Quetiapine ameliorates stress-induced cognitive inflexibility in rats

Nikiforuk, Agnieszka

doi:10.1016/j.neuropharm.2012.06.042

Cited by 13 publications

(8 citation statements)

References 56 publications

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“…While guanfacine has been reported to decrease impulsive choice in primates (Kim et al 2012), our results are consistent with those from a recent study showing that guanfacine had no effect on decision making in rats (Pardey et al 2013). As for propranolol, prazosin and guanfacine may have more impact on decision-making behaviors under conditions in which elevated noradrenergic signaling is present, as after exposure to acute stress (Fox et al 2012; Le et al 2011; Manion et al 2007; Nikiforuk 2013). …”

Section: Discussionmentioning

confidence: 99%

Impaired flexibility in decision making in rats after administration of the pharmacological stressor yohimbine

2014

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Rationale Stress-induced disruption of decision making has been hypothesized to contribute to drug-seeking behaviors and addiction. Noradrenergic signaling plays a central role in mediating stress responses. However, the effects of acute stress on decision making, and the role of noradrenergic signaling in regulating these effects, have not been well characterized. Objective To characterize changes in decision making caused by acute pharmacological stress, the effects of yohimbine (an α2-adrenergic antagonist) were examined in a delay discounting task. Noradrenergic contributions to decision making were further characterized by examining the effects of propranolol (a β antagonist), prazosin (an αl antagonist), and guanfacine (an α2 agonist). Methods Sprague-Dawley rats were administered drugs prior to performance on a delay discounting task, in which the delay preceding the large reward increased within each session (ascending delays). To dissociate drug-induced changes in delay sensitivity from behavioral inflexibility, drug effects were subsequently tested in a modified version of the discounting task, in which the delay preceding the large reward decreased within each session (descending delays). Results Yohimbine increased choice of the large reward when tested with ascending delays but decreased choice of the same large reward when tested with descending delays, suggesting that drug effects could be attributed to perseverative choice of the lever preferred at the beginning of the session. Propranolol increased choice of the large reward when tested with ascending delays. Prazosin and guanfacine had no effect on reward choice. Conclusions The stress-like effects of yohimbine administration may impair decision making by causing inflexible, perseverative behavior.

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Section: Discussionmentioning

confidence: 99%

Impaired flexibility in decision making in rats after administration of the pharmacological stressor yohimbine

2014

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“…For instance, long-term administration of imipramine or electroconvulsive therapy increase the expression of α 1 Rs (Nalepa et al, 2002), but the antidepressant effects of other tricyclic antidepressants (TCAs) (Ramakrishna and Subhash, 2012) or quetiapine (Nikiforuk, 2013) reduce α 1 Rs expression. The interpretation of these results is further complicated by the age-dependence of α 1 Rs function (Deupree et al, 2007).…”

Section: α1rs Central Modulationmentioning

confidence: 99%

Locus Ceruleus Norepinephrine Release: A Central Regulator of CNS Spatio-Temporal Activation?

Atzori

Cuevas-Olguín

Esquivel-Rendón

et al. 2016

Front. Synaptic Neurosci.

115

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Norepinephrine (NE) is synthesized in the Locus Coeruleus (LC) of the brainstem, from where it is released by axonal varicosities throughout the brain via volume transmission. A wealth of data from clinics and from animal models indicates that this catecholamine coordinates the activity of the central nervous system (CNS) and of the whole organism by modulating cell function in a vast number of brain areas in a coordinated manner. The ubiquity of NE receptors, the daunting number of cerebral areas regulated by the catecholamine, as well as the variety of cellular effects and of their timescales have contributed so far to defeat the attempts to integrate central adrenergic function into a unitary and coherent framework. Since three main families of NE receptors are represented—in order of decreasing affinity for the catecholamine—by: α2 adrenoceptors (α2Rs, high affinity), α1 adrenoceptors (α1Rs, intermediate affinity), and β adrenoceptors (βRs, low affinity), on a pharmacological basis, and on the ground of recent studies on cellular and systemic central noradrenergic effects, we propose that an increase in LC tonic activity promotes the emergence of four global states covering the whole spectrum of brain activation: (1) sleep: virtual absence of NE, (2) quiet wake: activation of α2Rs, (3) active wake/physiological stress: activation of α2- and α1-Rs, (4) distress: activation of α2-, α1-, and β-Rs. We postulate that excess intensity and/or duration of states (3) and (4) may lead to maladaptive plasticity, causing—in turn—a variety of neuropsychiatric illnesses including depression, schizophrenic psychoses, anxiety disorders, and attention deficit. The interplay between tonic and phasic LC activity identified in the LC in relationship with behavioral response is of critical importance in defining the short- and long-term biological mechanisms associated with the basic states postulated for the CNS. While the model has the potential to explain a large number of experimental and clinical findings, a major challenge will be to adapt this hypothesis to integrate the role of other neurotransmitters released during stress in a centralized fashion, like serotonin, acetylcholine, and histamine, as well as those released in a non-centralized fashion, like purines and cytokines.

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“…Moreover, that it would also attenuate the decrease in brainderived neurotrophic factor (BDNF) expression in the rat cortex and hippocampus (Park et al, 2006). It is possible that mitigating this decrease in BDNF is one of the mechanisms contributing to quetiapine's procognitive action (Nikiforuk, 2013).…”

Section: Discussionmentioning

confidence: 99%

Quetiapine attenuates cognitive impairment and decreases seizure susceptibility possibly through promoting myelin development in a rat model of malformations of cortical development

Feng

Zhao

et al. 2015

Brain Research

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Quetiapine ameliorates stress-induced cognitive inflexibility in rats

Cited by 13 publications

References 56 publications

Impaired flexibility in decision making in rats after administration of the pharmacological stressor yohimbine

Impaired flexibility in decision making in rats after administration of the pharmacological stressor yohimbine

Locus Ceruleus Norepinephrine Release: A Central Regulator of CNS Spatio-Temporal Activation?

Quetiapine attenuates cognitive impairment and decreases seizure susceptibility possibly through promoting myelin development in a rat model of malformations of cortical development

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