Scopolamine model of dementia: electroencephalogram findings and cognitive performance

Ebert, Ulrike; Kirch, Wilhelm

doi:10.1046/j.1365-2362.1998.00393.x

Cited by 332 publications

(185 citation statements)

References 67 publications

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“…For example topically applied scopolamine to exposed feline cortex lead to the development of seizures but was prevented by application of the acetylcholinesterase inhibitor physostigmine (Tan et al, 1978). Systemic administration of scopolamine to healthy humans induces impairment to attentional processes, and memory, as well as decreases in higher frequency gamma/beta EEG power relative to lower frequency delta/theta power (Ebert and Kirch, 1998). Although not directly demonstrated in the current study, VNS has been shown to excite the nucleus basalis (NB) (Detari et al, 1983) and similarly to VNS, NB activation promotes arousal, suppresses seizure activity Berdiev et al, 2007), and promotes neural plasticity (Edeline et al, 1993;Engineer et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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Abstract-Vagus nerve stimulation (VNS) is an FDA approved treatment for drug-resistant epilepsy and depression.Recently, we demonstrated the capacity for repeatedly pairing sensory input with brief pulses of VNS to induce input specific reorganization in rat auditory cortex. This was subsequently used to reverse the pathological neural and perceptual correlates of hearing loss induced tinnitus. Despite its therapeutic potential, VNS mechanisms of action remain speculative. In this study, we report the acute effects of VNS on intra-cortical synchrony, excitability, and sensory processing in anesthetized rat auditory cortex. VNS significantly increased and decorrelated spontaneous multi-unit activity, and suppressed entrainment to repetitive noise burst stimulation at 6 -8 Hz but not after application of the muscarinic antagonist scopolamine. Collectively, these experiments demonstrate the capacity for VNS to acutely influence cortical synchrony and excitability and strengthen the hypothesis that acetylcholine and muscarinic receptors are involved in VNS mechanisms of action. These results are discussed with respect to their possible implications for sensory processing, neural plasticity, and epilepsy.

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Section: Discussionmentioning

confidence: 99%

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

et al. 2011

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“…Scopolamine-induced memory impairment was suggested for modeling some features of geriatric memory dysfunction and of Alzheimer's disease (AD) memory impairment (Bartus, Dean, Beer, & Lippa, 1982;Ebert & Kirch, 1998;Giacobini, 1990). This was proposed because a mild cholinergic dysfunction occurs in the elderly and at early stages of AD.…”

Section: Discussionmentioning

confidence: 99%

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Blake

Boccia

Krawczyk

et al. 2012

Neurobiology of Learning and Memory

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Please cite this article as: Blake, M.G., Boccia, M.M., Krawczyk, M.C., Delorenzi, A., Baratti, C.M., Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation, Neurobiology of Learning and Memory (2012), doi: http://dx.doi. org/10.1016/j.nlm.2012.07.001 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. were not subjected to memory reactivation, suggesting that the performance effects are not due to non-specific effects of the drug. The effects of Ch also depended on the age of the reactivated memory. Altogether, our results suggest that Ch exerts its effects by modulating memory reconsolidation, and that the memory impairment induced by low doses of SCP is a memory expression failure and not a storage deficit. Therefore, reconsolidation, among other functions, might serve to change memory expression in later tests. Summarizing, our results open new avenues about the behavioral significance and the physiological functions of memory reconsolidation, providing new strategies for recovering memories from some types of amnesia. Research highlights-Pre-training administration of scopolamine leads to memory impairment.-Intra-hippocampal administration of choline modulates memory reconsolidation -Choline reverses scopolamine-induced amnesia by enhancing memory reconsolidation -Low doses of scopolamine cause memory expression deficit, but not storage impairment -Reconsolidation could modify the ability of a memory for being expressed later

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“…Blockade of muscarinic acetylcholine receptors (mAChRs) has been shown to induce memory and attentional deficits in both animals and humans (Blokland, 1995;Ebert and Kirch, 1998;Everitt and Robbins, 1997;Green et al, 2005). Two of the cholinergic projections from the BF, those to the entorhinal cortex (EC) and the basolateral amygdala (BLA), have been shown to mediate distinct cognitive processes through mAChRs (Hasselmo, 2006;Hasselmo and McGaughy, 2004;Ingles et al, 1993;Power, 2004).…”

Section: Introductionmentioning

confidence: 99%

Differential Role of Muscarinic Transmission within the Entorhinal Cortex and Basolateral Amygdala in the Processing of Irrelevant Stimuli

Barak

Weiner

2010

Neuropsychopharmacol

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Cholinergic projections to the entorhinal cortex (EC) and basolateral amygdala (BLA) mediate distinct cognitive processes through muscarinic acetylcholine receptors (mAChRs). In this study, we sought to further differentiate the role of muscarinic transmission in these regions in cognition, using the latent inhibition (LI) phenomenon. LI is a cross-species phenomenon manifested as poorer conditioning to a stimulus experienced as irrelevant during an earlier stage of repeated non-reinforced pre-exposure to that stimulus, and is considered to index the ability to ignore, or to in-attend to, irrelevant stimuli. Given our recent findings that systemic administration of the mAChR antagonist scopolamine can produce two contrasting LI abnormalities in rats, ie, abolish LI under conditions yielding LI in non-treated controls, or produce abnormally persistent LI under conditions preventing its expression in non-treated controls, we tested whether mAChR blockade in the EC and BLA would induce LI abolition and persistence, respectively. We found that intra-EC scopolamine infusion (1, 10 mg per hemisphere) abolished LI when infused in pre-exposure or both pre-exposure and conditioning, but not in conditioning alone, whereas intra-BLA scopolamine infusion led to persistent LI when infused in conditioning or both stages, but not in pre-exposure alone. Although cholinergic innervation of the EC and BLA has long been implicated in attention to novel stimuli and in processing of motivationally significant stimuli, respectively, our results provide evidence that EC mAChRs also have a role in the development of inattention to stimuli, whereas BLA mAChRs have a role in re-attending to previously irrelevant stimuli that became motivationally relevant.

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Scopolamine model of dementia: electroencephalogram findings and cognitive performance

Cited by 332 publications

References 67 publications

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors

Choline reverses scopolamine-induced memory impairment by improving memory reconsolidation

Differential Role of Muscarinic Transmission within the Entorhinal Cortex and Basolateral Amygdala in the Processing of Irrelevant Stimuli

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