Abstract
Fear learning occurs in response to positive prediction error, when the expected outcome of a conditioning trial exceeds that predicted by the conditioned stimuli present. This role for error in Pavlovian association formation is best exemplified by the phenomenon of associative blocking, whereby prior fear conditioning of conditioned stimulus (CS) A is able to prevent learning to CSB when they are conditioned in compound. The midline and intralaminar thalamic nuclei (MIT) are well-placed to contribute to fear prediction error because they receive extensive projections from the midbrain periaqueductal gray—which has a key role in fear prediction error—and project extensively to prefrontal cortex and amygdala. Here we used an associative blocking design to study the role of MIT in fear learning. In Stage I rats were trained to fear CSA via pairings with shock. In Stage II rats received compound fear conditioning of CSAB paired with shock. On test, rats that received Stage I training expressed less fear to CSB relative to control rats that did not receive this training. Microinjection of bupivacaine into MIT prior to Stage II training had no effect on the expression of fear during Stage II and had no effect on fear learning in controls, but prevented associative blocking and so enabled fear learning to CSB. These results show an important role for MIT in predictive fear learning and are discussed with reference to previous findings implicating the midline and posterior intralaminar thalamus in fear learning and fear responding.
Highlights
Pavlovian fear conditioning involves the learning of predictive relationships between a conditioned stimulus (CS) and an aversive unconditioned stimulus (US)
Data from 5 rats were excluded because placements were lateral from the midline region, bordering on the mediodorsal thalamus and the habenular complex
Here we studied the role of midline and intralaminar thalamic nuclei (MIT) in the associative blocking of Pavlovian fear conditioning
Summary
Pavlovian fear conditioning involves the learning of predictive relationships between a conditioned stimulus (CS) and an aversive unconditioned stimulus (US). Principal cells of lateral and basolateral nuclei (BLA) receive glutamatergic inputs from thalamus and cortex conveying information about the CS and US (Sah et al, 2008, 2003; Marek et al, 2013). These neurons form fear memories in an NMDA receptor-dependent manner (Schafe et al, 2001; Maren and Quirk, 2004). CeAl output neurons tonically inhibit brainstem projecting-CeAm neurons and removal of this inhibition activates CeAm neurons causing fear expression (Ciocchi et al, 2010; Haubensak et al, 2010; Li et al, 2013)
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