Recent frameworks in cognitive neuroscience and behavioral neurology underscore interoceptive priors as core modulators of negative emotions. However, the field lacks experimental designs manipulating the priming of emotions via interoception and exploring their multimodal signatures in neurodegenerative models. Here, we designed a novel task that involves interoceptive and control-exteroceptive priming conditions followed by post-Intero and post-Extero facial emotion recognition (FER). We recruited 114 participants, including healthy controls (HCs) as well as patients with behavioral variant frontotemporal dementia (bvFTD), Parkinson's disease (PD), and Alzheimer's disease (AD). We measured online EEG modulations of the heart-evoked potential (HEP), and associations with both brain structural and resting-state functional connectivity patterns. Behaviorally, post-Intero negative FER was enhanced in HCs but selectively disrupted in bvFTD and PD, with AD presenting generalized disruptions across emotion types. Only BvFTD presented impaired interoceptive accuracy. Increased HEP modulations during post-Intero negative FER was observed in HCs and AD, but not in bvFTD or PD patients. Across all groups, post-Intero negative FER correlated with the volume of the insula and the anterior cingulate cortex. Also, negative FER was associated with functional connectivity along the (a) salience network in the post-Intero condition, and along the (b) executive network in the post-Extero condition. These patterns were selectively disrupted in bvFTD (a) and PD (b), respectively.Our approach underscores the multidimensional impact of interoception on emotion, while revealing a specific pathophysiological marker of bvFTD. These findings inform a promising theoretical and clinical agenda in the fields of interoception, emotion, allostasis, and neurodegeneration.

Fetal and neonatal ethanol-related alterations upon the respiratory system have been described in different mammals. Studies also indicate that perinates learn about the sensory attributes of ethanol and associate them with diverse physiological effects of the state of intoxication. The present study was conducted in rat neonates during a developmental stage equivalent to the third human gestational trimester. The major goal was to analyze the consequences of ethanol odor exposure, the state of intoxication, or the temporal contiguity between these factors upon breathing patterns. The main findings were as follows: (a) a conditioned breathing depression was observed following few trials defined by the association between ethanol odor and the state of intoxication and (b) sequential exposure to ethanol sensitizes the organism to the drug's respiratory depressant effects without affecting ethanol metabolism. These results indicate that early breathing disruptions caused by ethanol can be determined or modulated via learning processes. © 2016 Wiley Periodicals, Inc. Dev Psychobiol 58:670-686, 2016.

Different studies have focused on the deleterious consequences of binge-like or chronic exposure to ethanol during the brain growth spurt period (third human gestational trimester) that in the rat corresponds to postnatal days (PDs) 3-10. The present study analyzed behavioral and physiological disruptions caused by relatively brief binge-like exposures (PDs 3, 5, and 7) with an ethanol dose lower (3.0 g/kg) than those frequently employed to examine teratological effects during this stage in development. At PD 9, pups were exposed to ethanol doses ranging between .0-3.0 g/kg and tested in terms of breathing patterns and thermoregulation. At PDs 11 and 12, ethanol intake was examined. The main findings were as follows: i) pre-exposure to the drug resulted in brief depressions in breathing frequencies and an exacerbated predisposition toward apneic episodes; ii) these effects were not dependent upon thermoregulatory alterations; iii) early ethanol treatment increased initial consumption of the drug which also caused a marked hypothermia that appeared to regulate a subsequent decrement in ethanol consumption; and iv) ethanol exposure retarded overall body growth and even one exposure to the drug (PD 9) was sufficient to reduce brain weights although there were no indications of microcephaly. In conjunction with studies performed during the late gestational period in the rat, the results indicate that relatively brief binge-like episodes during a critical window of brain vulnerability disrupts the respiratory network and exacerbates initial acceptance of the drug. In addition, ethanol treatments were not found to induce tolerance relative to respiratory and thermal disruptions.

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As a whole, the results demonstrated that brief ethanol experience and stress-related factors significantly disorganize respiratory patterns as well as arousal responses linked to hypoxia in neonatal rats.

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