Involvement of dorsal hippocampal α-adrenergic receptors in the effect of scopolamine on memory retrieval in inhibitory avoidance task

Azami, Nasrin-Sadat; Piri, Morteza; Oryan, S; Jahanshahi, Mehrdad; Babapour, Vahab; Zarrindast, Mohammad‐Reza

doi:10.1016/j.nlm.2010.01.003

Cited by 46 publications

(29 citation statements)

References 51 publications

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“…This observation confirms that the sites identified with the present direct-agonist mapping approach have physiological relevance with regard to understanding the behavioral effects of endogenous NE transmission. Moreover, high concentrations of both a1 + b-NE receptors are found in many of the sites (anterior mPFC, DH, and CeA) in which the agonist cocktail had no effect on PPI (Pupo and Minneman, 2001;Rainbow et al, 1984;Swanson and Hartman, 1975;Young and Kuhar, 1980), and the dose range employed in the present study was sufficiently high to alter other behaviors in these 'PPI-null' sites (Azami et al, 2010;Ferry et al, 1999;Kerfoot et al, 2008). Hence, our negative results are not because of the use of behaviorally inactive doses.…”

Section: Discussionmentioning

confidence: 56%

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Alsene

Rajbhandari

Ramaker

et al. 2011

Neuropsychopharmacol

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Prepulse inhibition (PPI) refers to the reduction in the startle response when a startling stimulus is preceded by a weak prestimulus, and is an endophenotype of deficient sensorimotor gating in several neuropsychiatric disorders. Emerging evidence suggests that norepinephrine (NE) regulates PPI, however, the circuitry involved is unknown. We found recently that stimulation of the locus coeruleus (LC), the primary source of NE to the forebrain, induces a PPI deficit that is a result of downstream NE release. Hence, this study sought to identify LC-innervated forebrain regions that mediate this effect. Separate groups of male Sprague-Dawley rats received a cocktail solution of the a1-NE receptor agonist phenylephrine plus the b-receptor agonist isoproterenol (equal parts of each; 0, 3, 10, and 30 mg) into subregions of the medial prefrontal cortex (mPFC), nucleus accumbens (NAcc), extended amygdala, mediodorsal thalamus (MD-thalamus), or the dorsal hippocampus (DH) before PPI testing. NE agonist infusion into the posterior mPFC, NAcc shell, bed nucleus of the stria terminalis, basolateral amygdala, and the MD-thalamus disrupted PPI, with particularly strong effects in MD-thalamus. Sites in which NE receptor stimulation did not disrupt PPI (anterior mPFC, NAcc core, central amygdala, and DH) did support PPI disruptions with the dopamine D2 receptor agonist quinpirole (0, 10 mg). This pattern reveals new pathways in the regulation of PPI, and suggests that NE transmission within distinct thalamocortical and ventral forebrain networks may subserve the sensorimotor gating deficits that are seen in disorders such as schizophrenia, Tourette syndrome, and post-traumatic stress disorder.

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Section: Discussionmentioning

confidence: 56%

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Alsene

Rajbhandari

Ramaker

et al. 2011

Neuropsychopharmacol

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“…While many reports have suggested the dorsal hippocampus as the main site for modulation of memory (59,63), accumulating evidence have proposed that NAc or other sites of the brain may be involved in memory processes (7). According to the present data, the pre-training or pre-test injection of ethanol could decrease the step-through latency in a dose-dependent manner when animals were tested following 24 h. Other investigations have similarly shown that the pre-training ethanol inhibits the acquisition of memory in different paradigms such as inhibitory avoidance (7,8), working (9) and spatial memory (10)(11)(12).Our findings also showed that administration of the same dose of ethanol before retention, reverses the ethanol-induced amnesia.…”

