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Fig. 1 The bidirectional modulation of fear extinction by thalamic dual firing (tonic and burst) in MD.
This review will briefly describe neural mechanisms of fear extinction and highlight the role of MD in modulation of fear extinction.
An experiment combining genetics, pharmacology, physiology, and microstimulation revealed a role for the MD in extinction learning, especially suggesting that the firing mode of the MD is critical in modulation of fear extinction (Lee et al., 2012).
Despite the fact that tDCS has been used for the enhancement of memory and cognition, very few animal studies have addressed its impact on the modulation of fear memory.
However, a recent study reported that 10 minutes of social interaction with recently fear conditioned rats in the home cage enhanced the naïve partner rats' subsequent fear conditioning, suggesting that social transfer or modulation of fear transpired during brief social interaction [41]; see also [42].
The effects are relevant to endogenous TRPC5-containing channels, for example in S1P modulation of vascular smooth muscle cell migration [8] and cholecystokinin modulation of fear responses in the amygdala [7].
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These results provide initial evidence to support the timely use of tDCS for the modulation of fear-related memories.
Consistent with the modulation of fear-evoked plasticity in the LA, suppression of dopamine signaling attenuates acquisition of conditioned fear memory (Borowski and Kokkinidis, 1996; Lamont and Kokkinidis, 1998; Guarraci et al., 1999, 2000; Greba et al., 2001) and fear memory expression (Nader and LeDoux, 1999).
Research has also implicated glucocorticoids in modulation of extinction of fear memories.
The right amygdala parametric modulation of the upright fear > neutral responses during this time window peaked in vicinity to P4 (Z = 2.62, P = 0.004), while the parametric modulation due to left amygdala pathology peaked in vicinity to P8 (Z = 1.75, P = 0.04).
Our findings showed that stress-related placebo treatment in patients was accompanied by significantly increased fear-induced modulation of left fusiform gyrus→amygdala and right amygdala→OFC connectivity.
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