Article

Interactive effects of stress and aging on structural plasticity in the prefrontal cortex.

Fishberg Department of Neuroscience and Kastor Neurobiology of Aging Laboratories, Mount Sinai School of Medicine, New York, New York 10029, USA.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.75). 05/2010; 30(19):6726-31. DOI: 10.1523/JNEUROSCI.0759-10.2010
Source: PubMed

ABSTRACT Neuronal networks in the prefrontal cortex mediate the highest levels of cognitive processing and decision making, and the capacity to perform these functions is among the cognitive features most vulnerable to aging. Despite much research, the neurobiological basis of age-related compromised prefrontal function remains elusive. Many investigators have hypothesized that exposure to stress may accelerate cognitive aging, though few studies have directly tested this hypothesis and even fewer have investigated a neuronal basis for such effects. It is known that in young animals, stress causes morphological remodeling of prefrontal pyramidal neurons that is reversible. The present studies sought to determine whether age influences the reversibility of stress-induced morphological plasticity in rat prefrontal neurons. We hypothesized that neocortical structural resilience is compromised in normal aging. To directly test this hypothesis we used a well characterized chronic restraint stress paradigm, with an additional group allowed to recover from the stress paradigm, in 3-, 12-, and 20-month-old male rats. In young animals, stress induced reductions of apical dendritic length and branch number, which were reversed with recovery; in contrast, middle-aged and aged rats failed to show reversible morphological remodeling when subjected to the same stress and recovery paradigm. The data presented here provide evidence that aging is accompanied by selective impairments in long-term neocortical morphological plasticity.

Download full-text

Full-text

Available from: William Gm Janssen, Jul 05, 2015
1 Follower
 · 
104 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: This article is part of a Special Issue "Puberty and Adolescence". Learning and memory is affected by a myriad of factors, including exposure to stressors and the corresponding rise in circulating glucocorticoids. Nevertheless, the effects of stressors depend on the sex, species, the type of stressor used, the duration of exposure, as well as the developmental time-point in which stressors are experienced. Effects of stress in adolescence, however, have received less attention than other developmental periods. In adolescence, the hypothalamic-pituitary-adrenal axis and brain regions involved in learning and memory, which also richly express corticosteroid receptors, are continuing to develop, and thus the effects of stress exposures would be expected to differ from those in adulthood. We conclude from a review of the available literature in animal models that hippocampal function is particularly sensitive to adolescent stressors, and the effects tend to be most evident several weeks after the exposure, suggesting stressors alter the developmental trajectory of the hippocampus.
    Hormones and Behavior 07/2013; 64(2):364-79. DOI:10.1016/j.yhbeh.2012.09.012 · 4.51 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The adult brain is capable of considerable structural and functional plasticity and the study of hormone actions in brain has contributed to our understanding of this important phenomenon. In particular, stress and stress-related hormones such as glucocorticoids and mineralocorticoids play a key role in the ability of acute and chronic stress to cause reversible remodeling of neuronal connections in the hippocampus, prefrontal cortex, and amygdala. To produce this plasticity, these hormones act by both genomic and non-genomic mechanisms together with ongoing, experience-driven neural activity mediated by excitatory amino acid neurotransmitters, neurotrophic factors such as brain derived neurotrophic factor, extracellular molecules such as neural cell adhesion molecule, neuropeptides such as corticotrophin releasing factor, and endocannabinoids. The result is a dynamic brain architecture that can be modified by experience. Under this view, the role of pharmaceutical agents, such as antidepressants, is to facilitate such plasticity that must also be guided by experiences.
    Developmental Neurobiology 06/2012; 72(6):878-90. DOI:10.1002/dneu.20968 · 4.19 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Stressful life events, especially those that induce fear, can produce a state of anxiety that is useful for avoiding similar fearful and potentially dangerous situations in the future. However, they can also lead to exaggerated states, which over time can produce mental illness. These changing states of readiness versus illness are thought to be regulated, at least in part, by alterations in dendritic and synaptic structure within brain regions known to be involved in anxiety. These regions include the amygdala, hippocampus, and prefrontal cortex. In this article, we review the reciprocal relationships between the expression of stress- and anxiety-related behaviors and stress-induced morphological plasticity as detected by changes in dendrites and spines in these three brain regions. We begin by highlighting the acute and chronic effects of stress on synaptic morphology in each area and describe some of the putative mechanisms that have been implicated in these effects. We then discuss the functional consequences of stress-induced structural plasticity focusing on synaptic plasticity as well as cognitive and emotional behaviors. Finally, we consider how these structural changes may contribute to adaptive behaviors as well as maladaptive responses associated with anxiety.
    Neuroscience 04/2012; DOI:10.1016/j.neuroscience.2012.04.021 · 3.33 Impact Factor