Ventromedial prefrontal cortex

Summary

The ventromedial prefrontal cortex (vmPFC) is a part of the prefrontal cortex in the mammalian brain. The ventral medial prefrontal is located in the frontal lobe at the bottom of the cerebral hemispheres and is implicated in the processing of risk and fear, as it is critical in the regulation of amygdala activity in humans. It also plays a role in the inhibition of emotional responses, and in the process of decision-making and self-control. It is also involved in the cognitive evaluation of morality. While the ventromedial prefrontal cortex does not have a universally agreed on demarcation, in most sources, it is equivalent to the ventromedial reward network of Öngür and Price. This network includes Brodmann area 10, Brodmann area 14, Brodmann area 25, and Brodmann area 32, as well as portions of Brodmann area 11, Brodmann area 12, and Brodmann area 13. However, not all sources agree on the boundaries of the area. Different researchers use the term ventromedial prefrontal cortex differently. Sometimes, the term is saved for the area above the medial orbitofrontal cortex, while at other times, 'ventromedial prefrontal cortex' is used to describe a broad area in the lower (ventral) central (medial) region of the prefrontal cortex, of which the medial orbitofrontal cortex constitutes the lowermost part. This latter, broader area, corresponds to the area damaged in patients with decision-making impairments investigated by António Damásio and colleagues (see diagram, and below). The ventromedial prefrontal cortex is connected to and receives input from the ventral tegmental area, amygdala, the temporal lobe, the olfactory system, and the dorsomedial thalamus. It, in turn, sends signals to many different brain regions including; The temporal lobe, amygdala, the lateral hypothalamus, the hippocampal formation, the cingulate cortex, and certain other regions of the prefrontal cortex. This huge network of connections affords the vmPFC the ability to receive and monitor large amounts of sensory data and to affect and influence a plethora of other brain regions, particularly the amygdala.

Official source

https://en.wikipedia.org/wiki/Ventromedial_prefrontal_cortex

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Where does the engram come from? Study of prefrontal cortex inputs during memory consolidation

Lucie Pauline Dixsaut

The formation and storage of memories has been under deep investigation for several decades. Nevertheless, the precise contribution of each brain region involved in this process and the interplay between them across memory consolidation is still largely debated. Although memory encoding requires the hippocampus (HPC), it is becoming apparent that other brain regions are also important in early phases of memory formation, such as the medial prefrontal cortex (mPFC). In addition, engram cells have been found in the mPFC at memory encoding: these cells represent a close approximation of the "memory trace" insofar as they are activated at the time of learning, as they undergo enduring molecular modifications after learning, and as their reactivation drives memory recall. In contrast to HPC engram cells, mPFC engram cells are thought to be kept silent during a recent recall and until the memory is fully consolidated, becoming active only at remote recall. To explain the dynamics of these mPFC engram cells, we hypothesized that inputs to the mPFC could be differentially activated over the course of memory consolidation.We first determined that the prelimbic cortex (PL), a subregion of the mPFC, was specifically activated during the encoding phase of a fear memory in mice by measuring the expression of the Immediate Early Gene cFos, transcribed upon neuronal activation. We then traced the inputs of PL cells that were active during encoding, the putative PL engram cells, in order screen for relevant connections for further investigations. To achieve this, we used an activity-dependent monosynaptic retrograde tracing method based on rabies tracing. Then, to determine the activation patterns of these specific PL inputs, we measured their activity throughout consolidation of a contextual fear memory using an unbiased retrograde tracer coupled with cFos immunostaining. We further tested their functional relevance by chemogenetically inhibiting these projections during the different learning phases. This approach confirmed the roles of the Entorhinal Cortex and the Basolateral Amygdala inputs during the encoding phase of a fear memory to later recall remote memories. In addition, we found that the Claustrum (CLA) to PL projection was also required during the encoding phase, but to recall recent memories specifically. Moreover, the Insular Cortex (INS) to PL projection was necessary during recent recall. Eventually, we observed that the CLA and INS manipulations led to a modification of PL engram cells reactivation during recent recall.Overall, our results suggest that there is a functional shift in PL inputs during the course of memory consolidation, which is also impacting how PL engram cells are reactivated. In addition, we observed that the activity of PL inputs is part of a broader brain network, both through the presence of axon collaterals targeting other brain regions and by the existence of parallel and perhaps redundant pathways that could ensure efficient memory consolidation.Collectively, our data help to further refine the working model of memory formation by deciphering the interplay between brain regions during the process of systems consolidation of a fear memory, and open several questions for future investigations.

