Biology subjects

Rabinowitch, I.

Publications and source records attributed to Rabinowitch, I..

4 recordsLinked to original sources

bioRxiv2026

Effort experience as a driver of behavioral modulation in Caenorhabditis elegans

Effort is typically studied as a cost that influences choice, motivation, or persistence, but less is known about whether effort embedded within ordinary behavior can itself leave a trace that alters subsequent behavior. We developed a Caenorhabditis elegans paradigm in which animals reached the same food source under low or high effort conditions and were then tested in various behavioral contexts. Prior high effort enhanced subsequent food approach, generalized to more demanding tests including aversive barrier crossing, and persisted for at least 1 h but was lost by 24 h. The effect was distinct from food deprivation and was accompanied by context-dependent changes in locomotor dispersal rather than a uniform increase in activity. A monoamine screen implicated tyramine signaling. High effort also reduced ongoing activity in the tyraminergic RIM interneurons and enhanced the AWC OFF sensory response. These findings identify effort as a behaviorally consequential component of ordinary experience and suggest that ongoing behavior can generate internal state changes that may recursively influence future behavior.

neuroscience↗

bioRxiv2024

Asymmetry in synaptic connectivity balances redundancy and reachability in the C. elegans connectome

The brain is overall bilaterally symmetrical, but exhibits also considerable asymmetry. While symmetry may endow neural networks with robustness and resilience, asymmetry may enable parallel information processing and functional specialization. How is this functional tradeoff between symmetrical and asymmetrical brain architecture balanced? To address this, we focused on the C. elegans connectome, which comprises 99 classes of bilaterally symmetrical neuron pairs. We found symmetry in the number of synaptic partners between neuron class members, but pronounced asymmetry in the identity of these synapses. We developed graph theoretical metrics for evaluating Redundancy, the selective reinforcement of specific neural paths by multiple alternative synaptic connections, and Reachability, the extent of synaptic connectivity of each neuron class. We found Redundancy and Reachability to be stochastically tunable by the level of network asymmetry, driving the C. elegans connectome to favor Redundancy over Reachability. These results elucidate fundamental relations between lateralized neural connectivity and function.

neuroscience↗

bioRxiv2020

Repairing neural damage in a C. elegans chemosensory circuit using genetically engineered synapses

Neuronal loss can considerably diminish neural circuit function, impairing normal behavior by disrupting information flow in the circuit. We reasoned that by rerouting the flow of information in the damaged circuit it may be possible to offset these negative outcomes. We examined this possibility using the well-characterized chemosensory circuit of the nematode worm C. elegans. In this circuit, a main sensory neuron class sends parallel outputs to several interneuron classes. We found that the removal of one of these interneuron classes impairs chemotaxis to attractive odors, revealing a prominent path for information flow in the circuit. To alleviate these deficiencies, we sought to reinforce a remaining neural pathway. We used genetically engineered electrical synapses for this purpose, and observed the successful recovery of chemotaxis performance. However, we were surprised to find that the recovery was largely mediated by inadvertently formed left-right lateral electrical connections within individual neuron classes. Our analysis suggests that these additional electrical synapses help restore circuit function by amplifying weakened neuronal signals in the damaged circuit. These results demonstrate the power of genetically engineered synapses to regulate information flow and signal intensity in damaged neural circuits.

neuroscience↗

bioRxiv2019

INX-18 and INX-19 play distinct roles in electrical synapses that modulate aversive behavior in Caenorhabditis elegans

In order to respond to changing environments and fluctuations in internal states, animals adjust their behavior through diverse neuromodulatory mechanisms. In this study we show that electrical synapses between the ASH primary quinine-detecting sensory neurons and the neighboring ASK neurons are required for modulating the aversive response to the bitter tastant quinine in C. elegans. Mutant worms that lack the electrical synapse proteins INX-18 and INX-19 become hypersensitive to dilute quinine. Cell-specific rescue experiments indicate that inx-18 operates in ASK while inx-19 is required in both ASK and ASH for proper quinine sensitivity. Imaging analyses find that INX-19 in ASK and ASH localizes to the same regions in the nerve ring, suggesting that both sides of ASK-ASH electrical synapses contain INX-19. While inx-18 and inx-19 mutant animals have a similar behavioral phenotype, several lines of evidence suggest the proteins encoded by these genes play different roles in modulating the aversive quinine response. First, INX-18 and INX-19 localize to different regions of the nerve ring, indicating that they are not present in the same synapses. Second, removing inx-18 disrupts the distribution of INX-19, while removing inx-19 does not alter INX-18 localization. Finally, by using a fluorescent cGMP reporter, we find that INX-18 and INX-19 have distinct roles in establishing cGMP levels in ASK and ASH. Together, these results demonstrate that electrical synapses containing INX-18 and INX-19 facilitate modulation of ASH nociceptive signaling. Our findings support the idea that a network of electrical synapses mediates cGMP exchange between neurons, enabling modulation of sensory responses and behavior.\n\nAuthor SummaryAnimals are constantly adjusting their behavior to respond to changes in the environment or to their internal state. This behavior modulation is achieved by altering the activity of neurons and circuits through a variety of neuroplasticity mechanisms. Chemical synapses are known to impact neuroplasticity in several different ways, but the diversity of mechanisms by which electrical synapses contribute is still being investigated. Electrical synapses are specialized sites of connection between neurons where ions and small signaling molecules can pass directly from one cell to the next. By passing small molecules through electrical synapses, neurons may be able to modify the activity of their neighbors. In this study we identify two genes that contribute to electrical synapses between two sensory neurons in C. elegans. We show that these electrical synapses are crucial for proper modulation of sensory responses, as without them animals are overly responsive to an aversive stimulus. In addition to pinpointing their sites of action, we present evidence that they may be contributing to neuromodulation by facilitating passage of the small molecule cGMP between neurons. Our work provides evidence for a role of electrical synapses in regulating animal behavior.

neuroscience↗