Comparison of (stereotactic) parcellations in mouse prefrontal cortex

Werd, Henri J. J. M. Van De; Uylings, H.B.M.

doi:10.1007/s00429-013-0630-7

Cited by 50 publications

(35 citation statements)

References 29 publications

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“…As with our first study, visible NR1 deletions were detected within the rostrocaudal extent of the mPFC corresponding to ~1.9 to 2.6 mm anterior to bregma, with predominant involvement of the AC/PL subregions (Paxinos, 2001; Van De Werd and Uylings, 2014), and a rostrocaudal area of hippocampus corresponding to ~1.7 to 2.5 mm posterior to bregma, with predominant involvement of the dorsal CA3 subregion (Paxinos, 2001). Only social interaction data from mice with bilateral mPFC or CA3 NR1-deletions were included in the final results.…”

Section: Resultssupporting

confidence: 76%

“…mPFC NR1-deletions were readily visualized spanning a rostrocaudal area corresponding to ~1.9-2.6 mm anterior to bregma, involving predominantly the AC/PL subregions of the mPFC (Paxinos, 2001; Van De Werd and Uylings, 2014). Hippocampal NR1-deletions spanned a rostrocaudal area corresponding to ~1.7-2.5 mm posterior to bregma, involving predominantly the dorsal CA3 subregion of the hippocampus (Paxinos, 2001).…”

Section: Resultsmentioning

confidence: 99%

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Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

et al. 2015

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Glutamate N-methyl-D-aspartate receptors (NMDARs) in the medial prefrontal cortex (mPFC) and hippocampus may play an integral role in complex cognitive and social deficits associated with a number of psychiatric illnesses including autism, mood disorders, and schizophrenia. We used localized infusions of adeno-associated virus Cre-recombinase in adult, targeted knock-in mice with loxP sites flanking exons 11-22 of the NR1 gene, to investigate the effects of chronic NMDAR dysfunction in the mPFC and CA3 hippocampus on cognitive and social behavior. A 5-choice serial reaction time task (5-CSRTT) was used to monitor aspects of cognitive function that included attention and response inhibition. Social behavior was assessed using Crowley's sociability and preference for social novelty protocol. Chronic NMDAR dysfunction localized to the anterior cingulate/prelimbic mPFC or dorsal CA3 hippocampus differentially affected response inhibition and social interaction. mPFC NR1-deletion increased perseverative responding in the 5-CSRTT and enhanced preference for social novelty, whereas CA3 NR1-deletion increased premature responding in the 5-CSRTT and decreased social approach behavior. These findings suggest that mPFC and CA3 NMDARs may play selective roles in regulating compulsive and impulsive behavior, respectively. Furthermore, these findings are consistent with emerging evidence that these behaviors are mediated by distinct, albeit overlapping, neural circuits. Our data also suggest that NMDARs in these regions uniquely contribute to the expression of normal social behavior. In this case, mPFC and CA3 NMDARs appear to inhibit and facilitate aspects of social interaction, respectively. The latter dissociation raises the possibility that distinct circuits contribute to the expression of social intrusiveness and impoverished social interaction.

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Section: Resultssupporting

confidence: 76%

Section: Resultsmentioning

confidence: 99%

Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

et al. 2015

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“…As a neocortical structure, the mPFC is organized into six layers (I -VI) containing a majority of excitatory pyramidal neurons and a diverse array of inhibitory interneurons 99 . The mPFC can be parsed into distinct subregions based upon their cytoarchitecture, which are consistent with divergent functions among these regions 100 . The primary subdivisions of the mPFC in rodents include the prelimbic (PL) and infralimbic (IL) cortices.…”

Section: Evaluation Of Threat: Regulation Of Interpretationmentioning

confidence: 63%

Resolving the neural circuits of anxiety

2015

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Although anxiety disorders represent a major societal problem demanding new therapeutic targets, these efforts have languished in the absence of a mechanistic understanding of this subjective emotional state. While it is impossible to know with absolute certainty the subjective experience of a rodent, rodent models hold promise in dissecting wellconserved limbic circuits. The application of modern approaches in neuroscience has already begun to unmask the neural circuit intricacies underlying anxiety by allowing direct examination of hypotheses drawn from existing psychological concepts. This information points toward an updated conceptual model for what neural circuit perturbations could give rise to pathological anxiety, and thereby provides a roadmap for future therapeutic development.3

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“…There have been lots of efforts to resolve conflicts/confusions regarding regionalization in the rodent PFC (Van De Werd and Uylings, 2014; Vogt and Paxinos, 2014; Watson et al, 2011). The rodent PFC is located over the medial, orbital, and insular surfaces of the rostral cerebral hemispheres and consists of two major frontal areas with which the MD nuclei have connections.…”

Section: Neurobiological Framework For Cognitive Function: Pfcmentioning

confidence: 99%

Converging models of schizophrenia – Network alterations of prefrontal cortex underlying cognitive impairments

Sakurai

Gamo

Hikida

et al. 2015

Progress in Neurobiology

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The prefrontal cortex (PFC) and its connections with other brain areas are crucial for cognitive function. Cognitive impairments are one of the core symptoms associated with schizophrenia, and manifest even before the onset of the disorder. Altered neural networks involving PFC contribute to cognitive impairments in schizophrenia. Both genetic and environmental risk factors affect the development of the local circuitry within PFC as well as development of broader brain networks, and make the system vulnerable to further insults during adolescence, leading to the onset of the disorder in young adulthood. Since spared cognitive functions correlate with functional outcome and prognosis, a better understanding of the mechanisms underlying cognitive impairments will have important implications for novel therapeutics for schizophrenia focusing on cognitive functions. Multidisciplinary approaches, from basic neuroscience to clinical studies, are required to link molecules, circuitry, networks, and behavioral phenotypes. Close interactions among such fields by sharing a common language on connectomes, behavioral readouts, and other concepts are crucial for this goal.

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Comparison of (stereotactic) parcellations in mouse prefrontal cortex

Cited by 50 publications

References 29 publications

Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

Effects of prefrontal cortex and hippocampal NMDA NR1-subunit deletion on complex cognitive and social behaviors

Resolving the neural circuits of anxiety

Converging models of schizophrenia – Network alterations of prefrontal cortex underlying cognitive impairments

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