Stressful experience has opposite effects on dendritic spines in the hippocampus of cycling versus masculinized females

Abstract

Stress increases associative learning and the density of dendritic spines in the hippocampus of male rats. In contrast, exposure to the same stressor impairs associative learning and reduces spine density in females. These effects in females are most evident when they are in the proestrus phase of the estrous cycle. An injection of testosterone at the time of birth masculinizes the female brain. In adulthood, masculinized females respond like males do to stress, i.e. they learn better. Here, we hypothesized that stress would increase spine densities on pyramidal neurons in area CA1 of the hippocampus of masculinized females, because stress enhances learning ability in both males and masculinized females. To test this, we used Golgi impregnation to stain tissue from masculinized and cycling females that were exposed to the acute stressor and sacrificed one day later. There was a significant interaction between stressor exposure and testosterone treatment at birth (p<0.001). In general, cycling females that were stressed tended to possess fewer spines on apical and basal dendrites in the CA1 area of the hippocampus, whereas the masculinized females possessed significantly more spines after the stressor. These findings underscore the plastic nature of dendritic spines. They suggest that their response to stress in adulthood is organized by the presence of testosterone during very early development. Such a process may represent a mechanism for altering learning abilities after an acute traumatic experience.

Correlated memory defects and hippocampal dendritic spine loss after acute stress involve corticotropin-releasing hormone signaling

“…These diverse morphological effects of stress are not surprising, given the wide array of stress types and contexts (24) coupled with the biological variability of the hippocampus that is being stressed, including gender (53,69,70) and age (41,71). Therefore it is reasonable to propose that the plethora of structural and functional changes provoked by stress might be a result of a broad repertoire of stress-activated mediators acting via numerous mechanisms.…”

Divergent Functional Effects of Sazetidine-A and Varenicline During Nicotine Withdrawal

“…However, to do this, we first investigated hippocampal functional changes following in vivo treatment with chronic nicotine and withdrawal, which may impact the efficacy of these drugs. To do this, evoked responses were recorded from ventral Electrical stimulation of the Schaffer collateral pathway (Figure 5a and b) results in robust activation of the CA1, a region of the hippocampus sensitive to stress-induced synaptic remodeling (Dalla et al, 2009;Joels et al, 2004Joels et al, , 2008McEwen, 2001;McEwen and Magarinos, 2001;Shors et al, 1997Shors et al, , 2001) and shown to be selectively affected in individuals with anxiety disorders (Cole et al, 2010). As shown in Figure 5ci and ii ( þ 10ms), responses evoked in the CA1 by Schaffer collateral stimulation were significantly increased following chronic administration of nicotine relative to saline controls.…”

Chronic Stress- and Sex-Specific Neuromorphological and Functional Changes in Limbic Structures

“…Stress also influences CA1 dendritic/spine morphology, with chronic stress increasing CA1 branching [152] and postsynaptic density [215]. Moreover, sex differences in CA1 spine density emerge following an acute stressor, with males expressing increased apical and/or basal spine density compared to females (for review, see [216]), and this effect can be reproduced through the masculinization of females [217]. In addition, CA1 basal spine shape can be influenced by acute stress [218] and chronic stress [173,174] by facilitating the maturation of spines.…”