IGF-1 facilitates extinction of conditioned fear

Maglio, Laura E.; Noriega-Prieto, José Antonio; Maroto, Irene B.; Martín-Cortecero, Jesús; Muñoz‐Callejas, Antonio; Callejo-Móstoles, Marta; Sevilla, David Fernández de

doi:10.7554/elife.67267

Cited by 23 publications

(19 citation statements)

References 72 publications

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“…shown that fear conditioning decreases excitability, whereas extinction training enhances excitability and decreases medium-and slow AHP (Santini et al, 2008;Maglio et al, 2021). At the IC, chronic ethanol consumption has shown to decrease excitability and to increase AHP (Luo et al, 2021).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic excitability in layer IV-VI anterior insula to basolateral amygdala projection neurons encodes the confidence of taste valence

Chandran

Yiannakas

Kayyal

et al. 2022

Preprint

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Avoiding potentially harmful, and consuming safe food is crucial for the survival of living organisms. However, sensory information can change its valence following conflicting experiences. Novelty and aversiveness are the two crucial parameters defining the currently perceived valence of taste. Importantly, the ability of a given taste to serve as CS in conditioned taste aversion (CTA) is dependent on its valence. Activity in anterior insula (aIC) layer IV-VI pyramidal neurons projecting to the basolateral amygdala (BLA) is correlative and necessary for CTA learning and retrieval, as well as the expression of neophobia towards novel tastants, but not learning taste familiarity. Yet, the cellular mechanisms underlying the updating of taste valence representation in this specific pathway are poorly understood. Here, using retrograde viral tracing and whole cell patch-clamp electrophysiology in trained mice, we demonstrate that the intrinsic properties of deep-lying layer IV-VI, but not superficial layer I-III aIC-BLA neurons, are differentially modulated by both novelty and valence, reflecting the subjective predictability of taste valence arising from prior experience. These correlative changes in the profile of intrinsic properties of LIV-VI aIC-BLA neurons were detectable following both simple taste experiences, as well as following memory retrieval, extinction learning and reinstatement.

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Section: Discussionmentioning

confidence: 99%

Intrinsic excitability in layer IV-VI anterior insula to basolateral amygdala projection neurons encodes the confidence of taste valence

Chandran

Yiannakas

Kayyal

et al. 2022

Preprint

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“…Consistent with this finding, the current study demonstrated that intra-mPFC IGF-1 infusion produces antidepressant-like effects in the LPS-induced depression model mice via mTORC1 activation. Furthermore, IGF-1 increases cell surface GluA1 protein levels in the mPFC [ 15 ], and exogenous IGF-1 has also been reported to increase excitability and potentiate synaptic transmission in mPFC layer V pyramidal neurons [ 15 , 46 ]. Additionally, the frontoparietal cortex of IGF-1 null mice have reduced dendritic spine density in layers II/III and V pyramidal neurons [ 47 ], while IGF-1 treatment rescued decreased PSD-95 protein levels and dendritic spine density in the somatosensory cortex of a mouse model of cyclin-dependent kinase-like 5 deficiency disorder [ 48 ].…”

Section: Discussionmentioning

confidence: 99%

IGF-1 release in the medial prefrontal cortex mediates the rapid and sustained antidepressant-like actions of ketamine

et al. 2022

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Ketamine, an N-methyl-D-aspartate receptor antagonist, exerts rapid and sustained antidepressant actions. Preclinical studies demonstrated that the release of brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor in the medial prefrontal cortex (mPFC) is essential for the antidepressant-like effects of ketamine. However, the role of other neurotrophic factors in the antidepressant-like effects of ketamine has not been fully investigated. Since the intra-mPFC infusion of insulin-like growth factor 1 (IGF-1) reportedly produced antidepressant-like effects, the present study examined the role of endogenous intra-mPFC IGF-1 signaling in the antidepressant-like actions of ketamine. In vivo microdialysis showed that ketamine (10 and 30 mg/kg) significantly increased extracellular IGF-1 levels in the mPFC of male C57BL/6J mice for at least 5 h. Infusion of an IGF-1 neutralizing antibody (nAb; 160 ng/side) into the mPFC 15 min before or 2 h after ketamine injection blocked the antidepressant-like effects of ketamine in three different behavioral paradigms (forced swim, female urine sniffing, and novelty-suppressed feeding tests were conducted 1, 3 and 4 days post-ketamine, respectively). The ketamine-like antidepressant-like actions of the intra-mPFC infusion of BDNF (100 ng/side) and IGF-1 (50 ng/side) respectively were not blocked by co-infused IGF-1 nAb and BDNF nAb (200 ng/side). Moreover, intra-mPFC infusion of IGF-1 nAb 2 h post-ketamine blocked the antidepressant-like effects of ketamine in a murine lipopolysaccharide (LPS)-induced depression model. Intra-mPFC IGF-1 infusion also produced antidepressant-like effects in the LPS-challenged mice via mechanistic target of rapamycin complex 1 activation. These results suggest that persistent release of IGF-1, independently of BDNF, in the mPFC is essential for the antidepressant-like actions of ketamine.

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“…IGF-1 is a polypeptide hormone mainly produced in the hepatocytes and exerts its effect through high-affinity binding to the IGF-1R, located on the cell surface of target tissues [5]. IGF-1 affects a wide variety of biological activities such as somatic cell development, cell differentiation, cortical neuronal activity, regulation of brain development, and is involved, directly and indirectly, in longevity [6][7][8][9][10][11]. Interestingly, IGF-1 has a very potent physiological effect in vivo; however, its effects in vitro are relatively weak unless other hormones or growth factors are present [5].…”

Section: Introductionmentioning

confidence: 99%

The Role of Insulin-like Growth Factor-1 (IGF-1) in the Control of Neuroendocrine Regulation of Growth

Al-Samerria

Radovick

2021

Cells

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In mammals, the neuroendocrine system, which includes the communication between the hypothalamus and the pituitary, plays a major role in controlling body growth and cellular metabolism. GH produced from the pituitary somatotroph is considered the master regulator of somatic development and involved, directly and indirectly, in carbohydrate and lipid metabolism via complex, yet well-defined, signaling pathways. GH production from the pituitary gland is primarily regulated by the counter-regulatory effects of the hypothalamic GHRH and SST hormones. The role of IGF-1 feedback regulation in GH production has been demonstrated by pharmacologic interventions and in genetically modified mouse models. In the present review, we discuss the role of IGF-1 in the regulation of the GH-axis as it controls somatic growth and metabolic homeostasis. We present genetically modified mouse models that maintain the integrity of the GH/GHRH-axis with the single exception of IGF-1 receptor (IGF-1R) deficiency in the hypothalamic GHRH neurons and somatotroph that reveals a novel mechanism controlling adipose tissues physiology and energy expenditure.

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IGF-1 facilitates extinction of conditioned fear

Cited by 23 publications

References 72 publications

Intrinsic excitability in layer IV-VI anterior insula to basolateral amygdala projection neurons encodes the confidence of taste valence

Intrinsic excitability in layer IV-VI anterior insula to basolateral amygdala projection neurons encodes the confidence of taste valence

IGF-1 release in the medial prefrontal cortex mediates the rapid and sustained antidepressant-like actions of ketamine

The Role of Insulin-like Growth Factor-1 (IGF-1) in the Control of Neuroendocrine Regulation of Growth

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