Areal and synaptic interconnectivity of prelimbic (area 32), infralimbic (area 25) and insular cortices in the rat

Gabbott, P.L.A.; Warner, Tracy; Jays, Paul R.L.; Bacon, Sarah J.

doi:10.1016/j.brainres.2003.08.056

Cited by 136 publications

(103 citation statements)

References 56 publications

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“…Notably, it does not include IL, an important region within the medial network, nor does it include the insular orbital network structures [AIv, DI, and GI]. However, insular cortex sends projections to OMPFC, in particular LO, VLO, PrL, and IL (31,32), and thus, through corticocortical connections (32,33), highly integrated viscerosensory information reaches the medial and orbital networks of OMPFC.…”

Section: Discussionmentioning

confidence: 99%

Rat brains also have a default mode network

Zou

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

545

571

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The default mode network (DMN) in humans has been suggested to support a variety of cognitive functions and has been implicated in an array of neuropsychological disorders. However, its function (s) remains poorly understood. We show that rats possess a DMN that is broadly similar to the DMNs of nonhuman primates and humans. Our data suggest that, despite the distinct evolutionary paths between rodent and primate brain, a well-organized, intrinsically coherent DMN appears to be a fundamental feature in the mammalian brain whose primary functions might be to integrate multimodal sensory and affective information to guide behavior in anticipation of changing environmental contingencies.functional MRI | resting state | intrinsic activity | connectivity | spontaneous fluctuation I n the absence of an immediate need for goal-directed attention to the surrounding environment, our minds wander from recollection of past happenings to imagination of future events. Neuroimaging studies have consistently identified a set of interconnected brain areas that becomes less active during attentiondemanding cognitive tasks (1). This so-called default mode network (DMN) is posited to play a fundamental role in brain organization and supports a variety of self-referential functions such as understanding others' mental state, recollection and imagination (2), conceptual processing (3), and even in the sustenance of conscious awareness (4). Many of these functions have been considered to be unique to humans. Intriguingly, similar coherent structures have been shown to exist in anesthetized macaque monkeys and chimpanzees (5, 6). Furthermore, the functions of the default network are disrupted in such neuropsychological disorders as schizophrenia, Alzheimer's disease, and autism (7-9), underscoring the clear and critical need for further investigating the neurobiological basis of DMN using animal models.The evolutionary clade of rodents is about 35 million years earlier than that of old world monkeys and about 60 million years earlier than humans (10). Although many of the structures and functions of subcortical nuclei are conserved across these three species, the neocortex, in particular the "association" cortex, has extensively expanded in the primate as a result of evolutionary pressure, which is considered to be crucial in the development of higher cognitive and behavioral functions (10, 11). On the other hand, such structures as cingulate cortex, prefrontal cortex, and hippocampal formation, all of which are critical elements of the DMN, are also present in rodents (11). Given the distant evolutionary paths between rodent and primate brain, an intriguing question arises: Does the rat possess a similar DMN? Such a network, once demonstrated, would not only suggest that an operational DMN is a common feature in the mammalian brain, perhaps induced via parallel evolution as a result of natural selection, it would also offer a novel platform to explore the physiological basis and behavioral significance of the DMN. Such a demonstratio...

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Section: Discussionmentioning

confidence: 99%

Rat brains also have a default mode network

Zou

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

545

571

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“…However, the neural connections of the RAIC fit better into the description of a high-order cortex that might associate context with drug effect: The RAIC receives thalamic input from the medial subdivision of the mediodorsal thalamic nucleus (Krettek and Price, 1977;Allen et al, 1991), considered a high-order thalamic nucleus (Groenewegen and Witter, 2004), and from thalamic nuclei that are thought to convey the affective components of nociception (Jasmin et al, 2004). Interoceptive information may reach the RAIC from an intermediate, polysensory region of the granular insular cortex located rostral to the primary interoceptive cortex (Kimura et al, 2010) and from the adjacent dysgranular insular cortex (Shi and Cassell, 1998;Gabbott et al, 2003). Contextual information probably reaches the RAIC from brain regions representing spatial information or context, such as the entorhinal cortex (Insausti et al, 1997), closely interconnected with the hippocampus, and the posterior parietal cortex (Kerr et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

