Short communicationImpairment of working memory induced by scopolamine in rats with noradrenergic DSP-4 lesions
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Cited by (31)
Acute behavioral effects of deliriant hallucinogens atropine and scopolamine in adult zebrafish
2019, Behavioural Brain ResearchCitation Excerpt :In humans, acute scopolamine causes confusion, anxiety/fear, agitation and irritability [23,24]. In rodents, scopolamine impairs working memory [25], fear conditioning [26], social memory [27], and exhibits antidepressant-like effects [28]. Importantly, atropine, scopolamine and other M-receptor antagonists belong to a group of deliriant hallucinogens, as they commonly induce delirium-like states (hallucinations, hyperactivity, altered affective behaviors [29]) and cognitive deficits, consistently reported in both clinical [24] and rodent studies [27,30].
Hippocampal Noradrenaline Regulates Spatial Working Memory in the Rat
2017, Noradrenergic Signaling and AstrogliaSelective noradrenaline depletion impairs working memory and hippocampal neurogenesis
2016, Neurobiology of AgingCitation Excerpt :Surprisingly, in the present study, we found no lesion effect on reference memory, whereas working memory ability, as tested using the RAWM paradigm, was dramatically perturbed. Similar findings have been previously reported using electrolytic (Compton et al., 1995) or DSP4 lesions (Ohno et al., 1993; Sontag et al., 2008; Wenk et al., 1987), whereas in other studies, reference memory deficits have been observed as well following DSP4 (Connor et al., 1992; Langlais et al., 1993; Lapiz et al., 2001) or reversible LC inactivation (Khakpour-Taleghani et al., 2009). It should be noted, however, that the reference and/or working memory deficits observed in those studies were either inconsistently lesion- or dose-dependent or detectable only in the presence of a concurrent cholinergic lesion or receptor blockade.
Central noradrenergic depletion by DSP-4 prevents stress-induced memory impairments in the object recognition task
2009, NeuroscienceCitation Excerpt :This is, however, an acute effect of DSP-4 treatment without influence on the results 5 weeks post-treatment. The DSP-4-induced increase in NA release from remaining locus coeruleus neuronal terminals may function as a compensatory mechanism and could, at least in part, explain why memory measured in the object recognition task (this study) and in several other behavioural paradigms (Haroutunian et al., 1990; Ohno et al., 1993; Lapiz et al., 2001) is not affected after DSP-4 treatment. Various other compensatory adaptations have been described that may help to preserve the function of remaining locus coeruleus neurons.
Noradrenergic denervation facilitates the release of acetylcholine and serotonin in the hippocampus: Towards a mechanism underlying upregulations described in MCI patients?
2008, Experimental NeurologyCitation Excerpt :Histo- and neuropathologically, Alzheimer's disease (AD) is characterized by neurofibrillary tangles, amyloid plaques, degenerative alterations in hippocampal and retrohippocampal regions, loss of cholinergic neurons in the basal forebrain (Braak and Braak, 1993; deToledo-Morrell et al., 2004; Palmer, 2002; Perry et al., 1978; Stoub et al., 2005), and a decrease in noradrenergic functions in the locus coeruleus (Adolfsson et al., 1979; Forno, 1966; Haglund et al., 2006; Palmer, 1996, 2002). Although noradrenergic lesions generally do not affect memory functions in rats (e.g. Lapiz et al., 2001; Sirviö et al., 1994), they potentiate the amnesic effects that arise from either muscarinic blockade (Ohno et al., 1993, 1997) or damage to the nucleus basalis (Abe et al., 1997). Moreover, such lesions alter the retrieval of intermediate-term memories in both mice and rats (Murchison et al., 2004).
Noradrenergic mechanisms in neurodegenerative diseases: A theory
2004, Brain Research Reviews