EPFL2022

Context effects on probability estimation

Wei-Hsiang Lin

Many decisions rely on how we evaluate potential outcomes and estimate their corresponding probabilities of occurrence. Outcome evaluation is subjective because it requires consulting internal preferences and is sensitive to context. In contrast, probability estimation requires extracting statistics from the environment and therefore imposes unique challenges to the decision maker. Here, we show that probability estimation, like outcome evaluation, is subject to context effects that bias probability estimates away from other events present in the same context. However, unlike valuation, these context effects appeared to be scaled by estimated uncertainty, which is largest at intermediate probabilities. Blood-oxygen-level-dependent (BOLD) imaging showed that patterns of multivoxel activity in the dorsal anterior cingulate cortex (dACC), ventromedial prefrontal cortex (VMPFC), and intraparietal sulcus (IPS) predicted individual differences in context effects on probability estimates. These results establish VMPFC as the neurocomputational substrate shared between valuation and probability estimation and highlight the additional involvement of dACC and IPS that can be uniquely attributed to probability estimation. Because probability estimation is a required component of computational accounts from sensory inference to higher cognition, the context effects found here may affect a wide array of cognitive computations.

PUBLIC LIBRARY SCIENCE2020

Tourette syndrome is characterized by 'unvoluntary' tics, which are compulsive, yet often temporarily suppressible. The inferior frontal gyms is implicated in motor control, including inhibition of pre-potent actions through influences on downstream subcortical and motor regions. Although tic suppression in Tourette syndrome also engages the inferior frontal gyrus, it is unclear whether such prefrontal control of action is also dysfunctional: Tic suppression studies do not permit comparison with control groups, and neuroimaging studies of motor inhibition can be confounded by the concurrent expression or suppression of tics. Here, patients with Tourette syndrome were directly compared to control participants when performing an intentional inhibition task during functional MRL Tic expression was recorded throughout for removal from statistical models. Participants were instructed to make a button press in response to Go cues, withhold responses to NoGo cues, and decide whether to press or withhold to 'Choose' cues. Overall performance was similar between groups, for both intentional inhibition rates (% Choose-Go) and reactive NoGo inhibition commission errors. A subliminal face prime elicited no additional effects on intentional or reactive inhibition. Across participants, the task activated prefrontal and motor cortices and subcortical nuclei, including pre-supplementary motor area, inferior frontal gyrus, insula, caudate nucleus, thalamus and primary motor cortex. In Tourette syndrome, activity was elevated in the inferior frontal gyrus, insula and basal ganglia, most notably within the right inferior frontal gyrus during voluntary action and inhibition (Choose-Go and Choose-NoGo), and reactive inhibition (NoGo-correct). Anatomically, the locus of this inferior frontal gyrus hyperactivation during control of voluntary action matched that previously reported for tic suppression. In Tourette syndrome, activity within the caudate nucleus was also enhanced during both intentional (Choose-NoGo) and reactive (NoGo-correct) inhibition. Strikingly, despite the absence of overt motor behaviour, primary motor cortex activity increased in patients with Tourette syndrome but decreased in controls during both reactive and intentional inhibition. Additionally, severity of premonitory sensations scaled with functional connectivity of the pre-supplementary motor area to the caudate nucleus, globus pallidus and thalamus when choosing to respond (Choose-Go). Together, these results suggest that patients with Tourette syndrome use equivalent prefrontal mechanisms to suppress tics and withhold non-tic actions, but require greater inferior frontal gyrus engagement than controls to overcome motor drive from hyperactive downstream regions, notably primary motor cortex. Moreover, premonitory sensations may cue midline motor regions to generate tics through interactions with the basal ganglia.

OXFORD UNIV PRESS2020