Rostral agranular insular cortex and pain areas of the central nervous system: A tract‐tracing study in the rat

Jasmin, Luc; Granato, Alberto; Ohara, Peter T.

doi:10.1002/cne.10978

Cited by 202 publications

(180 citation statements)

References 120 publications

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“…The connectivity of RAIC suggests that it is involved in multiple aspects of pain behavior, and increasing evidence shows that the RAIC is important for the modulation of nociception in humans and rats. It is suggested that projections to the RAIC from medial thalamic nuclei are associated with motivational/ affective components of pain while RAIC projections to mesolimbic/mesocortical ventral forebrain circuits are likely to participate in the sensorimotor integration of nociceptive processing, and that its brainstem projections are most likely to contribute to descending pain-inhibitory control [44] . Clinical studies have also suggested that the insular cortex is involved in pain modulation.…”

Section: Rostral Agranular Insular Cortex (Raic) Involvement Of the Rmentioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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Pain is a complex experience encompassing sensory-discriminative, affective-motivational and cognitiv e-emotional components mediated by different mechanisms. Contrary to the traditional view that the cerebral cortex is not involved in pain perception, an extensive cortical network associated with pain processing has been revealed using multiple methods over the past decades. This network consistently includes, at least, the anterior cingulate cortex, the agranular insular cortex, the primary (SΙ) and secondary somatosensory (SΠ) cortices, the ventrolateral orbital cortex and the motor cortex. These cortical structures constitute the medial and lateral pain systems, the nucleus submedius-ventrolateral orbital cortex-periaqueductal gray system and motor cortex system, respectively. Multiple neurotransmitters, including opioid, glutamate, GABA and dopamine, are involved in the modulation of pain by these cortical structures. In addition, glial cells may also be involved in cortical modulation of pain and serve as one target for pain management research. This review discusses recent studies of pain modulation by these cerebral cortical structures in animals and human.

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Section: Rostral Agranular Insular Cortex (Raic) Involvement Of the Rmentioning

confidence: 99%

Cerebral cortex modulation of pain

2008

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“…Though the exact mechanism is unknown, IC outputs chronically regulate detection thresholds for painful stimuli in the periphery via GABAergic signais (Jasmin et al, 2003;Jasmin et aL, 2004). In addition, an unusually dense staining region for ~-opioid receptors (primary receptor targets for analgesia-producing opiates such as morphine) is present in the rostral agranular region (Delfs et aL, 1994;Burkey et aL, 1996).…”

Section: Extrahippocampal Involvement In Tle: the Insular Cortexmentioning

confidence: 99%

“…The rostral agranular IC, in particular, is important in regulating peripheral nociceptive thresholds via opioidergic, dopaminergic and GABAergic signaling (Burkey et aL, 1996;Burkey et aL, 1999;Jasmin et al, 2003;Jasmin et aL, 2004). In addition, the rostral agranular IC is reciprocally connected with the perirhinal cortex (PC) (Delatour and Witter, 2002), a structure central in object memory and recognition (Buckley, 2005;Murray et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

Sudbury

Avoli

2007

Eur J of Neuroscience

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The hippocampus plays a primary role in temporal lobe epilepsy, a common form of partial epilepsy in adults. Recent studies, however, indicate that extrahippocampal areas such as the perirhinal and insular cortices represent important participants in this epileptic disorder. By employing field potential recordings in the in vitro 4‐aminopyridine model of temporal lobe epilepsy, we have investigated here the contribution of glutamatergic and GABAergic signaling to epileptiform activity in these structures. First, we provide evidence of epileptiform synchronicity between the perirhinal and insular cortices, and resolve some pharmacological and network mechanisms involved in sustaining the interictal‐ and ictal‐like discharges recorded there. Second, we report that in the absence of ionotropic glutamatergic transmission, GABAergic networks produce synchronous potentials that spread between the perirhinal and insular cortices. Finally, we have established that such activity is modulated by activating µ‐opioid receptors. Our findings support clinical and experimental evidence concerning the involvement of the perirhinal and insular cortex networks in temporal lobe epilepsy, and provide observations that may impact research focussing on the role of the insular cortex in nociception.

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“…It is intensively connected with other cortical and subcortical regions via a cortico-striato-thalamic network (linking the insula also to the caudate nucleus; see Metzger et al 2010), with the lateral hypothalamus (Jasmin et al 2004), the hippocampus [at least with the entorhinal cortex (Mesulam and Mufson 1982)], and the brainstem via corticobulbar pathways (Jasmin et al 2004;Ruggiero et al 1987). We refer for further review of the neuroanatomy and function of the insula to the classical work by Mesulam and Mufson (1985) and an excellent new work by Nieuwenhuys (2012).…”

Section: Abnormal Yawning Due To Insular Lesionsmentioning

confidence: 99%

Insular and caudate lesions release abnormal yawning in stroke patients

Krestel

Weisstanner

Hess

et al. 2013

Journal of the Neurological Sciences

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Abnormal yawning is an underappreciated phenomenon in patients with ischemic stroke. We aimed at identifying frequently affected core regions in the supratentorial brain of stroke patients with abnormal yawning and contributing to the anatomical network concept of yawning control. Ten patients with acute anterior circulation stroke and C3 yawns/15 min without obvious cause were analyzed. The NIH stroke scale (NIHSS), Glasgow Coma Scale (GCS), symptom onset, period with abnormal yawning, blood oxygen saturation, glucose, body temperature, blood pressure, heart rate, and modified Rankin scale (mRS) were assessed for all patients. MRI lesion maps were segmented on diffusionweighted images, spatially normalized, and the extent of overlap between the different stroke patterns was determined. Correlations between the period with abnormal yawning and the apparent diffusion coefficient (ADC) in the overlapping regions, total stroke volume, NIHSS and mRS were performed. Periods in which patients presented with episodes of abnormal yawning lasted on average for 58 h. Average GCS, NIHSS, and mRS scores were 12.6, 11.6, and 3.5, respectively. Clinical parameters were within normal limits. Ischemic brain lesions overlapped in nine out of ten patients: in seven patients in the insula and in seven in the caudate nucleus. The decrease of the ADC within the lesions correlated with the period with abnormal yawing (r = -0.76, Bonferroni-corrected p = 0.02). The stroke lesion intensity of the common overlapping regions in the insula and the caudate nucleus correlates with the period with abnormal yawning. The insula might be the long sought-after brain region for serotonin-mediated yawning.

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Rostral agranular insular cortex and pain areas of the central nervous system: A tract‐tracing study in the rat

Cited by 202 publications

References 120 publications

Cerebral cortex modulation of pain

Cerebral cortex modulation of pain

Epileptiform synchronization in the rat insular and perirhinal cortices in vitro

Insular and caudate lesions release abnormal yawning in stroke patients

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