Biology subjects

Camprodon, J. A.

Publications and source records attributed to Camprodon, J. A..

3 recordsLinked to original sources

bioRxiv2025

Structural Connectivity Correlates of Response to Electroconvulsive Therapy in Treatment-Resistant Depression

BackgroundElectroconvulsive therapy (ECT) is the most effective option for treatment resistant depression (TRD). In this study, we sought to explore if structural connectivity of limbic networks has an association with response to ECT. MethodsWe studied 23 patients with TRD who underwent a course of bifrontal ECT, employing probabilistic tractography at baseline to assess structural connectivity between the thalamus (THA), posterior (PCC), subgenual cingulate cortices, anterior insula (aINS), amygdala and orbitofrontal and ventrolateral prefrontal cortices, hypothesizing that these hubs participate in the formation and refractoriness of depression symptoms. We also include 21 healthy subject as controls group (HC). ResultsConnectivity between left THA and left PCC was related to both baseline depression severity (R=0.504; p= 0.017) and clinical response (R=0.452; p=0.004). Right aINS-prefrontal connectivity was associated with less clinical response. Structural connectivity was globally higher in patients than in HC (F=2.488; p=0.007). ConclusionsThe association of ECT response with stronger structural connectivity between hubs supporting self-referential bodily experience as well as autobiographical memory encoding and retrieval deserves exploration as a predictor in persons with TRD. In turn, the right aINS is a major hub for the salience network and is involved in repetitive negative mentation. Stronger structural connectivity of this region may be a heuristically valid biomarker for refractory TRD. We discuss the potential of the present findings for the design of anatomically precise neuromodulation interventions that would be useful to treat TRD while circumventing cognitive side effects of ECT.

neuroscience↗

bioRxiv2025

A Clinically Aligned Murine Model of Electroconvulsive Stimulation Reverses Social Aversion and Displays Fear Memory Impairment After Chronic Social Defeat Stress

Electroconvulsive therapy (ECT) is the most effective treatment for patients with major depression, bipolar depression, mania, catatonia, and schizophrenia. Nonetheless, the mechanisms underlying its therapeutic effects largely remain unknown. While previous preclinical studies have noted a role for neurotropic signaling, neurogenesis, and alterations in monoamine neurotransmitter systems, these models were largely conducted using procedures that deviate from clinical practice. Therefore, we sought to develop a clinically relevant murine model of ECT, referred to as electroconvulsive stimulation (ECS) in animals, which more closely aligns with current clinical approaches to better explore its mechanisms. Using the well-established chronic social defeat stress (CSDS) paradigm, known to negatively impact reward processes, we investigated whether the behavioral changes after CSDS could be reversed following a clinically related course of ECS. Additionally, we observed induction of plasticity-related genes in the nucleus accumbens (NAcc) and amygdala, regions responsible for reward and fear-related memory, respectively. Lastly, we investigated ECS-related changes in the NAcc with bulk RNA-sequencing. Pathway analysis demonstrated cellular changes primarily involved in neuroplasticity and regulating cell migration and differentiation. Therefore, utilizing our novel and clinically relevant model of ECS, we have begun to elucidate mechanisms that contribute to ECTs therapeutic outcomes by examining murine behavior and RNA from brain regions associated with stress-induced states that model anxiety and depression and the effects of ECS.

neuroscience↗

bioRxiv2024

Anterior cingulate neurons display subregion-specific interaction with frontal eye fields as revealed by combined antidromic stimulation and resting state imaging

The anterior cingulate cortex (ACC) is thought to exert cognitive control over saccade generation in the frontal eye fields (FEF), but the nature of this interaction remains unclear. Although prior imaging studies have suggested ACC interacts with FEF, few studies have confirmed this by electrophysiological recordings. This study aimed to characterize the functional connectivity between ACC and medial and lateral FEF during cognitive saccade tasks. We combined resting-state functional MRI (rs-fMRI) with single-unit electrophysiology in two macaque monkeys performing memory-guided saccade and pro-/anti-saccade tasks. Anti- and ortho-dromic stimulation was used to electrophysiologically identify ACC neurons mono- and polysynaptically connected to FEF. We analyzed ACC neuronal selectivity for different task aspects and correlated these properties with both positive and negative rs-fMRI functional connectivity between ACC and FEF subregions. Anti- and ortho-dromically identified ACC neurons were predominantly connected to medial FEF, which showed stronger positive functional connectivity with ACC compared to lateral FEF. Sites with higher proportions of task-selective neurons yielded stronger functional connectivity with FEF. This stronger functional connectivity was particularly related to the delay and saccadic periods of different cognitive saccade tasks. Using combined imaging and electrophysiology, our findings provide converging evidence for functional interactions between ACC and FEF, predominantly medial FEF regions which encode large amplitude saccades. The correlation between functional connectivity and task-related neuronal selectivity supports ACCs interaction with FEF in the modulation of saccade generation and cognitive control. Additionally, we report suggestive evidence that mono- and poly-synaptic connections may be related to positive functional connectivity, but we found no such relationship for negative functional connectivity (anticorrelations). These results advance our understanding of prefrontal cortical interactions in oculomotor control and the electrophysiological mechanisms of positive and negative resting-state functional connectivity.

neuroscience↗