Spine Density In Prefrontal Cortex Research Articles

Social hierarchy differentially influences the anxiety-like behaviors and dendritic spine density in prefrontal cortex and limbic areas in male rats

Social hierarchy is a fundamental feature of social organization that can influence brain and emotional processing regarding social ranks. Several areas, including the medial prefrontal cortex (mPFC), the hippocampus, and the basolateral nucleus of the amygdala (BLA), are recognized to be involved in the regulation of emotional processing. However, its delicate structural correlates in brain regions are poorly understood. To address this issue, social hierarchy in home-caged sibling Wistar rats (three male rats/cage) was determined by employing a social confrontation tube test (postnatal weeks 9–12). Then, locomotor activity and anxiety-like behaviors were evaluated using an open-field test (OFT) and elevated plus-maze (EPM) at 13 weeks of age. The rapid Golgi impregnation method was conducted to quantify the spine density of the first secondary branch of the primary dendrite in 20 µm length. The results indicated that dominant rats had significantly higher anxiety-like behaviors compared to subordinates, as was evident by lower open-arm entries and time spent in the EPM and lower entries and time spent in the center of OFT. The spine density analysis revealed a significantly higher number of spines in subordinates compared to the dominant rats in dmPFC pyramidal neurons and the apical and basal dendrites of hippocampal CA1 pyramidal neurons. However, the spine density of pyramidal-like neurons in the BLA was higher in dominant rats. Our findings suggest that dominant social rank is associated with higher anxiety and differential density of the dendritic spine in the prefrontal cortex and limbic regions of the brain in male rats.

Impact of subchronic variable stress on ovariectomy and dendritic spine density in prefrontal cortex in mice.

Major depressive disorder affects both women and men but females are two times more susceptible to the incidence of depression. The majority of stress models used male rodents, whereas fewer studies included females. Volumetric reductions have been reported in brain areas critical for the stress response, such as prefrontal cortex, and remodeling of dendritic spines has been proposed as an underlying factor. The aim of this study was to determine the effects of subchronic variable stress (SCVS) in males, sham, and specifically in ovariectomized (OVX) female mice. Here, we used 6 days SCVS model to induce depressive-like behavior, and only the OVX female mice showed the depressive-like behavior, while males showed resilient type behavior. Only OVX female mice showed significant increase in dendritic spine density in SCVS paradigm. Overall, this study suggests that (1) the effects SCVS produced on the behavior of males and OVX females and (2) SCVS may induce rapid and sustained changes of PL neurons, which highlights the importance of gonadal hormones in studying depression.

Sleep deprivation induces differential morphological changes in the hippocampus and prefrontal cortex in young and old rats.

Sleep is a fundamental state necessary for maintenance of physical and neurological homeostasis throughout life. Several studies regarding the functions of sleep have been focused on effects of sleep deprivation on synaptic plasticity at a molecular and electrophysiological level, and only a few studies have studied sleep function from a structural perspective. Moreover, during normal aging, sleep architecture displays some changes that could affect normal development in the elderly. In this study, using a Golgi-Cox staining followed by Sholl analysis, we evaluate the effects of 24 h of total sleep deprivation on neuronal morphology of pyramidal neurons from Layer III of the prefrontal cortex (PFC) and the dorsal hippocampal CA1 region from male Wistar rats at two different ages (3 and 22 months). We found no differences in total dendritic length and branching length in both analyzed regions after sleep deprivation. Spine density was reduced in the CA1 of young-adults, and interestingly, sleep deprivation increased spine density in PFC of aged animals. Taken together, our results show that 24 h of total sleep deprivation have different effects on synaptic plasticity and could play a beneficial role in cognition during aging.

Ablation of ErbB4 from excitatory neurons leads to reduced dendritic spine density in mouse prefrontal cortex.

Dendritic spine loss is observed in many psychiatric disorders, including schizophrenia, and likely contributes to the altered sense of reality, disruption of working memory, and attention deficits that characterize these disorders. ErbB4, a member of the EGF family of receptor tyrosine kinases, is genetically associated with schizophrenia, suggesting that alterations in ErbB4 function contribute to the disease pathology. Additionally, ErbB4 functions in synaptic plasticity, leading us to hypothesize that disruption of ErbB4 signaling may affect dendritic spine development. We show that dendritic spine density is reduced in the dorsomedial prefrontal cortex of ErbB4 conditional whole-brain knockout mice. We find that ErbB4 localizes to dendritic spines of excitatory neurons in cortical neuronal cultures and is present in synaptic plasma membrane preparations. Finally, we demonstrate that selective ablation of ErbB4 from excitatory neurons leads to a decrease in the proportion of mature spines and an overall reduction in dendritic spine density in the prefrontal cortex of weanling (P21) mice that persists at 2 months of age. These results suggest that ErbB4 signaling in excitatory pyramidal cells is critical for the proper formation and maintenance of dendritic spines in excitatory pyramidal cells.

