The rostroventral part of the thalamic reticular nucleus modulates fear extinction

Lee, Joon-Hyuk; Latchoumane, Charles; Park, Jung-Joon; Kim, Jinhyun; Jeong, Jaeseung; Lee, Kwang-Hyung; Shin, Hee‐Sup

doi:10.1038/s41467-019-12496-9

Cited by 32 publications

(20 citation statements)

References 44 publications

(50 reference statements)

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“…6a ). There is a growing body of evidence suggesting that anterior part of the TRN is implicated in selective attention, fear conditioning, and flight behavior 20 , 22 , 23 , 71 , for which stable wakefulness is a prerequisite. Sensory TRN exhibits strong repetitive burst discharges 24 , 72 , which is essential for generating spindle oscillations and in turn promotes sleep onset 41 , 73 – 75 .…”

Section: Discussionmentioning

confidence: 99%

Microglia modulate stable wakefulness via the thalamic reticular nucleus in mice

et al. 2021

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Microglia are important for brain homeostasis and immunity, but their role in regulating vigilance remains unclear. We employed genetic, physiological, and metabolomic methods to examine microglial involvement in the regulation of wakefulness and sleep. Microglial depletion decreased stable nighttime wakefulness in mice by increasing transitions between wakefulness and non-rapid eye movement (NREM) sleep. Metabolomic analysis revealed that the sleep-wake behavior closely correlated with diurnal variation of the brain ceramide, which disappeared in microglia-depleted mice. Ceramide preferentially influenced microglia in the thalamic reticular nucleus (TRN), and local depletion of TRN microglia produced similar impaired wakefulness. Chemogenetic manipulations of anterior TRN neurons showed that they regulated transitions between wakefulness and NREM sleep. Their firing capacity was suppressed by both microglial depletion and added ceramide. In microglia-depleted mice, activating anterior TRN neurons or inhibiting ceramide production both restored stable wakefulness. These findings demonstrate that microglia can modulate stable wakefulness through anterior TRN neurons via ceramide signaling.

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Section: Discussionmentioning

confidence: 99%

Microglia modulate stable wakefulness via the thalamic reticular nucleus in mice

et al. 2021

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“…Briefly, the electrode was advanced slowly into the rostral reticular thalamus, guided by coordinates from the Franklin and Paxinos mouse brain atlas : −0.5 to −0.8 mm anteroposterior (AP) relative to Bregma, 0.8–1.2 mm mediolateral relative to the midline, 2.7–4 mm dorsoventral, relative to the dura mater ( Franklin, 2008 ). These coordinates were chosen to target the rostral part of the reticular thalamus ( Lee et al, 2019 ), which represents the limbic part of the reticular thalamus. This specific region receives projections from the striatum and medial prefrontal cortex (mPFC) ( Cornwall et al, 1990 ; Zikopoulos and Barbas, 2006 ), projects to the rostral mediodorsal thalamus ( Groenewegen, 1988 ), and in turn receives axon collaterals from the same thalamocortical nuclei that it inhibits ( Pinault and Deschênes, 1998 ).…”

Section: Methodsmentioning

confidence: 99%

Lysergic acid diethylamide differentially modulates the reticular thalamus, mediodorsal thalamus, and infralimbic prefrontal cortex: An in vivo electrophysiology study in male mice

et al. 2021

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Background: The reticular thalamus gates thalamocortical information flow via finely tuned inhibition of thalamocortical cells in the mediodorsal thalamus. Brain imaging studies in humans show that the psychedelic lysergic acid diethylamide (LSD) modulates activity and connectivity within the cortico-striato-thalamo-cortical (CSTC) circuit, altering consciousness. However, the electrophysiological effects of LSD on the neurons in these brain areas remain elusive. Methods: We employed in vivo extracellular single-unit recordings in anesthetized adult male mice to investigate the dose–response effects of cumulative LSD doses (5–160 µg/kg, intraperitoneal) upon reticular thalamus GABAergic neurons, thalamocortical relay neurons of the mediodorsal thalamus, and pyramidal neurons of the infralimbic prefrontal cortex. Results: LSD decreased spontaneous firing and burst-firing activity in 50% of the recorded reticular thalamus neurons in a dose–response fashion starting at 10 µg/kg. Another population of neurons (50%) increased firing and burst-firing activity starting at 40 µg/kg. This modulation was accompanied by an increase in firing and burst-firing activity of thalamocortical neurons in the mediodorsal thalamus. On the contrary, LSD excited infralimbic prefrontal cortex pyramidal neurons only at the highest dose tested (160 µg/kg). The dopamine D2 receptor (D2) antagonist haloperidol administered after LSD increased burst-firing activity in the reticular thalamus neurons inhibited by LSD, decreased firing and burst-firing activity in the mediodorsal thalamus, and showed a trend towards further increasing the firing activity of neurons of the infralimbic prefrontal cortex. Conclusion: LSD modulates firing and burst-firing activity of reticular thalamus neurons and disinhibits mediodorsal thalamus relay neurons at least partially in a D2-mediated fashion. These effects of LSD on thalamocortical gating could explain its consciousness-altering effects in humans.

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“…Fear extinction is a process involving progressive suppression of the salience of fear-associative cue or context. Manipulations of thalamic activities have been shown to bidirectionally modulate fear extinction ( Padilla-Coreano et al, 2012 ; Matyas et al, 2014 ; Paydar et al, 2014 ; Do-Monte et al, 2015 ; Lee et al, 2019 ; Ramanathan and Maren, 2019 ). Thalamic neurons exhibit two firing modes, tonic and burst, which could modulate behaviors in opposite directions ( Sherman, 2001 ).…”

Section: Connectivity Profiles Of Thalamic Nucleimentioning

confidence: 99%

The Contribution of Thalamic Nuclei in Salience Processing

Zhou

Zhu

Hou

et al. 2021

Front. Behav. Neurosci.

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The brain continuously receives diverse information about the external environment and changes in the homeostatic state. The attribution of salience determines which stimuli capture attention and, therefore, plays an essential role in regulating emotions and guiding behaviors. Although the thalamus is included in the salience network, the neural mechanism of how the thalamus contributes to salience processing remains elusive. In this mini-review, we will focus on recent advances in understanding the specific roles of distinct thalamic nuclei in salience processing. We will summarize the functional connections between thalamus nuclei and other key nodes in the salience network. We will highlight the convergence of neural circuits involved in reward and pain processing, arousal, and attention control in thalamic structures. We will discuss how thalamic activities represent salience information in associative learning and how thalamic neurons modulate adaptive behaviors. Lastly, we will review recent studies which investigate the contribution of thalamic dysfunction to aberrant salience processing in neuropsychiatric disorders, such as drug addiction, posttraumatic stress disorder (PTSD), and schizophrenia. Based on emerging evidence from both human and rodent research, we propose that the thalamus, different from previous studies that as an information relay, has a broader role in coordinating the cognitive process and regulating emotions.

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The rostroventral part of the thalamic reticular nucleus modulates fear extinction

Cited by 32 publications

References 44 publications

Microglia modulate stable wakefulness via the thalamic reticular nucleus in mice

Microglia modulate stable wakefulness via the thalamic reticular nucleus in mice

Lysergic acid diethylamide differentially modulates the reticular thalamus, mediodorsal thalamus, and infralimbic prefrontal cortex: An in vivo electrophysiology study in male mice

The Contribution of Thalamic Nuclei in Salience Processing

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