@article {70276,
	title = {Synchronization of behavioral and cardiac dynamics in larval zebrafish.},
	journal = {Cell Rep},
	volume = {45},
	year = {2026},
	month = {2026 Feb 03},
	pages = {116947},
	abstract = {<p>Animals reprioritize behavioral goals in response to internal physiological states. Using larval zebrafish, we investigated whether engagement with a visuomotor task, the optomotor response (OMR), is coupled to cardiac dynamics. We discovered that threats lead to tachycardia that is synchronized with behavioral suppression. The change in heart rate is represented in the activity of specific neuronal populations. Severing the input to the sympathetic ganglia or ablating the vagus nerve revealed that the threat-related changes to behavioral state do not require interoceptive pathways. Direct tachycardic optopacing of the heart similarly suppressed the OMR response, but by reducing cardiac filling during diastole, thereby impacting oxygen delivery to the CNS. Optopacing also changed the activity of specific brain regions but in neurons distinct from those associated with threat-induced tachycardia. These cardiac function-associated central changes may have relevance to autonomic imbalances in anxiety, stress, and orthostatic disorders.</p>
},
	issn = {2211-1247},
	doi = {10.1016/j.celrep.2026.116947},
	url = {https://doi.org/10.1016/j.celrep.2026.116947},
	author = {Herrera, Kristian J and Zarghani-Shiraz, Arman and Ahrens, Misha B and Engert, Florian and Fishman, Mark C}
}
@article {69703,
	title = {Ketamine induces plasticity in a norepinephrine-astroglial circuit to promote behavioral perseverance.},
	journal = {Neuron},
	year = {2024},
	month = {2024 Dec 16},
	pages = {1-15},
	abstract = {<p>Transient exposure to ketamine can trigger lasting changes in behavior and mood. We found that brief ketamine exposure causes long-term suppression of futility-induced passivity in larval zebrafish, reversing the "giving-up" response that normally occurs when swimming fails to cause forward movement. Whole-brain imaging revealed that ketamine hyperactivates the norepinephrine-astroglia circuit responsible for passivity. After ketamine washout, this circuit exhibits hyposensitivity to futility, leading to long-term increased perseverance. Pharmacological, chemogenetic, and optogenetic manipulations show that norepinephrine and astrocytes are necessary and sufficient for ketamine{\textquoteright}s long-term perseverance-enhancing aftereffects. In\&nbsp;vivo calcium imaging revealed that astrocytes in adult mouse cortex are similarly activated during futility in the tail suspension test and that acute ketamine exposure also induces astrocyte hyperactivation. The cross-species conservation of ketamine{\textquoteright}s modulation of noradrenergic-astroglial circuits and evidence that plasticity in this pathway can alter the behavioral response to futility hold promise for identifying new strategies to treat affective disorders.</p>
},
	issn = {1097-4199},
	doi = {10.1016/j.neuron.2024.11.011},
	url = {https://doi.org/10.1016/j.neuron.2024.11.011},
	author = {Duque, Marc and Chen, Alex B and Hsu, Eric and Narayan, Sujatha and Rymbek, Altyn and Begum, Shahinoor and Saher, Gesine and Cohen, Adam E and Olson, David E and Li, Yulong and Prober, David A and Bergles, Dwight E and Fishman, Mark C and Engert, Florian and Ahrens, Misha B}
}
