression of the clock genes clk, per, tim, vri, pdp1 and cwo in an HSD and in control fly heads with samples taken at ZT 1, 5, 9, 13, 17
The results show that an HSD alters the state of gene expression in the brain at a global level, and severely affects the normal function of neurons, especially biological processes related to neurotransmitters
Summary
Valentini Konstantinidou and Sodium is an essential nutrient that contributes to many physiological processes, including the transmission of nerve impulses and normal cellular function [1]. The amplitudes of circadian clock gene expression were found to be decreased in the heart, liver, and kidney of Dahl salt-sensitive rats fed HSD compared to a group fed a normal salt diet [14]. The circadian rhythm of plasma sodium could be disrupted in spontaneously hypertensive rats fed HSD [15]. This suggests that HSD disrupts the circadian clock and this could be a good way to study the effects of HSD on the neuron function. In the second feedback loop, CLK/CYC directly activates the transcription of vri and pdp1 Another level of regulation is provided by the core clock gene clockwork orange (cwo). We found that an HSD impairs morning anticipation in Drosophila by regulating the plasticity of pacemaker neurons. We found that an HSD significantly inhibits the biological processes of neurotransmitter levels and their secretion or transport, and even inhibits the regulation of axonogenesis
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