WorldCat Identities

Chigr, Fatiha

Overview
Works: 7 works in 9 publications in 2 languages and 13 library holdings
Roles: Other, Opponent, Author
Publication Timeline
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Most widely held works by Fatiha Chigr
Gestational and Lactational Exposure to Malathion Affects Antioxidant Status and Neurobehavior in Mice Pups and Offspring by Fatima Zahra Ouardi( )

1 edition published in 2019 in English and held by 2 WorldCat member libraries worldwide

Continuous Exposure to Inorganic Mercury Affects Neurobehavioral and Physiological Parameters in Mice by Hafsa Malqui( )

1 edition published in 2018 in English and held by 2 WorldCat member libraries worldwide

Distribution of delta sleep-inducing peptide in the newborn and infant human hypothalamus: an immunohistochemical study by Mohamed Najimi( )

1 edition published in 2001 in English and held by 2 WorldCat member libraries worldwide

The distribution of delta sleep-inducing peptide immunoreactive cell bodies, fibers, and terminal-like structures was investigated in the normal human hypothalamus during the first postnatal year, using immunohistofluorescence and peroxidase anti-peroxidase techniques. Immunolabeled perikarya were relatively few and were mostly scattered through the anterior (preoptic) and mediobasal regions (infundibular nucleus) of the hypothalamus. DSIP-immunoreactive fibers and terminal-like fibers were observed throughout the entire rostrocaudal extent of the hypothalamus. They exhibit high densities in the preoptic region, the organum vasculosum of lamina terminalis, infundibular nucleus and median eminence. Moderate to low densities of DSIP-immunoreactive fibers were observed in the other hypothalamic structures, located in the anterior and mediobasal regions of hypothalamus, such as periventricular, paraventricular, suprachiasmatic, ventromedial, dorsomedial and parafornical nuclei. In the present study, the analysis of the immunohistochemical pattern of DSIP-immunoreactive neuronal elements in the human infant hypothalamus during the first postnatal year provided evidence of the presence of several differences. We have found qualitative age-related changes in the density of DSIP immunoreactivity in several hypothalamic structures such as the anterior region and the median eminence. (Au)
Sensibilisation à la douleur chez un modèle murin de troubles du déficit de l'attention et de l'hyperactivité by Otmane Bouchatta( )

1 edition published in 2018 in French and held by 1 WorldCat member library worldwide

Attention deficit hyperactivity disorder (ADHD) is characterized by the core symptoms of inattention, hyperactivity and impulsivity. Neural pathways underlying these deficits point to deficits within frontal-subcortical catecholaminergic networks, involving dopaminergic and noradrenergic innervation. Hence, impairment of the dopaminergic neurotransmission is a frequent target of ADHD medication. Low-dose psychostimulants, including methylphenidate (MpH) and amphetamines (AMP) are the most widely used treatments of ADHD. Recent evidence pointed to pain hypersensitivity in subjects with ADHD history, and suggests possible comorbidity of ADHD with pain. However, the mechanisms and neural circuits involved in these interactions are unknown. In order to understand this comorbidity, the first objective was to create a good animal model of ADHD. We generated a mouse model at P5 by neonatal disruption of central dopaminergic pathways with 6-Hydroxydopamine (6-OHDA) and we demonstrated the validity of the model to mimic ADHD syndrome. Next, we analyzed nociceptive responses in the 6-OHDA mouse model of ADHD. We found that 6-OHDA mice exhibited a marked decrease of withdrawal thresholds, suggesting that ADHD increase nociceptive sensitivity. Interestingly, by using in vivo electrophysiological recordings, we demonstrated that allodynia and hyperalgesia may be caused by neuronal hyperexcitability in the dorsal spinal cord. Moreover, we found that both lowered wihdrawal threshold and increased activity of nociceptive neurons in ADHD-like mice was not normalized by MpH. We tested the hypothesis that descending controls are responsible for pain alterations through the modulation of spinal circuits. The 'anterior cingulate cortex (ACC) - posterior insular (PI)' connectivity is at the cross-road of ADHD and pain, being involved in executive functions and emotions, as well as sending projections to the dorsal horn of the spinal cord. By combining electrophysiological, optogenetic and behavioral analyzes, we have shown that the effects of ADHD on painful sensitization involve the implication of ACC and the ACC - PI pathway. In conclusion, we showed that ADHD conditions induce spinal cord nociceptive neurons hyperactivation and pain hypersensitivity. We also suggest that the ACC - PI circuit may trigger dysfunction of spinal cord neurons in ADHD conditions
Caractéristiques neurobiologiques de la résilience et de la susceptibilité au trouble de stress post-traumatique avec des modèles murins incluant l'utilisation de substances psychoactives (alcool et cocaïne) by Asmae Lguensat( )

1 edition published in 2020 in French and held by 1 WorldCat member library worldwide

Following exposure to traumatic events, only a small proportion of individuals (susceptible individuals) develops post-traumatic stress disorder (PTSD), while the others remain weakly affected (resilient individuals). In susceptible individuals, there is a high rate of co-morbidity with substance use disorder (SUD), especially with alcohol and cocaine use. Knowing that current treatments to reduce PTSD symptoms in co-morbid conditions show little efficacy, understanding the mechanisms underlying the individual differences and interactions between PTSD and SUD is needed to develop effective treatments. Thus, our work, carried out with rodent models aimed initially to elucidate the behavioral and neurobiological differences between the susceptible and the resilient phenotypes and to explore the consequences of exposure to alcohol on PTSD symptoms. Second, we studied the effects of chronic alcohol or cocaine use on PTSD. Finally, we tested the effectiveness of topiramate in co-morbid conditions. Our results show that the susceptible and resilient phenotypes are distinguished by opposite dendritic changes in the prelimibic (PrL) and infralimbic (IL) regions of the median prefrontal cortex (mPFC). These changes are associated with high levels of ACTH and corticosterone and low levels of BDNF. The consequences of comorbidity are the persistence of symptoms, the exacerbation of dendritic changes in the PrL region and the resistant to treatment with topiramate. We therefore suggest to provide more efforts to develop means of intervention to promote resilience
 
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