Self-Stimulation Rewarding Experience Restores Stress-Induced CA3 Dendritic Atrophy, Spatial Memory Deficits and Alterations in the Levels of Neurotransmitters in the Hippocampus

Abstract

Chronic restraint stress causes spatial learning and memory deficits, dendritic atrophy of the hippocampal pyramidal neurons and alterations in the levels of neurotransmitters in the hippocampus. In contrast, intracranial self-stimulation (ICSS) rewarding behavioral experience is known to increase dendritic arborization, spine and synaptic density, and increase neurotransmitter levels in the hippocampus. In addition, ICSS facilitates operant and spatial learning, and ameliorates fornix-lesion induced behavioral deficits. Although the effects of stress and ICSS are documented, it is not known whether ICSS following stress would ameliorate the stress-induced deficits. Accordingly, the present study was aimed to evaluate the role of ICSS on stress-induced changes in hippocampal morphology, neurochemistry, and behavioral performance in the T-maze. Experiments were conducted on adult male Wistar rats, which were randomly divided into four groups; normal control, stress (ST), self-stimulation (SS), and stress + self-stimulation (ST + SS). Stress group of rats were subjected to restraint stress for 6 h daily over 21 days, SS group animals were subjected to SS from ventral tegmental area for 10 days and ST + SS rats were subjected to restraint stress for 21 days followed by 10 days of SS. Interestingly, our results show that stress-induced behavioral deficits, dendritic atrophy, and decreased levels of neurotransmitters were completely reversed following 10 days of SS experience. We propose that SS rewarding behavioral experience ameliorates the stress-induced cognitive deficits by inducing structural and biochemical changes in the hippocampus.

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

“…Acetylcholinesterase activity was measured by modified Ellman's method (Ellman et al, 1961;Ramkumar et al, 2008;Srikumar et al, 2006;Sunanda et al, 2000). At the end of experimentation, rats were decapitated; the frontal cortex, hippocampus, and septum were dissected quickly.…”

“…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).…”

“…Several morphological, neurochemical, and neurogenic mechanisms have been proposed to underlie the stress-induced cognitive deficits (McEwen, 2000). 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).…”

The Same Antidepressant Elicits Contrasting Patterns of Synaptic Changes in the Amygdala vs Hippocampus

“…Brains were quickly removed and processed for rapid Golgi staining (Ramkumar et al, 2008). Dendritic arbors of Golgi-impregnated BLA neurons were quantified using Sholl's analysis as described earlier (Vyas et al, 2002;Supplementary Information).…”

Potential Applications of Euphorbia hirta in Pharmacology

“…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). The dopaminergic and cholinergic neurotransmitter systems have been shown to be involved in mediating the stress induced deficits (Srikumar et al, 2006(Srikumar et al, , 2007.…”