Abstract
It has been shown that applying transcranial direct current stimulation (tDCS) over the dorsolateral prefrontal cortex (DLPFC) influences declarative memory processes. This study investigates the efficacy of tDCS on emotional memory consolidation, especially experimental fear conditioning. We applied an auditory fear-conditioning paradigm, in which two differently colored squares (blue and yellow) were presented as conditioned stimuli (CS) and an auditory stimulus as unconditioned stimulus (UCS). Sixty-nine participants were randomly assigned into three groups: anodal, cathodal, and sham stimulation. The participants of the two active groups (i.e., anodal and cathodal) received tDCS over the left DLPFC for 12 min after fear conditioning. The effect of fear conditioning and consolidation (24 h later) was measured by assessing the skin conductance response (SCR) to the CS. The results provide evidence that cathodal stimulation of the left DLPFC leads to an inhibitory effect on fear memory consolidation compared to anodal and sham stimulation, as indicated by decreased SCRs to CS+ presentation during extinction training at day 2. In conclusion, current work suggests that cathodal stimulation interferes with processes of fear memory consolidation.
Highlights
Exaggerated fear is the root cause of the fear memory persistence, which further leads to the development of anxiety disorder [1, 2]
The results show that cathodal, but not anodal stimulation disrupts fear memory consolidation
Improvement in memory was due to anodal stimulation of the dorsolateral prefrontal cortex (DLPFC)
Summary
Exaggerated fear is the root cause of the fear memory persistence, which further leads to the development of anxiety disorder [1, 2]. A preponderance of neurobiological data from the past decades demonstrates that consolidation processes is responsible for making fear memories robust. Studies investigating the neurobiological nature of memory consolidation showed that memory consolidation is dependent on the interaction of neurons and their synapses [3,4,5]. Synaptic consolidation of memory highlights that synaptic plasticity plays an important role in learning and memory processes [4]. Research on learning and memory shows that the mechanism of synaptic plasticity depends upon several factors such as (i) initially activated neural circuit, (ii) release of second messengers, i.e., cyclic AMP (cAMP) and protein-kinase A (PKA), (iii) pre- and post-generated proteins, and (iv) the regulation of genes [4, 5]
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