The anxiolytic-like effect of nicotine undergoes rapid tolerance in a model of contextual fear conditioning in rats

Szyndler, Janusz; Sienkiewicz-Jarosz, Halina; Maciejak, Piotr; Siemiątkowski, Marek; Rokicki, Dariusz; Czlonkowska, A; Płaźnik, Adam

doi:10.1016/s0091-3057(01)00548-2

Cited by 40 publications

(23 citation statements)

References 33 publications

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“…27,28 Single injections of nicotine also decrease the freezing response of rats in the contextual fearconditioning test. 29 Furthermore, clinical evidence from patients with Alzheimer's disease also supports a relationship between the cholinergic system and anxiety. Alzheimer's disease is associated with decreased cholinergic levels, and roughly 33% of patients with Alzheimer's syndrome also suffer from anxiety disorders.…”

Section: Discussionmentioning

confidence: 98%

Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities

et al. 2008

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Mutations in SLITRK1 are found in patients with Tourette's syndrome and trichotillomania. SLITRK1 encodes a transmembrane protein containing leucine-rich repeats that is produced predominantly in the nervous system. However, the role of this protein is largely unknown, except that it can modulate neurite outgrowth in vitro. To clarify the role of Slitrk1 in vivo, we developed Slitrk1-knockout mice and analyzed their behavioral and neurochemical phenotypes. Slitrk1-deficient mice exhibited elevated anxiety-like behavior in the elevated plus-maze test as well as increased immobility time in forced swimming and tail suspension tests. Neurochemical analysis revealed that Slitrk1-knockout mice had increased levels of norepinephrine and its metabolite 3-methoxy-4-hydroxyphenylglycol. Administration of clonidine, an a2-adrenergic agonist that is frequently used to treat patients with Tourette's syndrome, attenuated the anxiety-like behavior of Slitrk1-deficient mice in the elevated plusmaze test. These results lead us to conclude that noradrenergic mechanisms are involved in the behavioral abnormalities of Slitrk1-deficient mice. Elevated anxiety due to Slitrk1 dysfunction may contribute to the pathogenesis of neuropsychiatric diseases such as Tourette's syndrome and trichotillomania.

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Section: Discussionmentioning

confidence: 98%

Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities

et al. 2008

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“…Alterations in cholinergic neurotransmission have been implicated in anxiety induction; muscarinic Ach receptor antagonists are anxiogenic in rodents (36,37), whereas nicotinic receptor agonists decrease anxiety (38)(39)(40) and AchE inhibitors reduce neophobia (41). Aged mice had elevated AchE expression in the NBM that coincided with elevated anxiety-like behavior occurring late in the dark phase.…”

Section: Discussionmentioning

confidence: 99%

Altered temporal patterns of anxiety in aged and amyloid precursor protein (APP) transgenic mice

Bedrosian

Herring

Weil

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Both normal aging and dementia are associated with dysregulation of the biological clock, which contributes to disrupted circadian organization of physiology and behavior. Diminished circadian organization in conjunction with the loss of cholinergic input to the cortex likely contributes to impaired cognition and behavior. One especially notable and relatively common circadian disturbance among the aged is "sundowning syndrome," which is characterized by exacerbated anxiety, agitation, locomotor activity, and delirium during the hours before bedtime. Sundowning has been reported in both dementia patients and cognitively intact elderly individuals living in institutions; however, little is known about temporal patterns in anxiety and agitation, and the neurobiological basis of these rhythms remains unspecified. In the present study, we explored the diurnal pattern of anxiety-like behavior in aged and amyloid precursor protein (APP) transgenic mice. We then attempted to treat the observed behavioral disturbances in the aged mice using chronic nightly melatonin treatment. Finally, we tested the hypothesis that time-of-day differences in acetylcholinesterase and choline acetyltransferase expression and general neuronal activation (i.e., c-Fos expression) coincide with the behavioral symptoms. Our results show a temporal pattern of anxiety-like behavior that emerges in elderly mice. This behavioral pattern coincides with elevated locomotor activity relative to adult mice near the end of the dark phase, and with time-dependent changes in basal forebrain acetylcholinesterase expression. Transgenic APP mice show a similar behavioral phenomenon that is not observed among agematched wild-type mice. These results may have useful applications to the study and treatment of age-and dementia-related circadian behavioral disturbances, namely, sundowning syndrome.Alzheimer's disease | cholinesterase | nucleus basalis of Meynert | behavioral and psychological signs and symptoms of dementia B oth normal aging and dementia are associated with disturbances in the biological clock that contribute to dramatic circadian disorganization, including the sleep-wake cycle, body temperature rhythm, and daily patterns of hormone release (1). Generally, aging is associated with reduced amplitudes among these daily rhythms; the most severe changes are associated with Alzheimer's disease (AD) (2). Circadian disorders affect more than 80% of individuals over age 65 (3) because of several converging factors; loss of neurons in the suprachiasmatic nucleus, decreased melatonin and melatonin receptor sensitivity, and minimal zeitgebers because of lifestyle all contribute to circadian dysfunction (1, 4).Normal aging and dementia are also associated with impairments in cognition and behavior, in part caused by loss of cholinergic input to the cortex (5). In particular, parts of the basal forebrain, most notably the nucleus basalis of Meynert (NBM), undergo degenerative changes, such as down-regulation of choline acetyltransferase (ChAT) activity (the r...

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“…However, no posttraining injection of nicotine was given, making it impossible to determine whether this effect was on acquisition or consolidation of fear conditioning. This behavioral effect is not present in animals receiving six daily nicotine injections prior to training (Szyndler et al 2001), indicating that they become tolerant to the effects of systemic nicotine. Gould and Wehner (1999) also examined the effects of systemic nicotine on Pavlovian fear conditioning in mice.…”

Section: Pharmacological Nicotinic Manipulations and Pavlovian Fear Cmentioning

confidence: 92%

“…Systemic, acute pretraining injections of nicotine, the archetypal agonist at nicotinic receptors, 5 to 20 min prior to Pavlovian fear conditioning in rats, reduce levels of context fear during a subsequent test session (Szyndler et al 2001). These effects are not caused by unconditional increases in freezing caused by the nicotine injection itself or are the result of changes in pain sensitivity.…”

Section: Pharmacological Nicotinic Manipulations and Pavlovian Fear Cmentioning

confidence: 98%

The Role of Muscarinic and Nicotinic Cholinergic Neurotransmission in Aversive Conditioning: Comparing Pavlovian Fear Conditioning and Inhibitory Avoidance

Tinsley

Quinn²,

Fanselow³

2004

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The anxiolytic-like effect of nicotine undergoes rapid tolerance in a model of contextual fear conditioning in rats

Cited by 40 publications

References 33 publications

Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities

Slitrk1-deficient mice display elevated anxiety-like behavior and noradrenergic abnormalities

Altered temporal patterns of anxiety in aged and amyloid precursor protein (APP) transgenic mice

The Role of Muscarinic and Nicotinic Cholinergic Neurotransmission in Aversive Conditioning: Comparing Pavlovian Fear Conditioning and Inhibitory Avoidance

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