A Role for the Insular Cortex in Long-Term Memory for Context-Evoked Drug Craving in Rats

Contreras

Billeke

Vicencio

et al. 2012

Neuropsychopharmacol

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Drug craving critically depends on the function of the interoceptive insular cortex, and may be triggered by contextual cues. However, the role of the insula in the long-term memory linking context with drug craving remains unknown. Such a memory trace probably resides in some neocortical region, much like other declarative memories. Studies in humans and rats suggest that the insula may include such a region. Rats chronically implanted with bilateral injection cannulae into the high-order rostral agranular insular cortex (RAIC) or the primary interoceptive posterior insula (pIC) were conditioned to prefer the initially aversive compartment of a 2-compartment place preference apparatus by repeatedly pairing it to amphetamine. We found a reversible but long-lasting loss (ca. 24 days) of amphetamineconditioned place preference (CPP) and a decreased expression in the insula of zif268, a crucial protein in memory reconsolidation, when anisomycin (ANI) was microinjected into the RAIC immediately after the reactivation of the conditioned amphetamine/context memory. ANI infusion into the RAIC without reactivation did not change CPP, whereas ANI infusion into pIC plus caused a 15 days loss of CPP. We also found a 24 days loss of CPP when we reversibly inactivated pIC during extinction trials. We interpret these findings as evidence that the insular cortex, including the RAIC, is involved in a context/drug effect association. These results add a drug-related memory function to the insular cortex to the previously found role of the pIC in the perception of craving or malaise.

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“…Further, adolescents with depression showed increased activation to social rejection (a non-reward outcome) relative to controls in the subgenual anterior cingulate as well as the supracallosal cingulate non-reward/punishment area and the amygdala, anterior insula and nucleus accumbens (Silk et al, 2014). However, the subgenual cingulate cortex is also implicated in autonomic function (Gabbott et al, 2003), and its role as an autonomic output region receiving information from the orbitofrontal and cingulate cortices could be related to some of the effects found in the subgenual cortex that are related to depression. Indeed, it is sometimes stated that a core symptom of depression is a "pervasive negative interoceptive state", and this may relate directly to the roles of the subgenual cingulate cortex in depression.…”

Section: Relation To Other Brain Systems Implicated In Depressionmentioning

confidence: 99%

A non-reward attractor theory of depression

Rolls

2016

Neuroscience & Biobehavioral Reviews

161

174

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Neuroscience and Biobehavioral Reviews, in press (May 2016) \papers\Emotion\depression\depression16b.docx 2 SummaryA non-reward attractor theory of depression is proposed based on the operation of the lateral orbitofrontal cortex and supracallosal cingulate cortex. The orbitofrontal cortex contains error neurons that respond to non-reward for many seconds in an attractor state that maintains a memory of the nonreward. The human lateral orbitofrontal cortex is activated by non-reward during reward reversal, and by a signal to stop a response that is now incorrect. Damage to the human orbitofrontal cortex impairs reward reversal learning. Not receiving reward can produce depression. The theory proposed is that in depression, this lateral orbitofrontal cortex non-reward system is more easily triggered, and maintains its attractor-related firing for longer. This triggers negative cognitive states, which in turn have positive feedback top-down effects on the orbitofrontal cortex non-reward system. Treatments for depression, including ketamine, may act in part by quashing this attractor. The mania of bipolar disorder is hypothesized to be associated with oversensitivity and overactivity in the reciprocally related reward system in the medial orbitofrontal cortex and pregenual cingulate cortex.

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Areal and synaptic interconnectivity of prelimbic (area 32), infralimbic (area 25) and insular cortices in the rat

Cited by 136 publications

References 56 publications

Rat brains also have a default mode network

Rat brains also have a default mode network

A Role for the Insular Cortex in Long-Term Memory for Context-Evoked Drug Craving in Rats

A non-reward attractor theory of depression

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