Medial prefrontal cortex circuit function during retrieval and extinction of associative learning under anesthesia.
Associative learning is encoded under anesthesia and involves the medial prefrontal cortex (mPFC). Neuronal activity in mPFC increases in response to a conditioned stimulus (CS+) previously paired with an unconditioned stimulus (US) but not during presentation of an unpaired stimulus (CS-) in anesthetized animals. Studies in conscious animals have shown dissociable roles for different mPFC subregions in mediating various memory processes, with the prelimbic (PL) and infralimbic (IL) cortex involved in the retrieval and extinction of conditioned responding, respectively. Therefore PL and IL may also play different roles in mediating the retrieval and extinction of discrimination learning under anesthesia. Here we used in vivo electrophysiology to examine unit and local field potential (LFP) activity in PL and IL before and after auditory discrimination learning and during later retrieval and extinction testing in anesthetized rats. Animals received repeated presentations of two distinct sounds, one of which was paired with footshock (US). In separate control experiments animals received footshocks without sounds. After discrimination learning the paired (CS+) and unpaired (CS-) sounds were repeatedly presented alone. We found increased unit firing and LFP power in PL and, to a lesser extent, IL after discrimination learning but not after footshocks alone. After discrimination learning, unit firing and LFP power increased in PL and IL in response to presentation of the first CS+, compared to the first CS-. However, PL and IL activity increased during the last CS- presentation, such that activity during presentation of the last CS+ and CS- did not differ. These results confirm previous findings and extend them by showing that increased PL and IL activity result from encoding of the CS+/US association rather than US presentation. They also suggest that extinction may occur under anesthesia and might be represented at the neural level in PL and IL.
School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK. Electronic address: stxgf@exmail.nottingham.ac.uk.
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GE
Fenton
Department of Electronics, University of York, Heslington, York YO10 5DD, UK. Electronic address: david.halliday@york.ac.uk.
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DM
Halliday
School of Life Sciences, University of Nottingham, Queen's Medical Centre, Nottingham NG7 2UH, UK. Electronic address: rob.mason@nottingham.ac.uk.
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Mason
School of Biosciences, University of Nottingham, Sutton Bonington Campus, Loughborough LE12 5RD, UK. Electronic address: carl.stevenson@nottingham.ac.uk.
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CW
Stevenson
D000161:Acoustic Stimulation; D000758:Anesthesia; D000818:Animals; D001245:Association Learning / Q000187:drug effects / Q000502:physiology; D004193:Discrimination Learning; D005108:Extinction, Psychological / Q000187:drug effects / Q000502:physiology; D007858:Learning / Q000187:drug effects* / Q000502:physiology; D008297:Male; D011939:Mental Recall / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects* / Q000502:physiology; D017397:Prefrontal Cortex / Q000187:drug effects* / Q000502:physiology; D051381:Rats
discrimination learning; extinction; in vivo electrophysiology; infralimbic; prelimbic; retrieval