@article{20101,
  abstract     = {Evading imminent threat from predators is critical for animal survival. Effective defensive strategies can vary, even between closely related species. However, the neural basis of such species-specific behaviours remains poorly understood1,2,3,4. Here we find that two sister species of deer mice (genus Peromyscus)5 show different responses to the same looming stimulus: Peromyscus maniculatus, which occupies densely vegetated habitats, predominantly escapes, whereas the open field specialist, Peromyscus polionotus, briefly freezes. This difference arises from species-specific escape thresholds, is largely context-independent, and can be triggered by both visual and auditory threat stimuli. Using immunohistochemistry and electrophysiological recordings, we find that although visual threat activates the superior colliculus in both species, the role of the dorsal periaqueductal grey (dPAG) in driving behaviour differs. Whereas dPAG activity scales with running speed in P. maniculatus, neural activity in the dPAG of P. polionotus correlates poorly with movement, including during visually triggered escape. Moreover, optogenetic activation of dPAG neurons elicits acceleration in P. maniculatus but not in P. polionotus, and their chemogenetic inhibition during a looming stimulus delays escape onset in P. maniculatus to match that of P. polionotus. Together, we trace species-specific escape thresholds to a central circuit node, downstream of peripheral sensory neurons, localizing an ecologically relevant behavioural difference to a specific region of the mammalian brain.},
  author       = {Baier, Felix and Reinhard, Katja and Nuttin, Bram and Sans-Dublanc, Arnau and Liu, Chen and Tong, Victoria and Murmann, Julie Stefanie and Wierda, Keimpe and Farrow, Karl and Hoekstra, Hopi E.},
  issn         = {1476-4687},
  journal      = {Nature},
  pages        = {439--447},
  publisher    = {Springer Nature},
  title        = {{The neural basis of species-specific defensive behaviour in Peromyscus mice}},
  doi          = {10.1038/s41586-025-09241-2},
  volume       = {645},
  year         = {2025},
}

@misc{20883,
  abstract     = {Evading imminent predator threat is critical for survival. Effective defensive strategies can vary, even between closely related species. However, the neural basis of such species-specific behaviours is still poorly understood. Here we find that two sister species of deer mice (genus Peromyscus) show different responses to the same looming stimulus: P. maniculatus, which occupies densely vegetated habitats, predominantly escapes, while the open field specialist, P. polionotus, briefly freezes. This difference arises from species-specific escape thresholds, is largely context-independent, and can be triggered by both visual and auditory threat stimuli. Using immunohistochemistry and electrophysiological recordings, we find that although visual threat activates the superior colliculus in both species, the role of the dorsal periaqueductal gray (dPAG) in driving behaviour differs. While dPAG activity scales with running speed in P. maniculatus, neural activity in the dPAG of P. polionotus correlates poorly with movement, including during visually triggered escape. Moreover, optogenetic activation of dPAG neurons elicits acceleration in P. maniculatus but not P. polionotus, while their chemogenetic inhibition during a looming stimulus delays escape onset in P. maniculatus to match that of P. polionotus. Together, we trace species-specific escape thresholds to a central circuit node, downstream of peripheral sensory neurons, localizing an ecologically relevant behavioural difference to a specific region of the mammalian brain.},
  author       = {Felix, Baier and Reinhard, Katja and Nuttin, Bram and Sans Dublanc, Arnau and Liu, Chen and Tong, Victoria and Murmann, Julie Stefanie and Wierda, Keimpe and Farrow, Karl and Hoekstra, Hopi},
  publisher    = {Dryad},
  title        = {{The neural basis of species-specific defensive behaviour in Peromyscus mice}},
  doi          = {10.5061/DRYAD.Q2BVQ83XC},
  year         = {2025},
}

@phdthesis{15352,
  abstract     = {Epilepsy affects about 50 to 65 million people globally. It summarizes a spectrum of neurological
disorders that have in common a hyperactivity of the neuronal network resulting in seizures. A common
assumption is that an imbalance between neuronal excitation and inhibition is a key mechanism in
seizure generation and epileptogeneisis. In at least one-third of the patients, current therapies have
proven unsuccessful in treating seizure progression. One potential reason could be that the therapies
only focus on neurons. Recent studies suggest that neuronal hyperactivity causes a microglial
response, which reinstates brain homeostasis. Additionally, interactions between microglia and neurons
have been shown to inhibit neuronal firing and dampen seizure activity. However, the exact relationship
between microglia and seizure progression in epilepsy is yet to be elucidated. A main bottleneck is that
several studies investigate microglia dynamics in ex vivo slice models, which can severely affect the
microglia dynamics due to their rapid response to environmental changes. On the other hand, in vivo
studies focus mostly on behavior characterization of the epileptic seizure phenotype and their long-term
consequences on microglia activity leaving out the direct consequences of acute seizure activity on
microglia dynamics.
Here, we perform a pilot study to combine electroencephalography (EEG) and in vivo live imaging to
directly monitor and correlate the onset of seizure activity with microglia response. To induce seizures,
we take advantage of the kainic acid (KA) model, which represents similar neuropathological and
electroencephalographic features seen in human patients with temporal lobe epilepsy (TLE). After
confirmation of induction of the seizure and microglia activity in the hippocampus as a focal point, we
investigated whether these changes also reached the primary visual cortex (V1) as a secondary
generalized seizure activity. Indeed, we found that microglia changed their morphology at high doses
of KA in the V1. Next, we optimized each of the two methodological components: for the EEG recording,
our initial attempts under the microscope suffered from extensive electrical noise, which overlaid the
actual signal. Thus, we built a customized Faraday-cage and confirmed that the signal-to-noise ratio
was sufficiently reduced to be able to record brain oscillatory activity. For the in vivo live imaging of
microglia, we had to optimize the imaging parameters, so that we would be able to detect microglial
processes in a sufficient resolution to track their process changes. Finally, we combined both
methodologies with the KA model. We confirmed that KA induced seizure activity and found first
indication that those correlate with microglia volume changes.
Overall, we have developed a first methodological approach, which allows the analysis of the acute
effects of seizure onset on microglia. Future studies will have to continue to optimize the drift during
imaging recording and the post-image analysis. },
  author       = {Murmann, Julie Stefanie},
  issn         = {2791-4585},
  pages        = {54},
  publisher    = {Institute of Science and Technology Austria},
  title        = {{Investigating acute microglia response to seizure activity in vivo: Combining 2-Photon imaging and EEG recording}},
  doi          = {10.15479/at:ista:15352},
  year         = {2024},
}