Biology subjects

Marrone, D. F.

Publications and source records attributed to Marrone, D. F..

3 recordsLinked to original sources

bioRxiv2026

Social Approach Dynamics in Freely-Moving Rat Dyads are Not Impacted by Lesions to the Retrosplenial Cortex

Social interaction in rodents can involve a dynamic interplay of approach and withdrawal movements, requiring the brain to rapidly update information about where others are and where they may intend to go. In mammals, the posterior parietal cortex (PPC) and adjacent, reciprocally-connected retrosplenial cortex (RSC) are high-level hubs for spatial information processing. To test the role of these regions in dynamic social approach, we evaluated rats' relative orientation, movement, and position (ROMP) with a freely-moving social-stimulus rat following bilateral lesions to the PPC or anterior RSC. RSC animals showed overall more and faster movements, and greater attention to environment boundaries across multiple behavioral conditions (open field, social, object, static social, and dynamic object) compared with sham-lesioned controls. Increased attention to boundaries was correlated with reduced orienting to a social stimulus; however, this appeared to have little observable impact on the social interactions themselves. Rear-sniffing was lower in RSC rats, but only during the latter half of the 10 minute social exposures, and there were no detected differences in the dynamics of their social approach compared with sham controls. PPC lesion spread was more limited, and social behavior was mostly indistinguishable from sham controls, though this group was more likely to chase the dynamic object. Results suggest that social approach within short (peripersonal) distances is largely accomplished through sensorimotor adjustments that do not require higher-level, spatial-predictive processing taking place in the RSC.

animal behavior and cognition↗

bioRxiv2022

A biophysical, minimal model to investigate age-related changes in CA1 pyramidal cell electrical activity

Aging is a physiological process that is still poorly understood, especially with respect to effects on the brain. There are open questions about aging that are difficult to answer with an experimental approach. Underlying challenges include the difficulty of recording in vivo single cell and network activity simultaneously with submillisecond resolution, and brain compensatory mechanisms triggered by genetic, pharmacologic, or behavioral manipulations. Mathematical modeling can help address some of these questions by allowing us to fix parameters that cannot be controlled experimentally and investigate neural activity under different conditions. We present a biophysical minimal model of CA1 pyramidal cells (PCs) based on general expressions for transmembrane ion transport derived from basic thermodynamical principles. The model allows directly varying the contribution of ion channels by changing their number. By analyzing the dynamics of the model, we find parameter ranges that reproduce the variability in electrical activity seen in PCs. In addition, increasing the L-type Ca2+ channel expression in the model reproduces age-related changes in excitability that are qualitatively and quantitatively similar to those observed in PCs from aged animals.

biophysics↗

bioRxiv2020

Norepinephrine as a Memory Reset Signal: Switching the System from Retrieval to Encoding During a Spatial Memory Task can be Both Adaptive and Maladaptive

Contextual information is represented in the hippocampus (HPC) partially through the recruitment of distinct neuronal ensembles. It is believed that reactivation of these ensembles underlies memory retrieval processes. Recently, we showed that norepinephrine (NE) input from phasic locus coeruleus (LC) activation induces hippocampal plasticity resulting in the recruitment of new neurons and a disengagement from previously established representations. We hypothesize that NE may provide a neuromodulatory, mnemonic switch signaling the HPC to move from a state of retrieval to encoding in the presence of novelty, and therefore, plays a role in memory updating. Here, we tested whether bilateral dorsal dentate gyrus (DG) infusions of the {beta}-adrenergic receptor (BAR) agonist isoproterenol (ISO), administered prior to encoding or retrieval, would impair spatial working and reference memory by reverting the system to encoding (thereby recruiting new neurons) potentially interfering with retrieval of the previously established spatial ensemble. We also investigated whether dDG infusions of ISO could promote cognitive flexibility by switching the system to encoding when it is adaptive (i.e. when new information is presented e.g. reversal learning). We found that intra-dDG infusions of ISO given prior to retrieval caused deficits in working and reference memory which was blocked by pre-treatment with the BAR-antagonist, propranolol (PRO). In contrast, ISO administered prior to reversal learning led to improved performance. These data support our hypothesis that NE serves as a novelty signal to update HPC contextual representations via BAR activation-facilitated recruitment of new neurons. This can be both maladaptive and adaptive depending on the situation. SIGNIFICANCE STATEMENTThe current work highlights the involvement of hippocampal BARs in determining the flexibility of contextual representations to promote new learning in a way that supports adaptive behavior. This work builds upon previous work showing that noradrenergic input to the hippocampus is involved in recruiting new neurons resulting in new contextual representations and may be involved in the underlying neural mechanisms that support memory updating. These data suggest targets for anxiety disorders such as PTSD, which are characterized by noradrenergic dysregulation, and may also involve impairments in memory updating mechanisms where the incorporation of new information is not effectively encoded. The further understanding of the neurobiological mechanisms involved in updating memories may provide insight into novel treatment strategies.

animal behavior and cognition↗