Effect of prenatal stress on memory, nicotine withdrawal and 5HT1A expression in raphe nuclei of adult rats

Said, Nadia; Lakehayli, S.; Khachibi, Meryam El; Ouahli, M. El; Nadifi, Sellama; Hakkou, F.; Tazi, A.

doi:10.1016/j.ijdevneu.2015.04.008

Cited by 14 publications

(10 citation statements)

References 67 publications

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“…5HT release in target areas is also dependent on the balance of activity on 5HT1A inhibitory autoreceptors on 5HT cell bodies and GABAergic inhibitory interneurons in the DRN. Although neither anxiety nor depressive-like behavior were assessed in the study, the number of 5HT1A receptors (5HT1AR) in the whole DRN region, measured by reversed transcription PCR, was significantly reduced in PS rats (sex not defined) ( Said et al., 2015 ). By means of fluorescence immunohistochemistry with specific antibodies directed to different cell groups, we found that anxiety and depressive-like behavior of PS, Wistar rats was accompanied by a decrease in the expression of 5HT1AR on 5HT cell bodies and GABAergic interneurons in the DRN and PFC in males.…”

Section: Neurochemical Basis Of Behavioral Alterationsmentioning

confidence: 99%

Prenatal stressors in rodents: Effects on behavior

Weinstock

2017

Neurobiology of Stress

216

156

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The current review focuses on studies in rodents published since 2008 and explores possible reasons for any differences they report in the effects of gestational stress on various types of behavior in the offspring. An abundance of experimental data shows that different maternal stressors in rodents can replicate some of the abnormalities in offspring behavior observed in humans. These include, anxiety, in juvenile and adult rats and mice, assessed in the elevated plus maze and open field tests and depression, detected in the forced swim and sucrose-preference tests. Deficits were reported in social interaction that is suggestive of pathology associated with schizophrenia, and in spatial learning and memory in adult rats in the Morris water maze test, but in most studies only males were tested. There were too few studies on the novel object recognition test at different inter-trial intervals to enable a conclusion about the effect of prenatal stress and whether any deficits are more prevalent in males. Among hippocampal glutamate receptors, NR2B was the only subtype consistently reduced in association with learning deficits. However, like in humans with schizophrenia and depression, prenatal stress lowered hippocampal levels of BDNF, which were closely correlated with decreases in hippocampal long-term potentiation. In mice, down-regulation of BDNF appeared to occur through the action of gene-methylating enzymes that are already increased above controls in prenatally-stressed neonates. In conclusion, the data obtained so far from experiments in rodents lend support to a physiological basis for the neurodevelopmental hypothesis of schizophrenia and depression.

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Section: Neurochemical Basis Of Behavioral Alterationsmentioning

confidence: 99%

Prenatal stressors in rodents: Effects on behavior

Weinstock

2017

Neurobiology of Stress

216

156

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“…In addition to data regarding the causal link between inter-individual differences in anxiety- and depression-like behaviors and appetence for nicotine, it was demonstrated that acute stressor exposure through a single episode of intermittent footshock administered 24 h before the start of place conditioning dose-dependently facilitated acquisition of CPP to nicotine in adolescent rats ( 256 ). Prenatal stress in rats also increased nicotine reinforcing properties in a CPP procedure and anxiety withdrawal symptom at the cessation of nicotine exposure ( 257 , 258 ). Finally, chronic mild stress, considered as a model of depression, which was delivered prior to nicotine exposure was found to exacerbate nicotine withdrawal syndrome in rats ( 259 ).…”

Section: Predisposing Endophenotypes For Nicotine Taking and Seeking mentioning

confidence: 99%

Cognitive Dysfunction, Affective States, and Vulnerability to Nicotine Addiction: A Multifactorial Perspective

Besson

Forget

2016

Front. Psychiatry

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Although smoking prevalence has declined in recent years, certain subpopulations continue to smoke at disproportionately high rates and show resistance to cessation treatments. Individuals showing cognitive and affective impairments, including emotional distress and deficits in attention, memory, and inhibitory control, particularly in the context of psychiatric conditions, such as attention-deficit hyperactivity disorder, schizophrenia, and mood disorders, are at higher risk for tobacco addiction. Nicotine has been shown to improve cognitive and emotional processing in some conditions, including during tobacco abstinence. Self-medication of cognitive deficits or negative affect has been proposed to underlie high rates of tobacco smoking among people with psychiatric disorders. However, pre-existing cognitive and mood disorders may also influence the development and maintenance of nicotine dependence, by biasing nicotine-induced alterations in information processing and associative learning, decision-making, and inhibitory control. Here, we discuss the potential forms of contribution of cognitive and affective deficits to nicotine addiction-related processes, by reviewing major clinical and preclinical studies investigating either the procognitive and therapeutic action of nicotine or the putative primary role of cognitive and emotional impairments in addiction-like features.

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“…Among others, impaired adaptation to stressful conditions, increased vulnerability to toxic and traumatic lesions, memory impairments and delayed psychomotor development have been described [43]. Changes in neurotransmitter levels and metabolism, hormonal alterations and gene expression patterns have been documented [12,42,44,45]. In this respect, it is worth mentioning that many neurobehavioral impairments may be related to changes in the dopamine (DA) neurotransmission.…”

Section: Discussionmentioning

confidence: 99%