Fos expression in the brains of rats performing an attentional set-shifting task

Abstract

Impairments in executive function and cognitive control are a common feature of neuropsychiatric and neurodegenerative disorders. A promising behavioral paradigm for elucidating the neural mechanisms of executive function is extradimensional/intradimensional (ED/ID) shifting, which places demands on executive function by requiring the adjustment of behavioral responses based on affective or attentional information. To augment the understanding of the brain systems required for these aspects of executive function, we examined the induction of Fos protein in rats tested in the ED/ID paradigm. We found increased Fos-like immunoreactivity (Fos-LI) in several cortical areas, including medial and orbital frontal cortex (OFC), in rats performing affective or attentional shifts relative to rats performing control discriminations. However, increased Fos-LI was also present in rats that performed a yoked number of additional control discrimination trials, without affective or attentional shifting. These observations suggest that cortical networks required for affective and attentional shifting are also activated during comparable discrimination tasks that do not require shifting, consistent with a role for these networks in monitoring ongoing behavior even in situations in which adaptation to changing behavioral demands is not required.

Identification of Immediate Early Genes in the Nervous System of SnailHelix lucorum

“…The activation of c-Fos in Pa2 neurons after the behavioral training was not directly linked to associative learning (Fig. 4 G , H ), consistent with studies conducted in mice and other vertebrates (Herdegen and Leah, 1998; Kovacs, 1998; Kaczmarek et al, 1999; Burnham et al, 2010; Lopez et al, 2018; Fredericksen et al, 2019; Möser et al, 2019). Intriguingly, a group of serotoninergic neurons located in PdG showed greater c-Fos upregulation after paired CS and US presentation compared to unpaired ones (Fig.…”

Impaired Cognitive Flexibility After Neonatal Perirhinal Lesions in Rhesus Macaques

“…This dissociation suggests that mechanisms of cognitive flexibility were more severely affected by the early damage than after the adult-onset damage. Given the early timing of the neonatal lesions, the deficits in cognitive flexibility may instead represent downstream effects of the neonatal lesions on the normal development and maturation of the brain area important for flexible cognition and preventing perseverative responding, such as the vlPFC (Iversen and Mishkin, 1970; Owen et al, 1991; Dias et al, 1997; Rogers et al, 2000; Monchi et al, 2001; Baxter et al, 2009; Burnham et al, 2010; Bissonette et al, 2013). The protracted anatomical and functional development of this prefrontal area has been well established (Fuster, 2002; Conklin et al, 2007; Kolb and Gibb, 2011), and a number of morphological and neurochemical changes in the lateral PFC have been reported following early damage to other MTL structures (Bertolino et al, 1997; Chlan-Fourney et al, 2000; Tseng et al, 2008; Meng et al, 2013).…”

“…The critical involvement of the dorsolateral PFC is well established in WM processes of monitoring/manipulation (Goldman and Rosvold, 1970; Alexander and Goldman, 1978; Petrides and Milner, 1982; Petrides, 1991a,b, 1995, 2000; Miller and Cohen, 2001), whereas ventrolateral and medial PFC regions are involved with perseveration and cognitive flexibility (Rogers et al, 2000; Monchi et al, 2001; Burnham et al, 2010; Bissonette et al, 2013). It is therefore noteworthy that the PFC regions critical for cognitive flexibility receive comparably heavier perirhinal inputs than do the regions involved in WM (dorsolateral PFC), and comparably fewer from other areas like inferotemporal cortex, parahippocampal cortex, and the hippocampus (Suzuki and Amaral, 1994a,b; Cavada et al, 2000; Lavenex et al, 2002; Croxson et al, 2005; Kondo et al, 2005; Saunders et al, 2005).…”

“…Lesion studies in monkeys have already demonstrated a double-dissociation between behavioral inhibition supported by the orbitofrontal cortex (OFC), and cognitive flexibility supported by the ventrolateral prefrontal cortex (vlPFC) (Dias et al, 1997; Rogers et al, 2000; Monchi et al, 2001; Burnham et al, 2010; Bissonette et al, 2013). Given that the PRh has robust interconnections with both of these cortical areas (Barbas and Pandya, 1989; Suzuki and Amaral, 1994a,b; Lavenex et al, 2002; Petrides and Pandya, 2002), it is possible that the PRh also contributes in mechanisms underlying behavioral inhibition and/or cognitive flexibility.…”

Long-term memory, synaptic plasticity and dopamine in rodent medial prefrontal cortex: Role in executive functions

“…mPFC lesions selectively impair shifting of the perceptual set, but not its acquisition (Birrell and Brown, 2000 ). In these tasks, learning is associated with neural activity changes in mPFC (Rich and Shapiro, 2009 ; Durstewitz et al, 2010 ; Singh et al, 2019 ) and with plasticity-related gene expression in mPFC (DeSteno and Schmauss, 2008 ; Burnham et al, 2010 ). The main learning components of these tasks are the selection of a new behavioral strategy and inhibition of a previously acquired one, following a contingency switch (Dalley et al, 2004 ).…”