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. 2014 Sep 8;8:160. doi: 10.3389/fnsys.2014.00160

Table 1.

The behavioral effects associated with changes in neuronal activity in anterior cingulate (AC), prelimbic (PL), and infralimbic (IL) sub-regions of medial prefrontal cortex (mPFC) in tasks measuring serial reaction time, latent inhibition, trace conditioning and object recognition, as well as related benchmark tests of learning and memory (for which the effects of similar interventions in different mPFC sub-regions have been examined).

Behavioral test Lesion, drug, neuronal activity mPFC sub-region
AC PL IL
Serial reaction time Excitotoxic lesion Reduced accuracy, increased latencies to collect reward, increased omissions (Passetti et al., 2002; note lesion centered on Cg1) Increased perseverative responding, transient effect on accuracy (Passetti et al., 2002; note lesion included PL and IL) Increased perseverative responding, transient effect on accuracy (Passetti et al., 2002; note lesion included PL and IL)
Reduced accuracy and decreased impulsive responding (Chudasama et al., 2003, 2012; note lesion included PL and IL) Reduced accuracy, slower response latencies, increased omissions and premature responses (Pezze et al., 2009; note lesion included PL and IL) Increased impulsive responding (Chudasama et al., 2003, 2012)
Single unit recording Neuronal responses higher when accurately responding to cue, lower before an incorrect response and increased after an incorrect response (Totah et al., 2009) Neuronal responses higher when accurately responding to cue, lower before an incorrect response, but no significant change after an incorrect response (Totah et al., 2009)
Reversible inactivation Lower dose muscimol increased premature responding (Paine et al., 2011; note injection coordinates included IL) Muscimol increased the number of premature responses (Murphy et al., 2012)
Higher dose muscimol decreased accuracy and impulsive responding (Pezze et al., 2014) and increased omissions (Murphy et al., 2012; Pezze et al., 2014)
Disinhibition SRB95531 decreased accuracy and increased omissions (Pehrson et al., 2013) Bicuculine decreased accuracy, increased omissions and increased latencies to collect rewards (Paine et al., 2011; note bicuculine likely spread to IL) Bicuculine blocked the increase in premature responding otherwise caused by CPP (Murphy et al., 2012)
Picrotoxin decreased accuracy and increased omissions (Pezze et al., 2014)
Micro-injection of NMDA antagonist MK801 increased omissions (Pehrson et al., 2013) CPP increased the number of premature responses (Murphy et al., 2012)
Reinforced responding in the Skinner box Excitotoxic lesions No effect (Risterucci et al., 2003) Increased premature responding and disrupted the distribution of preparatory responding during the intervals between cues (Risterucci et al., 2003) Increased premature responding and disrupted the distribution of preparatory responding during the intervals between cues (Risterucci et al., 2003)
Reinforced responding in the Skinner box (Continued) Single neuron recording Fast transient responses to sucrose delivery (Burgos-Robles et al., 2013) Delayed prolonged responses to sucrose delivery (Burgos-Robles et al., 2013)
Reversible inactivation Muscimol without effect on collection of earned sucrose rewards (Burgos-Robles et al., 2013) Muscimol delayed collection of earned sucrose rewards (Burgos-Robles et al., 2013)
Pre-pulse inhibition Excitotoxic lesion No effect (Lacroix et al., 1998; note lesion included AC and IL) No effect (Sullivan and Gratton, 2002; note lesion encroached on PL)
Increased by larger lesions (Lacroix et al., 2000b; note lesion included AC and IL)
Micro-injection of D1 antagonist Impaired (Ellenbroek et al., 1996; note injection coordinates included IL) Impaired (Shoemaker et al., 2005)
Impaired (Shoemaker et al., 2005)
Latent inhibition Electrolytic lesion No effect (Joel et al., 1997) No effect (Joel et al., 1997; note lesion included AC and IL) No effect (Joel et al., 1997)
