Extinction des espèces | EPFL Graph Search

thumb|Le dodo est un exemple emblématique d'extinction souvent cité. En biologie et en écologie, l' est la disparition totale d'une espèce ou d'un groupe de taxons, réduisant ainsi la biodiversité. Les écologues distinguent cette extinction numérique de l'extinction fonctionnelle, qui est la réduction de taille de la population d'une espèce telle qu'elle conduit à la raréfaction ou à l'extinction d'autres espèces dans la communauté, ce qui altère la fonctionnalité et la stabilité de l'écosystème. À travers l'évolution, de nouvelles espèces apparaissent par le processus de la spéciation — où de nouvelles variétés d'organismes émergent et se développent quand elles sont capables de trouver et d'exploiter une niche écologique — et des espèces disparaissent quand elles ne sont plus capables de survivre dans des conditions changeantes ou face à une concurrence qu'elles ne peuvent affronter. Typiquement, une espèce s'éteint en 5 à 10 millions d'années (hors période de crise bio géologique

Genetic selection for low glucocorticoid responsiveness recapitulates PTSD-related phenotypes: a behavioral, neuroimaging and sleep-physiology study

Silvia Monari

Humans show inter-individual differences in vulnerability to develop post-traumatic stress disorder (PTSD) following exposure to trauma. Several critical biobehavioral features have been consistently described in PTSD patients, including blunted cortisol levels, smaller hippocampal size, sleep disturbances. However, because of the delay between trauma exposure and the onset of symptoms characteristic of PTSD, only a few longitudinal studies have tried to dissect whether these features constitute pre-trauma risk factors or consequences of the trauma. Enormous effort in animal and human studies has been dedicated to understanding mechanisms of conditioned fear and fear extinction, processes that are at the core of PTSD. However, the same progress has not been translated into psychiatric practice for PTSD. Deepening our understanding of the contribution of key factors to PTSD-related alterations can serve to develop effective treatments.In particular, with regard to low cortisol levels in PTSD pathophysiology, a causative role for blunted glucocorticoid responsiveness in PTSD has not been demonstrated yet.Here, we have addressed this question in lines of Wistar rats genetically-selected for their differential habituation of glucocorticoid responses to stress (LOW-, INTER-, HIGH-CORT Responder rats) and focused on fear extinction, a hallmark of PTSD symptomology, as one of the key features. As a first step, we looked whether divergent trajectories of glucocorticoid responsiveness were associated with brain volume abnormalities, prompted by the influential role of glucocorticoid in brain development. Notably, rats with low or high corticosterone responsiveness exhibit smaller hippocampi, regardless of trauma exposure, compared to rats with normative corticosterone levels. Similarly, the distribution of corticosteroid receptors in the hippocampus presented similarities between the LOW-CR and the HIGH-CR rats with higher mineralocorticoid receptors (MR) and less glucocorticoid receptors (GR). Although LOW- and HIGH-CR rats displayed a similar hippocampal profile at the structural and molecular levels, only LOW-CR male rats exhibited strong deficits in extinction consolidation compared to rats with 'normative' glucocorticoid responses (INTER-CR rats), and showed higher fear response both at few days and at several weeks after trauma exposure. We next tested the causal involvement of corticosterone in the fear extinction consolidation, and found that post-extinction corticosterone treatment markedly prevented the deficits in extinction memory and attenuated fear relapse. In addition, pharmacological inhibition of corticosterone levels during extinction memory consolidation, but not during training, in the INTER-CR rats led to extinction deficits at retrieval one day later. These results indicate that blunted corticosterone levels contribute to confer major vulnerability than having a small hippocampus, and that consolidation processes following extinction are mainly affected by low corticosterone levels.It is well known that glucocorticoids play an important role in memory consolidation processes and that sleep disturbances are a diagnostic criterion of PTSD. Therefore, we investigated in greater detail the sleep architecture in undisturbed condition and during the consolidation period of the extinction phase, which is known to be supported by sleep-dependent processes. In polysomnographic recordings, we found that rats with blunted corticos

EPFL2022

Unaltered cocaine self-administration in the prenatal LPS rat model of schizophrenia

