Biology subjects

Jacquerie, K.

Publications and source records attributed to Jacquerie, K..

5 recordsLinked to original sources

bioRxiv2026

Compensation of the effects of temperature on a motor system in the crab, Cancer borealis

Rising ocean temperatures challenge ectothermic animals to maintain essential behaviors such as movement and feeding. We asked how a complete neuromuscular pathway preserves function when every component process responds differently to warming. In the pyloric system of the crab Cancer borealis, we simultaneously recorded motor nerve activity, muscle membrane potential, and contraction. Warming preserved rhythmic nerve activity and excitatory junctional potentials, but contraction declined and failed first. Fixed low-frequency stimulation, mimicking cold-temperature motor output, resulted in reduced contraction at warm temperatures, whereas higher-frequency stimulation, mimicking warm-temperature motor output, partially restored contraction. Warming hyperpolarized muscle fibers, moving them farther from contraction threshold, but also reduced input resistance, which together limited over-excitability. However, high-potassium stimulation revealed that the muscle contractile machinery remained functional. Thus, warming acts differently across levels, and overlapping compensatory mechanisms help preserve neuromuscular function across a wide range of temperatures. Significance statementCold-blooded animals that live in climates with significant seasonal changes in ambient temperature must have myriad mechanisms to function over a wide range of environmental conditions. We explore the effects of temperature at multiple levels of organization within the stomatogastric system of the crab, Cancer borealis. We find a series of compensatory mechanisms that cooperatively help maintain stable function despite the fact that the motor patterns, neuromuscular junctions and muscle functions are all differently temperature dependent.

neuroscience↗

bioRxiv2025

Temperature and pH-dependent Potassium Currents of Muscles of the Stomatogastric Nervous System of the Crab, Cancer borealis

Marine crustaceans, such as the crab Cancer borealis, experience large fluctuations in temperature and pH, yet their stomatogastric neuromuscular system must remain functional to support feeding. We examined 16 of the [~]40 pairs of stomach muscles and found that warming consistently hyperpolarized muscle fibers ([~]10 mV per 10 {degrees}C) and reduced excitatory junctional potentials and currents. Voltage-clamp analysis in the gastric muscle 5b (gm5b) revealed a temperature-activated conductance with a reversal potential near the potassium reversal potential, consistent with a potassium current, and insensitive to tetraethylammonium. Quantitative RT-PCR identified expression of two putative two-pore domain potassium (K2P) channels in these muscles. Muscle responses were also strongly influenced by extracellular pH. We observed an optimal operating window between pH 6.7-8.8; outside this range, responses diminished and abnormal activity, including spontaneous firing, appeared. Voltage-clamp recordings confirmed pH modulation of the same potassium conductance. Together, these results demonstrate that muscle excitability in Cancer borealis is shaped by temperature- and pH-sensitive currents, presumably carried by K2P channels. Functionally, these channels provide a plausible mechanism for stabilizing neuromuscular output despite environmental perturbations. As temperature increases, the pyloric and gastric rhythms accelerate, increasing synaptic drive to muscles. Activation of K2P channels counterbalances this input by reducing excitability, thereby preventing over-contraction and extending its dynamic range. This work highlights a muscle-intrinsic contribution to the well-known robustness of the stomatogastric system and identifies K2P channels as key players in adapting motor performance to changing environments. HighlightsO_LICancer borealis stomach muscles are sensitive to temperature and pH. C_LIO_LIWarming hyperpolarizes fibers and reduces synaptic response amplitude. C_LIO_LIKCNK1 and KCNK2, K2P channels mediate temperature- and pH-dependent conductances. C_LIO_LIMuscle K2Ps lower excitability, extending the functional range at high temperatures. C_LI In BriefThe crab Cancer borealis experiences large fluctuations in temperature and pH. We show that its stomach muscles hyperpolarize with warming and operate optimally within a narrow pH window. These effects are mediated by K2P channels (KCNK1, KCNK2), which reduce excitability and help maintain robust neuromuscular function under environmental change. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=114 SRC="FIGDIR/small/680680v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@bec881org.highwire.dtl.DTLVardef@15d91a3org.highwire.dtl.DTLVardef@4777forg.highwire.dtl.DTLVardef@141444b_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2025

Switches from tonic to burst firing enable memory consolidation through late-phase synaptic plasticity