Sleep deprivation induce morphology changes in the hippocampus and prefrontal cortex in young and old rats

Introduction During normal aging several changes in sleep/wake patterns are observed, which include frequent awakenings during sleep and increased daytime naps, among others. Likewise, aging has also been associated with a deterioration of cognitive function, learning and memory, although widespread loss of nerve cells does not occur, the most of age-related structural changes observed in nerve cells are modifications in dendrites, dendritic spines or even axons. Evidence accumulated over the last years indicates that these functional changes observed during sleep loss, aging, or both could be due to modifications in synaptic connectivity and intracellular signaling; for example, excitatory synaptic transmission at the hippocampal CA1 region is affected by sleep deprivation; in the locus coeruleus (involved in both arousal system and cognitive performance) the number of neurons projecting to areas such as the cortex and the hippocampus declines with age. Therefore, it has been hypothesized that sleep deprivation may compromise neurophysiological and behavioral events; however, relatively few studies have investigated links between sleep loss and structural changes in neurons and, despite the seemingly similar effects of age and sleep deprivation on cognition and the prevalence of sleep changes with age, little is known about the impact of sleep loss on cellular morphology in aging neurons. For that reasons, the aim of this study was to evaluate the effects of total sleep deprivation on neuronal morphology in the hippocampus and prefrontal cortex of both young and aged animals. Materials and methods A total of 28 male Wistar rats (14 “young-adult” rats, 3–4 months old; 14 “aged rats”, 22–23 months old; 7 for control and 7 for sleep deprivation for each age) were used in this study. Total sleep deprivation was carried out in both experimental groups (young-adult and aged, n = 7 per group) by gentle handling: once sleep-behaviour was observed or low amplitude waves first appear in sleep recording, rats were softly touched in their tails, whiskers or handling them to prevent falling asleep during 24 h. Immediately after sleep deprivation finished, animals were deeply anesthetized with sodium pentobarbital (75 mg/kg, i.p.) and then perfused intracardially with 0.9% saline solution. Brains were removed and stained by modified Golgi-Cox method. Pyramidal neurons from layer 3 of prefrontal cortex and hippocampus (CA1 area) were selected for study. Five neurons from each region of each brain hemisphere per animal were drawn using a camera lucida. Basal dendrites, including all branches, were reconstructed for each neuron and their dendritic tracings were quantified by Sholl analysis. Results Results showed that total dendritic length of prefrontal cortex and hippocampus was not affected either age or after 24 h of sleep deprivation compared to their corresponding control group. However, after 24 h of sleep deprivation (SD) aged animals had an increase in spine density in prefrontal cortex but not in hippocampus. Conclusion Sleep deprivation could be considered a factor that induces neuronal plasticity, which may depend on age. Acknowledgement This study was supported by CONACYT grant 133178.

Chronic phencyclidine treatment increases dendritic spine density in prefrontal cortex and nucleus accumbens neurons

We examined whether repeated exposure to the noncompetitive NMDA receptor antagonist phencyclidine (PCP) produces enduring changes in dendritic structure in a manner similar to the stimulants cocaine and amphetamine. Adult rats were treated with i.p. injections of PCP (5 mg/kg) or saline, twice a day, for 5 consecutive days, for a total of 4 weeks. One month after the last injection, their brains were removed and processed for Golgi-Cox staining. Prior exposure to PCP increased dendritic spine density in the mPFC and NAcc core, but not in the parietal cortex. These findings, which are similar to those observed after chronic treatment with cocaine and amphetamine, raise the possibility that, despite differences in their mechanisms of action, PCP and stimulant drugs may induce some of their enduring effects via common processes.

Weaning age, social isolation, and gender, interact to determine adult explorative and social behavior, and dendritic and spine morphology in prefrontal cortex of rats

We tested the effect of weaning at 21 or 30 days, followed by individual or group housing, on explorative and social behavior in adult male and female rats, and in males, on dendritic length and spine density in prefrontal cortex. In the open field, rats weaned early were the most active, while those weaned late and group housed were the most explorative. In the social interaction test, behavior in adult females was relatively impervious to weaning age or rearing condition. Isolated males sought out social interaction, whereas, group-reared males tended to avoid it. Social behaviors in males weaned early or group-reared correlated with decreased dendrite length and spine density, whereas, non-social behaviors correlated with increased dendritic length. Such changes are consistent with neural pruning in the development of social behavior. Although our experimental manipulations were mild, and serve as standard rearing conditions in many laboratories, their effects on brain and behavior were marked, and differed by gender. Early rearing conditions may have few appreciable effects when studied in isolation, but their interactive effects on adult social behavior are significant and varied.