Topic: Caenorhabditis elegans

Locomotor behaviors are composed of ordered transitions between motor states required to produce a functional outcome. However, the circuit mechanisms by which the brain generates a sequential ordering of motor actions for constructive behavioral output, particularly in freely-behaving animals, is largely unknown. With 302 neurons within a well-defined connectome and a library of genetic tools, complex yet discernible behaviors, and recent advances in brain-wide imaging, the nematode Caenorhabditis elegans offers a unique opportunity to study how the brain generates behavior. To better underst

Achyrocline satureoides aqueous extract (ASAE) protective effects were evaluated on dopaminergic neurodegeneration induced by reserpine in Caenorhabditis elegans (C. elegans). Strain BY200 was cultured following standard procedure. The worms (L1 stage) were exposed to the treatments, ASAE (10 or 25 mg/ml) or no for 24 hours, followed by the induction of dopaminergic damage (reserpine, 60 µM, positive control; PC) or no (negative control; NC). Worm’s images (n=20) were captured using a fluorescence microscope and quantified using the ImageJ software. The locomotor behavior (body bends) of the w

How neuronal wiring architecture supports coordinated brain dynamics is an unsolved problem in neuroscience.The worm Caenorhabditis elegans (C.elegans) is a tractable model organism with a fully mapped connectome. C.elegans displays stereotyped behaviour, with specific gaits of locomotion (like forward/backward movement) matching distinct neuronal brain activity dynamics, which are comprised of synchronous network activity patterns (Kato 2015, Uzel 2022). Here, we aim to understand how the C.elegans connectome supports such dynamics.Our studies (Avila 2023) have suggested that these network sy

Ageing has been defined as a gradual functional decline with a progressive physiological integrity loss, increasing the organism’s vulnerability to death. Otherwise, this described deterioration is the major risk factor for most current human pathologies, including neurodegenerative diseases, cancer, cardiovascular disorders, and diabetes. However, in the last decades, non-pharmacological treatments like physical exercise have provided general health benefits against ageing decline. In this study, we aim to analyze how lifestyle factors such as physical exercise can modify the molecular expres

CHARGE syndrome (CS) is a rare genetic disease, mainly due to mutations in the chromatin remodeler gene CHD7 and characterized by multiple neuronal dysfunctions and malformations of neural-crest derived organs, for which no pharmacological treatments are available. CS high phenotypic variability could be explained by mutations in genes with an epistatic relationship to CHD7, that may alter the expressivity of disease traits. In this context, recent evidence revealed that genes encoding semaphorins (SEMA) and their receptors might be good candidates as CHD7 genetic interactors. Thus, we generat

Neurons rely on mitochondria for an efficient supply of ATP and other metabolites. However, while neurons are highly elongated, mitochondria are discrete and limited in number. Due to the slow rates of diffusion over long distances it follows that neurons would benefit from an ability to control the distribution of mitochondria to sites of high metabolic activity, such as synapses. It is assumed that neurons’ possess this capacity, but ultrastructural data over substantial portions of a neuron’s extent that would allow for tests of such hypotheses are scarce. Here, we mined the Caenorhabditis