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Haak, R.

Publications and source records attributed to Haak, R..

2 recordsLinked to original sources

LatenZy, non-parametric, binning-free estimation of latencies from neural spiking data

Precisely estimating the onset of neural spiking responses and the timing at which activity begins to diverge between conditions is crucial for understanding temporal dynamics in brain information processing. Conventional methods require arbitrary parameter choices such as bin widths and response thresholds, limiting reproducibility and comparability. Here, we present latenZy and latenZy2, two non-parametric, binning-free methods that directly analyze spike times using cumulative statistics and iterative refinement, without assumptions about response shape. LatenZy estimates neuronal response onset latency, while latenZy2 detects when spiking activity diverges between conditions. We validate these methods on electrophysiological datasets from mouse and macaque visual cortex, and show that they outperform standard approaches in precision, robustness, sensitivity, and statistical power. LatenZy captures contrast-dependent latency shifts and hierarchical timing across visual areas, and latenZy2 reveals earlier attentional modulation in higher visual cortex consistent with top-down feedback. Together, they offer scalable, parameter-free tools for reliable latency estimation in large-scale neural recordings. Open-source implementations are available in Python and MATLAB.

neuroscience↗

A prefrontal cortex-lateral hypothalamus circuit controls stress-driven food intake

Stress can drive overconsumption of high-fat foods. The medial prefrontal cortex (mPFC) is implicated in such stress-eating, but the underlying circuit mechanisms remain unclear. Here we show that mPFC projections to the lateral hypothalamus (LHA) are required for stress-induced fat intake in male mice. We find that mPFC-LHA stimulation in sated states increases fat intake. Social stress acutely engages mPFC-LHA neurons, and inhibiting this pathway selectively prevents stress-driven excess fat intake. Circuit mapping shows that mPFC neurons innervate GABAergic and glutamatergic LHA (LHAVGLUT2) neurons, but that social stress preferentially engages mPFC-LHAVGLUT2 neurons and causes plasticity at mPFC-LHAVGLUT2 synapses. Specifically, stress weakens mPFC synapses onto LHAVGLUT2 neurons that curtail food intake, while strengthening mPFC synapses onto midbrain-projecting LHAVGLUT2 neurons linked to stress-eating. We show that LHAVGLUT2 neurons are required downstream mPFC targets for transforming stress into heightened fat intake. Overall, we identify the mPFC-LHA as a multi-branched network, indispensable for stress-eating.

neuroscience↗