Prefrontal somatostatin interneurons encode fear memory

Abstract

Theories stipulate that memories are encoded within networks of cortical projection neurons (PNs). Conversely, GABAergic interneurons (INs) are thought to function primarily to inhibit PNs and thereby impose network gain control, an important but purely modulatory role. Here we show in male mice that associative fear learning potentiates synaptic transmission and cue-specific activity of medial prefrontal cortex (mPFC) somatostatin interneurons (SST-INs), and that activation of these cells controls both memory encoding and expression. Furthermore, the synaptic organization of SST-and parvalbumin (PV)-INs provides a potential circuit basis for SST-INevoked disinhibition of mPFC output neurons and recruitment of remote brain regions associated with defensive behavior. These data suggest that rather than constrain mnemonic processing, potentiation of SST-IN activity represents an important causal mechanism for conditioned fear.

Sleep deprivation triggers somatostatin neurons in prefrontal cortex to initiate nesting and sleep via the preoptic and lateral hypothalamus

“…As to be expected, the SOM cells within the PFC are involved in many functions; for example, some PFC SOM cells contribute to reading emotions (affective state discrimination) 52 , others encode fear memories 53 ; and locally opto-activating neocortical NOS1 and SOM cells increases cerebral blood flow 54,55 . The c-fosdependent activity-tagging technique allows the SOM/GABA cells that become activated by sleep deprivation to be highlighted from the other functions that these cells carry out.…”

Learning-induced plasticity in the barrel cortex is disrupted by inhibition of layer 4 somatostatin-containing interneurons

“…Increasing L4 SOM-IN activity may decrease the activity of PV-INs, resulting in increased activity of excitatory neurons (Xu et al, 2013), and increased SOM-IN activity during learning has been reported earlier (Cummings and Clem, 2020;Cybulska-Klosowicz et al, 2013b).…”

A Computational Model Integrating Multiple Phenomena on Cued Fear Conditioning, Extinction, and Reinstatement

“…Even in the absence of the brake, CeM is not active without an input from BA. BA receives afferent connections from LA and projects to the PL, the IL, and CeM (Courtin et al, 2014 ; Senn et al, 2014 ; Asede et al, 2015 ; McGarry and Carter, 2016 ; Cummings and Clem, 2020 ). The PL and IL, in turn, project back to BA (Vertes, 2004 ; Cho et al, 2013 ; Courtin et al, 2014 ).…”

“…The PL and IL receive afferent connections from BA and project back to it (Vertes, 2004 ; Cho et al, 2013 ; Courtin et al, 2014 ; Bloodgood et al, 2018 ). To do this, the inhibitory control of parvalbumin interneurons of the mPFC, respectively the units PLpv in the PL and ILpv in the IL, must be removed through the activation of somatostatin interneurons, respectively PLs and ILs (Courtin et al, 2014 ; McGarry and Carter, 2016 ; Lucas and Clem, 2018 ; Cummings and Clem, 2020 ).…”