Ventral hippocampal projections to the medial prefrontal cortex regulate social memory

Phillips, Mary L.; Robinson, Holly; Pozzo-Miller, Lucas

doi:10.7554/elife.44182

Cited by 160 publications

(183 citation statements)

References 69 publications

Supporting

Mentioning

170

Contrasting

Order By: Relevance

“…The amygdala is one of the major target of vHPC projection neurons (Pitkänen et al, 2000), suggesting that the vHPC-to-BLA pathway is not involved in the beneficial effect of silencing vHPC excitatory neurons on long-term ORM. The vHPC involvement in memory processes also involves other projections to the nucleus accumbens or the ventromedial prefrontal cortex (Barker et al, 2019;Hsu et al, 2018;Okuyama et al, 2016;Phillips et al, 2019) and future studies are warranted to determine the role of these circuits in HFD-induced memory deficits.…”

Section: Effects Of Chemogenetic Manipulation Of Vhpc and Bla On Perimentioning

confidence: 99%

Chemogenetic silencing of hippocampus and amygdala reveals a double dissociation in periadolescent obesogenic diet-induced memory alterations

Naneix

Bakoyiannis

Santoyo-Zedillo

et al. 2020

Preprint

View full text Add to dashboard Cite

1ABSTRACTIn addition to numerous metabolic comorbidities, obesity is associated with several adverse neurobiological outcomes, especially learning and memory alterations. Obesity prevalence is rising dramatically in youth and is persisting in adulthood. This is especially worrying since adolescence is a crucial period for the maturation of certain brain regions playing a central role in memory processes such as the hippocampus and the amygdala. We previously showed that periadolescent exposure to obesogenic high-fat diet (HFD) had opposite effects on hippocampus- and amygdala-dependent memory, impairing the former and enhancing the latter. However, the causal role of these two brain regions in periadolescent HFD-induced memory alterations remains unclear. Here, we first showed that periadolescent HFD induced long-term, but not short-term, object recognition memory deficits, specifically when rats were exposed to a novel context. Using chemogenetic approaches to inhibit targeted brain regions, we then demonstrated that recognition memory deficits are dependent on the activity of the ventral hippocampus, but not the basolateral amygdala. On the contrary, the HFD-induced enhancement of conditioned odor aversion requires specifically amygdala activity. Taken together, these findings suggest that HFD consumption throughout adolescence impairs long-term object recognition memory through the overactivation of the ventral hippocampus during memory acquisition. Moreover, these results further highlight the bidirectional effects of adolescent HFD on hippocampal and amygdala functions.

show abstract

Section: Effects Of Chemogenetic Manipulation Of Vhpc and Bla On Perimentioning

confidence: 99%

Chemogenetic silencing of hippocampus and amygdala reveals a double dissociation in periadolescent obesogenic diet-induced memory alterations

Naneix

Bakoyiannis

Santoyo-Zedillo

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…cortex, one of the brain regions involved in social behavior 39,40 , using transcranial two-photon microscopy 41 . We found that Mecp2 308/Y mice with neurological dysfunction and social behavioral deficits exhibited increased dendritic spine elimination ( Fig.…”

Section: Resultsmentioning

confidence: 99%

P2X7 receptor inhibition ameliorates dendritic spine pathology and social behavioral deficits in Rett syndrome mice

et al. 2020

View full text Add to dashboard Cite

Dysregulated immunity has been implicated in the pathogenesis of neurodevelopmental disorders but its contribution to synaptic and behavioral deficits in Rett syndrome (RTT) remains unknown. P2X7 receptors (P2X7Rs) are unique purinergic receptors with proinflammatory functions. Here, we report in a MECP2-deficient mouse model of RTT that the border of the cerebral cortex exhibits increased number of inflammatory myeloid cells expressing cell-surface P2X7Rs. Total knockout of P2X7Rs in MECP2 deficient mice decreases the number of inflammatory myeloid cells, restores cortical dendritic spine dynamics, and improves the animals' neurological function and social behavior. Furthermore, either genetic depletion of P2X7Rs in bone-marrow derived leukocytes or pharmacological block of P2X7Rs primarily outside of the central nervous system parenchyma, recapitulates the beneficial effects of total P2X7R depletion on the social behavior. Together, our results highlight the pathophysiological roles of P2X7Rs in a mouse model of RTT.

show abstract

“…Rodents rely on olfactory information to recognize other individuals, and olfactory inputs are required for social buffering in rats [11,58]. Olfactory-based identity information eventually contributes to social memory engram in the ventral CA1 (vCA1) region of the hippocampus (HPC) [59] and projections from this region to the PFC are required for social recognition memory [42,60]. Thus, the social memory trace in the IL-PFC may represent an advanced level of social information processing reliant on social engram projections from vCA1 feeding into mPFC.…”

Section: Discussionmentioning

confidence: 99%

Optogenetic reactivation of prefrontal social memory trace mimics social buffering of fear

Ahuna

Santos

et al. 2019

Preprint

View full text Add to dashboard Cite

Social buffering occurs when the presence of a companion attenuates the physiological and/or behavioral effects of a stressful or fear-provoking event. It represents a way in which social interactions can immediately and potently modulate behavior. As such, social buffering is one mechanism by which strong social support increases resilience to mental illness. While the behavioral and neuroendocrine impacts of social buffering are well studied in multiple species, including humans, the neuronal bases of this behavioral phenomenon remain largely unexplored. Previous work has shown that the infralimbic prefrontal cortex (IL-PFC) is important for processing social information and, in separate studies, for modulating fear and anxiety. Thus, we hypothesized that socially-active cells within the IL-PFC may integrate social information to modulate fear responsivity. To test this hypothesis, we employed social buffering paradigms in male and female mice. Similar to prior studies in rats, we found that the presence of a cagemate reduced freezing in fear and anxiety-provoking contexts. In accordance with previous work, we demonstrated that interaction with a novel or familiar conspecific induces activity in the IL-PFC as evidenced by increased immediate early gene (IEG) expression. We then utilized an activity-dependent tagging murine line, the ArcCreER T2 mice, to express channelrhodopsin (ChR2) in neurons active during the social encoding of a new cagemate. We found that optogenetic reactivation of these sociallyactive neuronal ensembles phenocopied the effects of cagemate presence in male and female mice in learned and innate fear contexts without being inherently rewarding or altering locomotion. These data suggest that a social neuronal ensemble within the IL-PFC may contribute to social buffering of fear. These neurons may represent a novel therapeutic target for fear and anxiety disorders.

show abstract

Ventral hippocampal projections to the medial prefrontal cortex regulate social memory

Cited by 160 publications

References 69 publications

Chemogenetic silencing of hippocampus and amygdala reveals a double dissociation in periadolescent obesogenic diet-induced memory alterations

Chemogenetic silencing of hippocampus and amygdala reveals a double dissociation in periadolescent obesogenic diet-induced memory alterations

P2X7 receptor inhibition ameliorates dendritic spine pathology and social behavioral deficits in Rett syndrome mice

Optogenetic reactivation of prefrontal social memory trace mimics social buffering of fear

Contact Info

Product

Resources

About