Excitotoxic lesion No effect (Lacroix et al., 1998, 2000b; Schiller and Weiner, 2004; note lesions centered on PL, encroached on IL and/or AC) Enhanced (George et al., 2010)
No effect (George et al., 2010)
6-OHDA lesion Enhanced (Nelson et al., 2010) No effect (Nelson et al., 2010)
Trace conditioning Aspiration lesion Impaired acquisition (Kronforst-Collins and Disterhoft, 1998; Weible et al., 2000)
Electrolytic lesion Impaired acquisition but only at longer CS duration (McLaughlin et al., 2002)
Erk inhibition Impaired retention but not acquisition (Runyan et al., 2004)
Single neuron recording Attentional responses to CSs (Weible et al., 2003; Hattori et al., 2014) Increased activity to the trace conditioned CS, including within the trace interval (Gilmartin and McEchron, 2005) Decreased activity to the trace conditioned CS, no change in trace interval activity (Gilmartin and McEchron, 2005)
Persistent activity within the trace interval during retention tests (Hattori et al., 2014)
Trace conditioning (Continued) Reversible inactivation Impaired acquisition (Kalmbach et al., 2009; note “caudal” placement included PL)
Excitotoxic lesion c-fos expression Impaired by lesion and associated with increased neuronal activity in Cg1 but not Cg2 (Han et al., 2003)
Excitotoxic lesion Impaired by immediate-post-training lesions (Oswald et al., 2010) Impaired by 1-week-post-training lesions (Oswald et al., 2008, 2010)
Fear conditioning Microstimulation No effect on the expression or extinction of conditioned fear (Vidal-Gonzalez et al., 2006) Increased the expression of conditioned fear and prevented extinction (Vidal-Gonzalez et al., 2006) Decreased the expression of conditioned fear and facilitated extinction (Vidal-Gonzalez et al., 2006)
Single neuron recording Decreased activity during extinction and extinction memory in male rats; females showed increased activity during extinction (Fenton et al., 2014) Increased activity during extinction and extinction memory (no sex difference; Fenton et al., 2014)
Reversible inactivation Muscimol impaired fear expression, but had no effect on extinction memory (Sierra-Mercado et al., 2011) Muscimol had no effect of fear expression, but impaired extinction memory (Sierra-Mercado et al., 2011)
Object recognition—identity Excitotoxic lesion No effect (Ennaceur et al., 1997) No effect (Ennaceur et al., 1997; Barker et al., 2007)
Reversible inactivation No effect (Hannesson et al., 2004a)
6-OHDA lesion No effect (Nelson et al., 2011a) No effect (Nelson et al., 2011a)
Object recognition—recency Excitotoxic lesion Impaired (Barker et al., 2007; note lesion encroached on IL)
Reversible inactivation Impaired (Hannesson et al., 2004a)
6-OHDA lesion Impaired (Nelson et al., 2011a; note PL lesion anatomically selective) Impaired (Nelson et al., 2011a; note IL lesion encroached on PL)
Single neuron recording Increased activity when in location of a “missing” object at 6 h or 30 day delay (Weible et al., 2012)
Object recognition—location Excitotoxic lesion No effect unless lesion extended to include retrosplenial cortex (Ennaceur et al., 1997) No effect (Ennaceur et al., 1997; Barker et al., 2007)
Object recognition—location (Continued) 6-OHDA lesion No effect (Nelson et al., 2011a) Impaired (Nelson et al., 2011a)
Spatial recognition memory Reversible inactivation No effect on spatial recognition memory, impaired spatial temporal order memory (Hannesson et al., 2004b)
Spatial memory Reversible inactivation Impaired working memory in radial arm maze (Seamans et al., 1995) Impaired reference memory (Seamans et al., 1995)
Micro-injection of D1 antagonist Disrupted performance if 30 min delay between training and test (Seamans et al., 1998)
Electrolytic lesions No effect on non-matching to position (Joel et al., 1997) Some transient impairment in non-matching to position but more marked impairment in rule reversal (Joel et al., 1997; note lesion extended to AC)