Neural circuits routinely alternate between input-driven tonic activity and collective burst firing. In the presence of Hebbian plasticity, bursts generate a robust attractor in weight space, creating a built-in drift that can be repurposed into a stabilizing trace of prior learning. We show that this phenomenon can be harnessed for memory consolidation through the introduction of a two-stage synaptic rule. The effective synaptic weight is defined as the product of a primary weight--updated by a Hebbian rule during both tonic and burst periods--and a secondary weight that updates in proportion with a coupling gain to the negative time-derivative of the primary weight. In a MNIST-like task, alternating tonic and burst epochs preserves earlier patterns, improves generalization to unseen inputs, and resists interference and noise, whereas replacing burst by quiescence or additional tonic epochs does not. Parameter sweeps reveal that coupling gain and the initial synaptic weights control whether bursts consolidate ("up-selection") or prune ("down-selection") synapses. Pairing the rule with alternative primary plasticity models yields distinct treatments of overlapping inputs, enabling either integration or separation. Studying switches in firing activity with a two-stage synaptic plasticity provides a plausible route to consolidation in biological and neuromorphic networks. Significance StatementNeural circuits alternate between tonic spiking and burst firing, yet most models of synaptic plasticity are limited to a single firing regime. We introduce a two--stage synaptic rule in which a primary weight encodes activity during both states, while a secondary weight--engaged only during bursts-- stabilizes learning from tonic periods. In conductance-based networks and a pattern recognition task, this rule preserves memories, improves generalization, and resists interference, whereas quiescence or extended tonic activity do not. The model further shows that bursts can consolidate or prune synapses depending on coupling gain and initial conditions. These findings identify a plausible, biologically motivated mechanism for how activity state transitions shape memory consolidation. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=160 HEIGHT=200 SRC="FIGDIR/small/648539v2_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@7a8922org.highwire.dtl.DTLVardef@c13425org.highwire.dtl.DTLVardef@46a505org.highwire.dtl.DTLVardef@1fc0820_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2022

Switches to rhythmic brain activity lead to a plasticity-induced reset in synaptic weights

1Neural circuits often alternate between tonic and burst firing - two distinct activity regimes that reflect changes in excitability and neuromodulatory state. While tonic firing produces asynchronous spiking driven by diverse external inputs, collective burst firing consists of rapid clusters of spikes followed by a period of silence, happening synchronously within the network. Synaptic plasticity has typically been studied only in either one of these regimes, leaving unclear how alternating states jointly shape long-term weight dynamics. Here, we use a conductance-based network model endowed with calcium-based or spike-timing-based plasticity rules to examine how synaptic weights evolve across state transitions. During tonic firing, synaptic weights are driven by the statistics of external inputs, producing a broad distribution across the network. In contrast, during collective burst firing, weights converge to a narrow region in weight space: a burst-induced attractor. We derive the location of this attractor analytically in terms of plasticity parameters and activity statistics, and confirm its emergence across diverse plasticity rules. The attractor reflects the synchronization of plasticity-driving signals during bursts, which homogenizes synaptic dynamics and forces convergence toward shared fixed points. We further show that neuromodulation and synaptic tagging can shift or split the burst-induced attractor, stabilizing selected synapses while weakening others. This mechanism reconciles flexibility during tonic-driven learning with stability during burst-driven consolidation. These results identify burst-induced attractors as a robust emergent property of networks combining collective bursting with soft-bound plasticity rules. By showing how they can be analytically predicted and experimentally modulated, our work provides a general computational framework linking state transitions, synaptic plasticity, and memory organization. 2 Author SummaryBrains operate in different activity states, reflecting different behaviors or neuromodulatory states. Neurons can fire isolated spikes in a tonic mode that encodes information about external inputs. They can fire rapid bursts of spikes, generating large synchronized oscillations that dominate population activity. Both tonic and burst firing are linked to learning and memory, yet their distinct contributions to shaping synaptic plasticity remain poorly understood. In this study, we use biophysical network models equipped with well-established plasticity rules to investigate how synaptic weights evolve under tonic and burst firing. We show that during tonic activity, synapses diverge toward a wide variety of values, reflecting the diversity of input statistics. In contrast, when the network enters a collective bursting state, synaptic weights collapse into a narrow region of weight space--a "burst-induced attractor." We derive the attractor mathematically and show that its position depends directly on the plasticity parameters, meaning it can be shifted or split through neuromodulatory and tag-dependent processes. Our results suggest that bursts provide a robust and controllable stage for synaptic consolidation. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=170 SRC="FIGDIR/small/500198v3_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@2ab6aeorg.highwire.dtl.DTLVardef@3f8199org.highwire.dtl.DTLVardef@155900borg.highwire.dtl.DTLVardef@63f520_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

bioRxiv2020

Robust switches in thalamic network activity require a timescale separation between sodium and T-type calcium channel activations

Switches in brain states, synaptic plasticity and neuromodulation are fundamental processes in our brain that take place concomitantly across several spatial and timescales. All these processes target neuron intrinsic properties and connectivity to achieve specific physiological goals, raising the question of how they can operate without interfering with each other. Here, we highlight the central importance of a timescale separation in the activation of sodium and T-type calcium channels to sustain robust switches in brain states in thalamic neurons that are compatible with synaptic plasticity and neuromodulation. We quantify the role of this timescale separation by comparing the robustness of rhythms of six published conductance-based models at the cellular, circuit and network levels. We show that robust rhythm generation requires a T-type calcium channel activation whose kinetics are situated between sodium channel activation and T-type calcium channel inactivation in all models despite their quantitative differences.

neuroscience↗