Figure 2. Chronic sexual experience enhances cell proliferation and
adult neurogenesis without altering glucocorticoid levels.
Well, now, sex is good for your brain! As if we needed another reason to get intimate with our loved one. We have known for quite some time that exercise (especially aerobic exercise) stimulates neurogenesis (the creation of new brain neurons), and we also know that SSRI antidepressants also stimulate neurogenesis, so now we can add sex to that list.
Personally, given the option, I'd rather get some exercise and have sex than take SSRIs, so this is good news.
As far as the study is concerned, they were looking at acute vs. chronic sexual experience in mice. Acute = a single experience; chronic = repeated sexual experience over a 14-day period. The acute experience produced stress hormones as well as neurogenesis, while in the chronic experience, the stress hormones dissipated after the initial experience, while the neurogenesis continued.
Sexual Experience Promotes Adult Neurogenesis in the Hippocampus Despite an Initial Elevation in Stress Hormones
Benedetta Leuner, Erica R. Glasper, Elizabeth Gould*Department of Psychology, Neuroscience Institute, Princeton University, Princeton, New Jersey, United States of America
Abstract
Aversive stressful experiences are typically associated with increased anxiety and a predisposition to develop mood disorders. Negative stress also suppresses adult neurogenesis and restricts dendritic architecture in the hippocampus, a brain region associated with anxiety regulation. The effects of aversive stress on hippocampal structure and function have been linked to stress-induced elevations in glucocorticoids. Normalizing corticosterone levels prevents some of the deleterious consequences of stress, including increased anxiety and suppressed structural plasticity in the hippocampus. Here we examined whether a rewarding stressor, namely sexual experience, also adversely affects hippocampal structure and function in adult rats. Adult male rats were exposed to a sexually-receptive female once (acute) or once daily for 14 consecutive days (chronic) and levels of circulating glucocorticoids were measured. Separate cohorts of sexually experienced rats were injected with the thymidine analog bromodeoxyuridine in order to measure cell proliferation and neurogenesis in the hippocampus. In addition, brains were processed using Golgi impregnation to assess the effects of sexual experience on dendritic spines and dendritic complexity in the hippocampus. Finally, to evaluate whether sexual experience alters hippocampal function, rats were tested on two tests of anxiety-like behavior: novelty suppressed feeding and the elevated plus maze. We found that acute sexual experience increased circulating corticosterone levels and the number of new neurons in the hippocampus. Chronic sexual experience no longer produced an increase in corticosterone levels but continued to promote adult neurogenesis and stimulate the growth of dendritic spines and dendritic architecture. Chronic sexual experience also reduced anxiety-like behavior. These findings suggest that a rewarding experience not only buffers against the deleterious actions of early elevated glucocorticoids but actually promotes neuronal growth and reduces anxiety.
Citation: Leuner B, Glasper ER, Gould E (2010) Sexual Experience Promotes Adult Neurogenesis in the Hippocampus Despite an Initial Elevation in Stress Hormones. PLoS ONE 5(7): e11597. doi:10.1371/journal.pone.0011597
Editor: Melissa Coleman, Claremont Colleges, United States of America
Received: March 30, 2010; Accepted: June 17, 2010; Published: July 14, 2010
Copyright: © 2010 Leuner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The work was supported by a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression (B.L.), grants from the National Institute of Mental Health (MH084148 to B.L. and MH54970 to E.G.) and a Ruth L. Kirschstein postdoctoral NRSA fellowship from the National Institute on Aging (E.R.G.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The authors have declared that no competing interests exist.
Introduction
Negative or aversive stressful experiences are associated with deleterious consequences for the brain and behavior. Indeed, aversive stress and trauma are major predisposing factors for the development of psychopathology [1]. The hippocampus is particularly sensitive to aversive stress, responding with diminished adult neurogenesis [2], [3], [4], dendritic complexity [5], [6], [7] and synaptic plasticity [8]. Negative stress enhances anxiety [9], the regulation of which has been linked to the hippocampus [10]. Elevated glucocorticoid levels have been implicated in these effects – blocking stress-induced increases in corticosterone levels prevents detrimental effects on adult neurogenesis [4], dendritic complexity [6], and anxiety [9].
Despite evidence linking elevated stress hormones with impaired structural plasticity and hippocampal function, physical exercise increases glucocorticoid levels but is generally beneficial to health. Running increases glucocorticoid levels in rodents and humans [11], [12], while paradoxically enhancing structural plasticity, including adult neurogenesis [13], [14], dendritic spine density, and dendritic complexity [15], [16] in the hippocampus. Furthermore, exercise reduces anxiety [17] and improves learning and memory functions associated with the hippocampus [13]. Running also increases blood flow to the brain, improves cardiovascular fitness, and stimulates angiogenesis, all factors that could lead to improved neuronal growth and, ultimately, enhanced brain function [18]. However, a recent study showed that rewarding intracranial self-stimulation is sufficient to increase adult neurogenesis [19], suggesting that the hedonic aspect of physical exercise may be responsible for its beneficial effects on structural plasticity.
Exercise appears to be universally rewarding for rodents – rats and mice voluntarily run considerable distances if given access to a running wheel. Rats also develop place preferences for a running wheel [17], [20] and will bar press to gain access to running [21]. Collectively, these results suggest that the emotional valence or hedonic value of the stressor may play a role in determining whether an experience will produce negative or positive effects despite elevated glucocorticoid levels [22]. That is, positive or rewarding stress may buffer the brain from the potentially adverse consequences of physical exertion. To explore this possibility further, we examined whether sexual behavior, a natural rewarding experience, is associated with alterations in hippocampal structure, glucocorticoids, and anxiety.
This is an open source publication, so go read the whole article.
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