The involvement of cholinergic and noradrenergic systems in behavioral recovery following oxotremorine treatment to chronically stressed rats

Srikumar, B.N.; Raju, T.R.; Rao, B.S. Shankaranarayana

doi:10.1016/j.neuroscience.2006.08.041

Cited by 71 publications

(84 citation statements)

References 68 publications

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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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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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“…In addition to anxiety, stress is also known to produce learning and memory deficits. For example, chronic stress impaired learning in the T-maze and radial arm maze (Ramkumar et al, 2008;Srikumar et al, 2006Srikumar et al, , 2007 or in other paradigms such as the Barnes maze and Morris water maze (Bodnoff et al, 1995;McLay et al, 1998). Several morphological, neurochemical, and neurogenic mechanisms have been proposed to underlie the stress-induced cognitive deficits (McEwen, 2000).…”

Section: Introductionmentioning

confidence: 99%

“…Detailed evaluation of the hippocampal morphology over the past several years clearly indicates atrophy of the hippocampal CA3 neurons following stress (Magarinos & McEwen, 1995;Ramkumar et al, 2008). Further, the dopaminergic and cholinergic neurotransmitter systems have been shown to be involved in mediating the stressinduced deficits (Srikumar et al, 2006(Srikumar et al, , 2007Sunanda et al, 2000). Several studies have examined the possible amelioration of stress-induced cognitive deficits or other types of anxiety (Barros et al, 2007;Rajarao et al, 2007;Srikumar et al, 2006Srikumar et al, , 2007.…”

Section: Introductionmentioning

confidence: 99%

Restoration of acetylcholinesterase activity byEuphorbia hirtain discrete brain regions of chronically stressed rats

Anuradha¹,

Srikumar²,

Deepti³

et al. 2010

Pharmaceutical Biology

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“…Prior studies linking cholinergic function to anxiety levels (Srikumar et al, 2006;Degroot and Dallas, 2002;Millan, 2003;Sienkiewicz-Jarosz et al, 2000) initially led us to hypothesize that the different effects of in utero MSF exposure as shown in the 8AFM versus the 8AWM may have been due to an altered stress response, in this case a blunted response to anxiety when exposed to noxious stimuli. Clearly we found no such change in the open field maze or the elevated plus maze, though the animals were tested only at basal levels of anxiety and not in responses to induced stress (e.g., 8AWM).…”

Section: Discussionmentioning

confidence: 99%

In utero methanesulfonyl fluoride differentially affects learning and maze performance in the absence of long-lasting cholinergic changes in the adult rat

Carcoba

Santiago

Moss

et al. 2008

Pharmacology Biochemistry and Behavior

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There is increasing evidence that acetylcholinesterase (AChE) may have various specific developmental roles in brain development. Nevertheless, specific effects of AChE inhibition during early brain development have not been adequately described. Therefore, methanesulfonyl fluoride (MSF), an irreversible AChE inhibitor that shows high selectivity for the CNS was used to produce AChE inhibition in utero to study subsequent adult behaviors, sleep, and cholinergic markers. Rats exposed to MSF in utero showed a deficit in spatial learning tasks using appetitive motivation but, surprisingly, they performed equally well or better than controls when aversive motivation was used. One hypothesis was that MSF treatment in utero affected the response to stress. Tests of anxiety however showed no differences in basal levels of anxiety. Studies of sleep behavior, however, indicated a higher level of REM sleep which is only seen during the light phase of male rats exposed to MSF in utero as compared to controls. No differences in cholinergic markers in the brains of adults were found except that females exposed to MSF in utero had a higher level of ChAT activity in the synaptosomal fraction of the hippocampus. Even so, whether cholinergic alterations accompany the in utero MSF exposure remains to be determined. The failure to find widespread changes in cholinergic markers in the adult brains suggests changes in behaviors should be further investigated by testing the participation of postsynaptic mechanisms, measuring of cholinergic markers during earlier development periods and the possible participation of other neurotransmitter systems to clearly reveal the role of the cholinergic system following in utero MSF exposure.

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The involvement of cholinergic and noradrenergic systems in behavioral recovery following oxotremorine treatment to chronically stressed rats

Cited by 71 publications

References 68 publications

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

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

Restoration of acetylcholinesterase activity byEuphorbia hirtain discrete brain regions of chronically stressed rats

In utero methanesulfonyl fluoride differentially affects learning and maze performance in the absence of long-lasting cholinergic changes in the adult rat

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