Section: Discussionmentioning

confidence: 99%

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Raoufi¹,

Moshfegh²,

Piri³

et al. 2016

Journal of Advanced Medical Sciences and Applied Technologies

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The present study investigated the possible involvement of the nucleus accumbens' (NAc) nitric oxide system in nicotine's reversal effect upon ethanol-induced amnesia. The hypothesis was tested through ethanol state-dependent memory assessment in adult male Wistar rats. Bilateral chronic cannulae were implanted in the NAc and the animals were trained in a step-through type inhibitory avoidance memory task. The step-through latency was examined 24 h after animals' training. The pre-training or pre-test intraperitoneal (i.p.) injection of ethanol (0.9 g/kg) decreased the step-through latency, indicating an amnesic effect of the drug. Meanwhile, the pre-test administration of ethanol (0.6 and 0.9 g/kg) could reverse the pre-training ethanol (0.9 g/kg)-induced amnesia, suggesting a state-dependent effect. Similar to ethanol, the pre-test intra-NAc microinjection of nicotine (0.25 and 0.5 µg/rat) alone or nicotine (0.1, 0.25 and 0.5 µg/mouse, intra-NAc) in combination with an ineffective dose of ethanol (0.3 g/kg) could significantly reverse the (pre-training) ethanol-induced memory impairment. The ethanol (0.9 g/kg)-induced amnesia was similarly prevented following the pre-test intra-NAc administration of a nitric oxide synthase (NOS) inhibitor, L-NAME (0.4 and 0.8 µg/rat). Of note, the co-administration of L-NAME (0.04 and 0.08 µg/rat, intra-NAc) with an ineffective dose of nicotine (0.1 µg/rat, intra-NAc) could significantly potentiate the memoryimproving effect of nicotine on ethanol-induced amnesia and resembled the effects of pretest administration of a higher dose of nicotine. Furthermore, while the pre-test intra-NAc injection of L-NAME impaired the memory retrieval by itself, the pre-test intra-NAc administration of L-arginine, a nitric oxide precursor (0.3 and 0.6 µg/rat, intra-NAc), did not exert any effect either alone or in combination with an effective dose of nicotine (0.5 µg/rat, intra-NAc) on pre-training ethanol-induced memory impairment. Our findings indicated a possible role of the nucleus accumbens' nitric oxide system in the improving effects of nicotine on ethanol-induced amnesia and the related state-dependent learning.

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“…Taking into account the pharmacokinetics and pharmacodynamics, scopolamine is distributed to the brain 20 -30 min after i.p. injection (Watanabe and Shimizu 1989) and its central effect persists beyond 120 min after application (Perlstein et al 2002); scopolamine could have impaired retrieval (Barros et al 2001;Azami et al 2010), since it was still present in the brain at significant concentration during STM test. Although we cannot fully discard this possibility, it appears unlikely since pretreatment with caffeine preserved both kinds of memories when scopolamine was given post-training, being still present in the brain when STM was assessed (Botton et al 2010); thus, it seems that scopolamine would not affect STM retrieval directly.…”

Section: Amnesia By Ip Scopolamine and The "Of Effect"mentioning

confidence: 99%

Amnesia of inhibitory avoidance by scopolamine is overcome by previous open-field exposure

et al. 2014

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The muscarinic cholinergic receptor (MAChR) blockade with scopolamine either extended or restricted to the hippocampus, before or after training in inhibitory avoidance (IA) caused anterograde or retrograde amnesia, respectively, in the rat, because there was no long-term memory (LTM) expression. Adult Wistar rats previously exposed to one or two open-field (OF) sessions of 3 min each (habituated), behaved as control animals after a weak though over-threshold training in IA. However, after OF exposure, IA LTM was formed and expressed in spite of an extensive or restricted to the hippocampus MAChR blockade. It was reported that during and after OF exposure and reexposure there was an increase in both hippocampal and cortical ACh release that would contribute to "prime the substrate," e.g., by lowering the synaptic threshold for plasticity, leading to LTM consolidation. In the frame of the "synaptic tagging and capture" hypothesis, plasticity-related proteins synthesized during/after the previous OF could facilitate synaptic plasticity for IA in the same structure. However, IA anterograde amnesia by hippocampal protein synthesis inhibition with anisomycin was also prevented by two OF exposures, strongly suggesting that there would be alternative interpretations for the role of protein synthesis in memory formation and that another structure could also be involved in this "OF effect."[Supplemental material is available for this article.]

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Involvement of dorsal hippocampal α-adrenergic receptors in the effect of scopolamine on memory retrieval in inhibitory avoidance task

Cited by 46 publications

References 51 publications

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Discrete Forebrain Neuronal Networks Supporting Noradrenergic Regulation of Sensorimotor Gating

Activation of the Nitric-Oxide System in Nucleus Accumbens Inhibits the Nicotine Reversal Effects upon Ethanol-Induced Amnesia

Amnesia of inhibitory avoidance by scopolamine is overcome by previous open-field exposure

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