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Gastambide, F.

Publications and source records attributed to Gastambide, F..

3 recordsLinked to original sources

GESTURE: unsupervised genotype-specific behavioral phenotyping in rodents via graph-based representation learning

Objective quantification of complex animal behavior is fundamental to neuroscience and pharmacology, yet extracting biologically meaningful insights from high-dimensional pose data remains challenging. This is especially true for subtle phenotypic differences caused by genetic mutations, which frequently evade conventional evaluation metrics. Here, we introduce GESTURE, an unsupervised, graph-based deep generative framework that autonomously discovers and quantifies behavioral structure from raw pose dynamics. Analyzing mice with motor dysfunction alongside wild-type controls, GESTURE identifies a shared vocabulary of behavioral motifs. We show that genotype-specific differences arise from the differential usage of these motifs, yielding distinct "behavioral fingerprints" that reliably separate genotypes without supervision. By modeling behavior as a sequence rather than a static partition, GESTURE measures temporal organization directly: affected animals held motifs longer and transitioned more predictably, revealing a slowing and stereotyping of behavioral sequences rather than a simple reduction in activity. Importantly, GESTUREs graph-based representation enables training across multiple recordings and embedding behaviors into a shared latent space, supporting robust cross-animal comparisons and future cross-experiment alignment. Furthermore, automatically derived metrics of behavioral divergence track the temporal dynamics of expert-annotated disability scores, reaching agreement comparable to independent human raters. Finally, node- and edge-level explainability analyses indicate that the models latent representations are shaped by a biologically plausible focus on the animals core motor scaffold. Together, these results position GESTURE as an interpretable and scalable framework for automated behavioral phenotyping, linking genetic perturbation to quantitative behavioral phenotypes. Author summaryHow can we measure, objectively, the subtle changes in behavior caused by a disease-causing mutation? Such changes are hard for human observers to judge consistently, and scoring them by hand is slow and does not scale. We studied mice carrying a mutation in a calcium-channel gene. In people, mutations in the same gene cause episodic ataxia and related movement disorders. We developed GESTURE, which learns recurring patterns of movement directly from video of a freely moving mouse, without being told what to look for. It treats the body as a set of connected landmarks and follows how their arrangement changes over time, discovering a shared vocabulary of movements. Affected and healthy mice drew on the same vocabulary but used it differently. Each animals pattern of use formed a distinctive "behavioral fingerprint", and these fingerprints alone identified which animals carried the mutation --in every case. They also revealed something a simple activity measure would miss: affected mice hold each movement longer, and string movements together more predictably. A severity score read automatically from them matched expert judgement as closely as two trained raters matched each other, and returned the same answer every time.

neuroscience↗

T-401 binding to monoacylglycerol lipase (MAGL) in the brains of patients and mice with temporal lobe epilepsy

Monoacylglycerol lipase (MAGL) inhibitors are considered as drug candidates for epilepsy. In order to determine the level of MAGL and evaluate changes in the epileptic brain, we have validated and used autoradiography and the MAGL radiotracer [3H]T-401 on resected temporal neocortex specimens obtained from patients with temporal lobe epilepsy and in brains from mice with chronic reoccurring seizures. Saturation experiments revealed a KD around 4 nM for the human temporal cortex and 7 nM for the mouse brain. In the human brain, binding of [3H]T-401 was detected mostly in the grey matter, and in the subcortical white matter in lower amounts. The levels were strongly correlated in the two cortical compartments. The level of [3H]T-401 binding in the human temporal cortex varied about a 4-fold among the patients, but was not correlated to either epilepsy duration or the age of the patients. In the epileptic mouse brain, a significant reduction was observed bilaterally in the hippocampus, as well as in other cortical regions, including the temporal cortex. Interestingly, a highly significant negative correlation was seen between MAGL and binding to the translocator protein 18 kDa (TSPO) expressed in glia. These data support the presence of MAGL in neuronal and non-neuronal cells, and indicate that MAGL levels in the brains of either patients with epilepsy or mice after intra-hippocampal kainite injection are reduced not only in the epileptic zone in the hippocampus, but more widespread in the brain.

neuroscience↗

Amphetamine disrupts haemodynamic correlates of prediction errors in nucleus accumbens and orbitofrontal cortex

In an uncertain world, the ability to predict and update the relationships between environmental cues and outcomes is a fundamental element of adaptive behaviour. This type of learning is typically thought to depend on prediction error, the difference between expected and experienced events, and in the reward domain this has been closely linked to mesolimbic dopamine. There is also increasing behavioural and neuroimaging evidence that disruption to this process may be a cross-diagnostic feature of several neuropsychiatric and neurological disorders in which dopamine is dysregulated. However, the precise relationship between haemodynamic measures, dopamine and reward-guided learning remains unclear. To help address this issue, we used a translational technique, oxygen amperometry, to record haemodynamic signals in the nucleus accumbens (NAc) and orbitofrontal cortex (OFC) while freely-moving rats performed a probabilistic Pavlovian learning task. Using a model-based analysis approach to account for individual variations in learning, we found that the oxygen signal in the NAc correlated with a reward prediction error, whereas in the OFC it correlated with an unsigned prediction error or salience signal. Furthermore, an acute dose of amphetamine, creating a hyperdopaminergic state, disrupted rats ability to discriminate between cues associated with either a high or a low probability of reward and concomitantly corrupted prediction error signalling. These results demonstrate parallel but distinct prediction error signals in NAc and OFC during learning, both of which are affected by psychostimulant administration. Furthermore, they establish the viability of tracking and manipulating haemodynamic signatures of reward-guided learning observed in human fMRI studies using a proxy signal for BOLD in a freely behaving rodent.

neuroscience↗