A Subpopulation of Prefrontal Cortical Neurons Is Required for Social Memory

Xing, Bo; Mack, Nancy R.; Guo, Kaiming; Zhang, Yu-Xiang; Ramirez, Billy; Yang, Sha-Sha; Lin, Li; Wang, Dong V.; Li, Yanchun; Gao, Wen-Jun

doi:10.1016/j.biopsych.2020.08.023

Cited by 53 publications

(40 citation statements)

References 75 publications

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“…We also examined the role of the mPFC PL-NAcSh circuit in social behaviors and found that this circuit is involved in both social preference and recognition. Recently, however, Xing et al (2021) reported that inactivation of NAcSh-projecting PL neurons impairs social recognition without affecting social preference; these findings conflict with our results. Although the reason for this discrepancy is not clear, different experimental conditions, including the dosage of CNO, might be responsible.…”

Section: Discussioncontrasting

confidence: 99%

Social isolation impairs the prefrontal-nucleus accumbens circuit subserving social recognition in mice

et al. 2021

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Section: Discussioncontrasting

confidence: 99%

Social isolation impairs the prefrontal-nucleus accumbens circuit subserving social recognition in mice

et al. 2021

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“…Previous studies have suggested that cortical neurons expressing dopamine D1 receptors contribute to facilitating social behavior 31,32 . In contrast, the activation of prefrontal neurons expressing D2 receptors inhibits social interactions 33 .…”

Section: Resultsmentioning

confidence: 99%

“…In this present study, we were able to determine that the persistence of excessive dopamine in the prefrontal cortex significantly reduced the induction of c‐Fos triggered by a social stimulus in the prefrontal neurons expressing dopamine D1 receptors. A recent study revealed that the selective inhibition of prefrontal neurons expressing c‐Fos induced by a social stimulus impaired social recognition 31 . In addition, these neurons exhibited the morphological and physiological characteristics of neurons expressing D1 receptors 31 .…”

Section: Discussionmentioning

confidence: 99%

The dual role of dopamine in the modulation of information processing in the prefrontal cortex underlying social behavior

et al. 2022

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Dopamine in the prefrontal cortex is essential for the regulation of social behavior. However, stress‐causing social withdrawal also promotes dopamine release in the prefrontal cortex. Thus, this evidence suggests opposite functions of dopamine in the prefrontal cortex. However, the influence of dopamine on prefrontal functions is yet to be fully understood. Here, we show that dopamine differentially modulated the neuronal activity triggered by social stimuli in the prefrontal cortex, depending on the duration of the dopamine activation (transient or sustained activation). Using chemogenetic techniques, we have found that social behavior was negatively regulated by a sustained increase in dopamine neuronal activity in the ventral tegmental area, while it was positively regulated by an acute increase. The duration of social interactions was positively correlated with the transient dopamine release triggered by social stimuli in the prefrontal cortex and negatively correlated with the sustained increase in prefrontal dopamine levels. Furthermore, the elevation of neural calcium signal, triggered by social stimuli, in the prefrontal cortex was attenuated by the persistent elevation of prefrontal dopamine levels, whereas an acute increase in dopamine levels enhanced it. Additionally, the chronic excess of dopamine suppressed c‐Fos induction triggered by social stimuli in prefrontal neurons expressing dopamine D1 receptors, but not D2 receptors. These results suggest that sustained activation of prefrontal dopamine, at the opposite of its transient activation, can reduce prefrontal activity associated with social behavior, even for identical dopamine concentrations. Thus, dopamine plays opposite roles in modulating prefrontal activity depending on the duration of its action.

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“…A vibratome (Leica VT1000S, Germany) was used to cut BLAcontaining coronal brain slices (thickness: 320 µm) in icecold N-methyl-D-glucamine (NMDG)-based cutting solution comprising 93 mM NMDG, 2.5 mM KCl, 30 mM NaHCO 3 , 1.2 mM NaH 2 PO 4 , 20 mM HEPES, 25 mM D-glucose, 2 mM thiourea, 5 mM sodium ascorbate, 3 mM sodium pyruvate, 10 mM MgSO 4 , and 0.5 mM CaCl 2 (Xing et al, 2021). Brain slices were then transferred to a holding chamber containing artificial cerebrospinal fluid (ACSF) composed of 92 mM NaCl, 2.5 mM KCl, 1.2 mM NaH 2 PO 4 , 30 mM NaHCO 3 , 20 mM HEPES, 25 mM D-glucose, 2 mM thiourea, 5 mM sodium ascorbate, 3 mM sodium pyruvate, 2 mM MgSO 4 , and 2 mM CaCl 2 (Feng et al, 2021) to recover for at least 1 h at room temperature before being transferred to a recording chamber continually perfused (∼2 ml/min) with oxygenated ACSF (124 mM NaCl, 2.5 mM KCl, 1.2 mM NaH 2 PO 4 , 24 mM NaHCO 3 , 5 mM HEPES, 12.5 mM D-glucose, 2 mM MgSO 4 , and 2 mM CaCl 2 (Feng et al, 2021).…”

Section: Whole-cell Patch-clamp Recordingsmentioning

confidence: 99%

Deficiency of the CYLD Impairs Fear Memory of Mice and Disrupts Neuronal Activity and Synaptic Transmission in the Basolateral Amygdala

Yang

et al. 2021

Front. Cell. Neurosci.

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Fear learning and memory are crucial for animal survival. Abnormal fear memory is a hallmark of many neuropsychiatric disorders. Appropriate neuronal activation and excitability in the basolateral amygdala (BLA) are necessary for the formation of fear memory. The gene cylindromatosis (Cyld), which encodes a lysine-63 deubiquitinase, is expressed in several brain regions including the amygdala. The functions of the cylindromatosis protein (CYLD) in the regulation of the neuronal activity, neural circuits and fear memory, remain largely unknown, however. Here, we report that Cyld knockout impairs amygdala-dependent tone-cued fear memory. The number of c-Fos+ neurons responding to the tone-cued fear test was reduced in the BLA of Cyld–/– mice, suggesting that the absence of CYLD causes aberrant neuronal activation. We found that this aberrant neuronal activation in the BLA of Cyld–/– mice may relate to the decreased excitability of principal neurons. Another possibility of aberrant neuronal activation could be the impaired excitatory synaptic transmission in the BLA of Cyld–/– mice. Specifically, both the frequency of spontaneous excitatory postsynaptic currents and the amplitude of miniature excitatory postsynaptic currents in BLA principal neurons were decreased. In addition, Cyld mutation caused an increase in both the frequency of miniature inhibitory postsynaptic currents in principal neurons and the number of parvalbumin+ interneurons, consistent with excessive local circuit inhibition in the BLA of Cyld–/– mice. Taken together, these results suggest that CYLD deficiency disrupts the neuronal activity and synaptic transmission in the BLA of mice which may contribute to the impaired fear memory observed in Cyld–/– mice.

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A Subpopulation of Prefrontal Cortical Neurons Is Required for Social Memory

Cited by 53 publications

References 75 publications

Social isolation impairs the prefrontal-nucleus accumbens circuit subserving social recognition in mice

Social isolation impairs the prefrontal-nucleus accumbens circuit subserving social recognition in mice

The dual role of dopamine in the modulation of information processing in the prefrontal cortex underlying social behavior

Deficiency of the CYLD Impairs Fear Memory of Mice and Disrupts Neuronal Activity and Synaptic Transmission in the Basolateral Amygdala

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