Effects of restraint stress on the expression of proteins involved in synaptic vesicle exocytosis in the hippocampus

Gao, Yan; Bezchlibnyk, Yarema B.; Sun, Xiao; Wang, J.-F.; McEwen, Bruce S.; Young, L. Trevor

doi:10.1016/j.neuroscience.2006.04.066

Cited by 52 publications

(30 citation statements)

References 68 publications

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“…For example, stress that occurs as a result of restraining rats has been shown to increase synatophysin expression in the hippocampus (Gao et al, 2006). Given that the rats in the present study were restrained during robot testing, it is possible that restraintrelated stress was induced and that this influenced synatophysin expression.…”

Section: Wstt Enhanced Synaptic Plasticity In the Lumbar Spinal Cord mentioning

confidence: 89%

Differential Effects of Low versus High Amounts of Weight Supported Treadmill Training in Spinally Transected Rats

Leon

See

Chow

2011

Journal of Neurotrauma

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Intensive weight-supported treadmill training (WSTT)improves locomotor function following spinal cord injury. Because of a number of factors, undergoing intensive sessions of training may not be feasible. Whether reduced amounts of training are sufficient to enhance spinal plasticity to a level that is necessary for improving function is not known. The focus of the present study was to assess differences in recovery of locomotor function and spinal plasticity as a function of the amount of steps taken during WSTT in a rodent model of spinal cord injury. Rats were spinally transected at 5 days of age. When they reached 28 days of age, a robotic system was used to implement a weight-supported treadmill training program of either 100 or 1000 steps/training session daily for 4 weeks. Antibodies for brain-derived neurotrophic factor (BDNF), TrkB, and the pre-synaptic marker, synaptophysin, were used to examine the expression of these proteins in the ventral horn of the lumbar spinal cord. Rats that received weight-supported treadmill training performed better stepping relative to untrained rats, but only the rats that received 1000 steps/training session recovered locomotor function that resembled normal patterns. Only the rats that received 1000 steps/training session recovered normal levels of synaptophysin immunoreactivity around motor neurons. Weight-supported treadmill training consisting of either 100 or 1000 steps/ training session increased BDNF immunoreactivity in the ventral horn of the lumbar spinal cord. TrkB expression in the ventral horn was not affected by spinal cord transection or weight-supported treadmill training. Synaptophysin expression, but not BDNF or TrkB expression was correlated with the recovery of stepping function. These findings suggested that a large amount of weight-supported treadmill training was necessary for restoring synaptic connections to motor neurons within the locomotor generating circuitry. Although a large amount of training was best for recovery, small amounts of training were associated with incremental gains in function and increased BDNF levels.

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Section: Wstt Enhanced Synaptic Plasticity In the Lumbar Spinal Cord mentioning

confidence: 89%

Differential Effects of Low versus High Amounts of Weight Supported Treadmill Training in Spinally Transected Rats

Leon

See

Chow

2011

Journal of Neurotrauma

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“…Gray levels were measured on the photomicrographs by placing open circles with diameters of 100 mm along different regions of the hippocampus (see Figure 1a). We followed procedures of Gao et al (2006). Specifically, optical density (OD) of synaptophysin was assessed in each of the hilus and inner molecular layer of the dentate gyrus (DGhilus and DGin), the stratum radiatum of the CA3 and CA1 (CA3ra and CA1ra), and the stratum oriens of the CA3 and CA1 (CA3or and CA1or).…”

Section: Quantitative Image Analysismentioning

confidence: 99%

“…Then the mean OD was obtained by subtracting each mean gray level from 255 (the maximum white intensity). Then the mean OD for each ROI was obtained by subtracting the mean reference OD from the corpus callosum from the mean OD for each ROI on each section (Gao et al, 2006).…”

Section: Quantitative Image Analysismentioning

confidence: 99%

Low Doses of 17α-Estradiol and 17β-Estradiol Facilitate, Whereas Higher Doses of Estrone and 17α- and 17β-Estradiol Impair, Contextual Fear Conditioning in Adult Female Rats

