Chronic but not acute nicotine treatment reverses stress-induced impairment of LTP in anesthetized rats.
ABSTRACT Stress impairs long-term potentiation (LTP) and is a major cause for starting or increasing tobacco smoking. We have previously shown that chronic concurrent nicotine treatment prevents stress-induced LTP impairment. Nicotine reduces stress-induced impairment of LTP, probably, through activation of nicotinic acetylcholine receptors in the hippocampus. Herein, we investigated the effects of acute and chronic nicotine treatments on the chronic-stress-induced impairment of LTP in area CA1 of the hippocampus of urethane-anesthetized rats. Extracellular in vivo recording from the hippocampal area CA1 showed that pre-treatment with nicotine (1 mg/kg; sc twice/day for 2 weeks prior to stress) protected LTP from the inhibitory effect of subsequent chronic psychosocial stress (4 additional weeks concurrently with nicotine). In another series of experiments, 2 weeks of psychosocial stress was followed by 4 weeks of nicotine treatment concurrently with continuing stress. Nicotine treatment reversed established stress-induced impairment of LTP. However, acute nicotine treatment of rats (a single dose of 1 mg/kg; sc.) did not reverse chronic-stress-induced impairment of LTP. The results show that the impairment of LTP during chronic stress can be blocked by chronic, but not acute, nicotine treatment.
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ABSTRACT: Stress is a biologically significant factor that, by altering brain cell properties, can disturb cognitive processes such as learning and memory, and consequently limit the quality of human life. Extensive rodent and human research has shown that the hippocampus is not only crucially involved in memory formation, but is also highly sensitive to stress. So, the study of stress-induced cognitive and neurobiological sequelae in animal models might provide valuable insight into the mnemonic mechanisms that are vulnerable to stress. Here, we provide an overview of the neurobiology of stress memory interactions, and present a neural endocrine model to explain how stress modifies hippocampal functioning.Nature reviews. Neuroscience 07/2002; 3(6):453-62. · 31.67 Impact Factor
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ABSTRACT: Although Alzheimer's disease (AD) is a disorder involving multiple neurotransmitter systems, the basal forebrain cholinergic system (Ch system) is severely and consistently affected in this condition. In both animals and man, the nature of age-associated alterations in the Ch system is unclear. In addition, available studies of cholinergic receptors in AD and aging are not consistent. In normal aging, the density of muscarinic cholinergic receptors (MCR) is reported to be either unchanged or decreased. In AD, increased, unchanged, or decreased densities have been reported. Recently, a subtype of MCR (M2), thought to be located presynaptically, has been reported to be reduced in neocortex and amygdala. In both AD and aging, nicotinic cholinergic receptors (NCR) have not been adequately studied. Our recent studies using [3H] acetylcholine and [3H] nicotine have demonstrated a reduction in NCR in AD. Possible explanations for some of the inconsistent findings are discussed, and directions for future studies are suggested.Progress in Neuro-Psychopharmacology and Biological Psychiatry 02/1986; 10(3-5):665-76. · 3.55 Impact Factor
- Annals of the New York Academy of Sciences 12/2006; 746(1):411 - 414. · 4.38 Impact Factor