Erika Myrna Borcel Novoa

Although cocaine abuse is up to three times more frequent among schizophrenic patients, it remains unclear why this should be the case and whether sex influences this relationship. Using a maternal immune activation model of schizophrenia, we tested whether animals at higher risk of developing a schizophrenia-like state are more prone to acquire cocaine self-administration behavior, and whether they show enhanced sensitivity to the reinforcing actions of cocaine or if they are resistant to extinction. Pregnant rats were injected with lipopolysaccharide on gestational day 15 and 16, and the offspring (both male and female) were tested in working memory (T-maze), social interaction and sensorimotor gating (prepulse inhibition of the acoustic startle response) paradigms. After performing these tests, the rats were subjected to cocaine self-administration regimes (0.5 mg/kg), assessing their dose-response and extinction. Male rats born to dams administered lipopolysaccharide showed impaired working memory but no alterations to their social interactions, and both male and female rats showed prepulse inhibition deficits. Moreover, similar patterns of cocaine self-administration acquisition, responsiveness to dose shifts and extinction curves were observed in both control and experimental rats. These results suggest that the higher prevalence of cocaine abuse among schizophrenic individuals is not due to a biological vulnerability directly associated to the disease and that other factors (social, educational, economic, familial, etc.) should be considered given the multifactorial nature of this illness. (C) 2016 Elsevier Inc. All rights reserved.

Pergamon-Elsevier Science Ltd2016

Analysis of taste processing in rat gustatory cortex

Riccardo Accolla

Gustatory perception is a complex phenomenon involving the recognition of sensory properties of a food (taste modality and intensity, flavour, texture, fat content, temperature) as well as its reward value (pleasantness and nutritional value). The sense of taste lies at the core of this process and has the fundamental task of guiding the individual towards the decision on which substances to ingest and which others to reject. Remarkable progress has been made through molecular and genetic manipulations in the understanding of the coding of taste at the receptor level. However, much less is known about the cortical processing of taste sensation and the organizing principles of the gustatory cortex (GC). Functional maps are evident in many sensory regions of the neocortex, where neurons are arranged in spatially distinct networks to process sensory inputs. In contrast, in the GC, the existence of functional domains encoding different taste modalities has not been shown yet. In this thesis we used in vivo optical imaging techniques to investigate the functional architecture of the GC in regard to pure taste attributes (modality and intensity) and stimulus hedonic value (or pleasantness). In a first study we found that four of the primary taste modalities (sweet, bitter, salty and sour) are represented by distinctive spatial patterns, but that no region was specific to a single modality. In addition, we found that two tastants of similar hedonic value (pleasant or unpleasant) activated areas with more common regions than two tastants with opposite hedonic value. To better investigate the role of GC in representing the hedonic value, in a second study we coupled intrinsic imaging with conditioned taste aversion (CTA), a learning paradigm whereby a subject learns to avoid a taste stimulus previously associated with visceral malaise. We imaged intrinsic signals from the rat GC after inducing CTA to a pleasant stimulus (saccharin) and compared the resulting map to the response to a naturally unpleasant compound (quinine). Our results show that saccharin maps undergo plastic changes after CTA acquisition and after the extinction of the aversion, although this second change did not seem to reflect a simple reversal of the CTA acquisition. This result would be consistent with the evidence that extinction represents a new state of learning. Interestingly, this GC maps plasticity appears to be strongly correlated with the behavioral changes in the stimulus hedonic value. When saccharin shifts from attractive (Ctrl) to aversive (CTA acquisition) and attractive again (CTA extinction) its cortical representation changes in its relative position with respect to the pattern of the reference aversive stimulus, becoming highly correlated to the quinine pattern only after the CTA acquisition. In summary, we propose that the specific cortical patterns can be used to discriminate among various taste modalities, according to a spatial model of taste coding. We also show that GC maps reshape following conditioned learning induced by an internal state of malaise. Overall the present thesis provides new evidence for the GC as a site where multiple taste attributes are processed, including taste modality, intensity, aversive memory and hedonic value.

EPFL2007