Barha

Dalton

Galea

2009

Neuropsychopharmacol

109

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Estrogens are known to exert significant structural and functional effects in the hippocampus of adult rodents. In particular, 17b-estradiol can improve, impair, or have no effect on hippocampus-dependent learning and memory depending on dose and time of administration. The effects of other forms of estrogen, such as estrone and 17a-estradiol, on hippocampus-dependent learning have not been as thoroughly investigated. Therefore, the purpose of this study was to investigate the effects of 17b-estradiol, estrone, and 17a-estradiol at three different doses on two different tasks: hippocampus-dependent contextual fear conditioning and hippocampusindependent cued fear conditioning. Adult ovariectomized female rats were injected with one of the estrogens at one of the three doses 30 mins before conditioning to assess the rapid effects of these estrogens on acquisition. Twenty-four hours later memory for the context was examined and 1 h later memory for the cue (tone) was assessed. Levels of synaptophysin were examined in the dorsal hippocampus of rats to identify a potential synaptic correlate of hormonal effects on contextual fear conditioning. Low 17b-estradiol and 17a-estradiol enhanced, whereas high 17b-estradiol and 17a-estradiol impaired, contextual fear conditioning. Only the middle dose of estrone severely impaired contextual fear conditioning. Estrogens did not alter performance in the hippocampus-independent cued task. Synaptophysin expression was increased by estrone (at a middle and high dose) and 17b-estradiol (at a middle dose) in the CA3 region of the hippocampus and was not correlated with cognition. The results of this study indicate that estradiol can positively or negatively influence hippocampus-dependent learning and memory, whereas estrone impairs hippocampus-dependent learning and memory in a dose-dependent manner. These results have important therapeutic implications, as estrone, a main component of a widely used hormone replacement therapy, was shown to have either a negative effect or no effect on learning and memory. It may be possible to use 17a-estradiol and lower doses of estrogens as potential alternatives in hormone replacement therapies.

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“…This type of restraint involves a physical component (immobilization), but acts primarily as a psychological stressor through awareness of the inability to escape (Glavin et al, 1994;Servatius et al, 2000). In addition to inducing hippocampal dendritic retraction, chronic restraint stress has also been widely used to assess other hippocampal properties including molecular expression and synaptic activity (Donahue et al, 2006;Ejchel-Cohen et al, 2006;Gao et al, 2006;McEwen, 1999;Stewart et al, 2005;Venero et al, 2002), and hippocampal-dependent behaviors such as spatial memory (Bowman et al, 2003;Conrad et al, 1996;Kleen et al, 2006;Luine et al, 1996;McLaughlin et al, 2005;Sandi et al, 2003;Srikumar et al, 2006). Earlier work with chronic restraint has emphasized that 6h/13d of restraint does not alter hippocampal dendritic complexity, and males tested under this paradigm actually show a slight enhancement in spatial memory on the radial arm maze (Luine et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

The effects of chronic stress on hippocampal morphology and function: An evaluation of chronic restraint paradigms

et al. 2007

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Chronic restraint stress for 6h/21d causes hippocampal CA3 apical dendritic retraction, which parallels spatial memory impairments in male rats. Recent research suggests that chronic immobilization stress for 2h/10d induces CA3 dendritic retraction (Vyas et al., 2002) and questions whether CA3 dendritic retraction and spatial memory deficits can be produced sooner than found following 6h/21d of restraint stress. Therefore, this study investigated the effects of four different durations of chronic restraint stress (varied by hours/day and total number of days) and the subsequent effects on hippocampal CA3 morphology and spatial memory in the same male Sprague-Dawley rats. The results showed that only rats exposed to the 6h/21d restraint paradigm exhibited CA3 apical dendritic retraction, consistent spatial memory deficits, and decreased body weight gain compared to experimental counterparts and controls. While chronically stressing a rat with wire mesh restraint has a physical component, it acts primarily as a psychological stressor, and these findings support the interpretation that chronic psychological stress produces hippocampal-dependent cognitive deficits that are consistent with hippocampal structural changes. Differences in stress effects observed across different studies may be due to rat strain, type of stressor, and housing conditions; however, the current findings support the use of chronic restraint stress, with wire mesh, for 6h/21d as a reliable and efficient method to produce psychological stress and to cause CA3 dendritic retraction and spatial memory deficits in male Sprague-Dawley rats.

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Effects of restraint stress on the expression of proteins involved in synaptic vesicle exocytosis in the hippocampus

Cited by 52 publications

References 68 publications

Differential Effects of Low versus High Amounts of Weight Supported Treadmill Training in Spinally Transected Rats

Differential Effects of Low versus High Amounts of Weight Supported Treadmill Training in Spinally Transected Rats

Low Doses of 17α-Estradiol and 17β-Estradiol Facilitate, Whereas Higher Doses of Estrone and 17α- and 17β-Estradiol Impair, Contextual Fear Conditioning in Adult Female Rats

The effects of chronic stress on hippocampal morphology and function: An evaluation of chronic restraint paradigms

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