Figure 4 - uploaded by Barbara B. Oswald
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Histology: Sample photomicrograph of a coronal section of rabbit brain with double-barreled bilateral infusion cannulas implanted, directed at infralimbic cortex (IL). Arrows indicate terminal ends of cannulas, and this representative slice indicates the most dorsal infusion points (i.e., those closest to PL). Muscimol or vehicle infusions would be expected to diffuse approximately 1 to 2 mm from these points. See the online article for the color version of this figure.
Source publication
This study assessed the effects of reversible lesions with microinfusions of the GABAA agonist muscimol (MUSC) to infralimbic cortex (IL; Brodmann’s area 25) of the medial prefrontal cortex (mPFC) on trace eyeblink conditioning and extinction in rabbits (Oryctolagus cuniculus). Four groups were tested: rabbits receiving MUSC infusions 5 min before...
Context in source publication
Context 1
... the remaining 27 animals (n 5 VEH/VEH, 8 MUSC/MUSC, 6 MUSC/VEH, 8 VEH/MUSC) both barrels of each bilateral cannulas were directed at IL (Brodmann's area 25, as described by Vogt, Sikes, Swadlow, & Weyand, 1986; see Figure 3). Histological analyses revealed virtually no cell loss due to tissue displacement caused by repeated infusions of MUSC or VEH; see Figure 4. ...
Citations
... Similarly, enhancing IL, but not PL, activity during tone-shock extinction training facilitates extinction acquisition and consolidation (Do-Monte et al., 2015;Thompson et al., 2010) and enhancing IL activity immediately following tone-shock extinction training facilitates consolidation (Do-Monte et al., 2010Thompson et al., 2010). Additionally, evidence supports that the IL is important for extinction learning when the CS and US are separated by a trace interval, as chemogenetic IL inhibition impairs the extinction of trace fear conditioning (Mukherjee and Caroni, 2018), and pharmacological IL inhibition via GABA A agonism impairs the extinction of trace eyeblink conditioning (Oswald et al., 2015). Taken together, a large body of evidence supports that IL activity is important for the extinction of learned associations with footshock stimuli. ...
NETT, K.E., and R.T. LaLumiere. Infralimbic cortex functioning across motivated behaviors: Can the differences be reconciled? NEUROSCI BIOBEHAV REV 21(1) XXX-XXX, 2021.-The rodent infralimbic cortex (IL) is implicated in higher order executive functions such as reward seeking and flexible decision making. However, the precise nature of its role in these processes is unclear. Early evidence indicated that the IL promotes the extinction and ongoing inhibition of fear conditioning and cocaine seeking. However, evidence spanning other behavioral domains, such as natural reward seeking and habit-based learning, suggests a more nuanced understanding of IL function. As techniques have advanced and more studies have examined IL function, identifying a unifying explanation for its behavioral function has become increasingly difficult. Here, we discuss evidence of IL function across motivated behaviors, including associative learning, drug seeking, natural reward seeking, and goal-directed versus habit-based behaviors, and emphasize how context-specific encoding and heterogeneous IL neuronal populations may underlie seemingly conflicting findings in the literature. Together, the evidence suggests that a major IL function is to facilitate the encoding and updating of contingencies between cues and behaviors to guide subsequent behaviors.
... The rodent infralimbic (IL) subregion of the medial prefrontal cortex has been shown to modulate the specificity and generalization attributes of cued and contextual fear memories at the acquisition stage: pre-training damage to the IL 11 or inactivation of both IL and prelimbic (PL) 12 was sufficient to produce memory overgeneralization. Similarly, lesioning or inactivating the IL before cued or contextual fear memory acquisition induced a relative resistance to extinction 11,13,14 . The IL has also been associated with aversive memory consolidation. ...
... Animals in which the IL was inactivated during consolidation extinguished similarly to controls within the session but were unable to recall the extinction memory the following day. This result is in line with that found when the IL was lesioned or inactivated before cued and contextual fear memory acquisition [12][13][14] , suggesting that the IL controls the formation of extinction-sensitive fear memories at both stages. Of note, activity in the IL similarly has a role not only after consolidation, in maintaining extinction-sensitive fear memories 47 , but also during their extinction acquisition and consolidation [48][49][50] . ...
Lesioning or inactivating the infralimbic (IL) subregion of the medial prefrontal cortex before acquisition produces more generalized and extinction-resistant fear memories. However, whether and how it modulates memory specificity and extinction susceptibility while consolidation takes place is still unknown. The present study aims to investigate these questions using muscimol-induced temporary inactivation and anisomycin-induced protein synthesis inhibition in the rat IL following contextual fear conditioning. Results indicate that the IL activity immediately after acquisition, but not six hours later, controls memory generalization over a week, regardless of its strength. Such IL function depends on the context-shock pairing since muscimol induced no changes in animals exposed to immediate shocks or the conditioning context only. Animals in which the IL was inactivated during consolidation extinguished similarly to controls within the session but were unable to recall the extinction memory the following day. Noteworthy, these post-acquisition IL inactivation-induced effects were not associated with changes in anxiety, as assessed in the elevated plus-maze test. Anisomycin results indicate that the IL protein synthesis during consolidation contributes more to producing extinction-sensitive fear memories than memory specificity. Collectively, present results provide evidence for the IL's role in controlling generalization and susceptibility to extinction during fear memory consolidation.
