MinireviewNeural Topography and Chronology of Memory Consolidation: A Review of Functional Inactivation Findings☆,☆☆
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Cited by (111)
Recruitment of neurons in basolateral amygdala after intense training produces a stronger memory trace
2021, Neurobiology of Learning and MemoryCitation Excerpt :Brains of naïve animals are characterized by a low number of c-Fos positive cells while some structures show a relatively high number of c-Fos positive neurons after learning (Bertaina-Anglade, Tramu, & Destrade, 2000; Casanova et al., 2016; He, Yamada, & Nabeshima, 2002; Martinez et al., 2013; Robins, Li, & Ryabinin, 2020; Zhang, Fukushima, & Kida, 2011), and the distribution of c-Fos positive neurons in different brain structures seems to depend on the learning paradigm (e.g., Filipkowski, Knapska, & Kaczmarek, 2006; Gill, Bernstein, & Mizumori, 2007) although there is a lack of reports dealing with the amount of neurons expressing c-Fos after intense training1. Numerous studies have shown that the amygdala plays a central role in learned fear and in forming and expressing fear memories (Ambrogi, Baldi, Bucherelli, Sacchetti, & Tassoni, 1999; Fanselow & LeDoux, 1999; LeDoux, 2000; McGaugh, 2000, 2015; McGaugh, Cahill, & Roozendaal, 1996; Roozendaal, McEwen, & Chattarji, 2009; Wilensky, Schafe, Kristensen, & LeDoux, 2006). Many experimental findings regarding Pavlovian fear conditioning have led to the proposal that, within the amygdala, the lateral nucleus (LA) is necessary for the association of conditioned and unconditioned stimuli, which results in plastic changes necessary for the formation of a memory trace in the basolateral nucleus (BL), while subsequent exposure to the conditioned stimulus induces the expression of the conditioned fear response through the activation of the central nucleus (CE) (for a recent review see Ressler & Maren, 2019).
Inhibition of transcription and translation in dorsal hippocampus does not interfere with consolidation of memory of intense training
2019, Neurobiology of Learning and MemoryQuercetin ameliorates chronic unpredicted stress-induced behavioral dysfunction in male Swiss albino mice by modulating hippocampal insulin signaling pathway
2017, Physiology and BehaviorCitation Excerpt :Memory acquisition, retention, and retrieval is a complex phenomenon, which depends on the morphological and functional integrity of neurons in different regions of the brain, especially the hippocampus. Hypercortisolemia adversely affect the neuronal integrity and normal functioning and is known to affect neuronal survival and induce neurodegeneration [38,39]. Accumulated evidence suggest that quercetin is having neuroprotective potential and improve neuronal survival by attenuating hippocampal oxidative stress, inflammatory stress, mitochondrial dysfunction and apoptotic pathway [40–42].
Rutin alleviates chronic unpredictable stress-induced behavioral alterations and hippocampal damage in mice
2017, Neuroscience LettersCitation Excerpt :The behavioral dysfunction due to CUS on a cellular level is associated with CA3 hippocampal neurodegeneration, possibly because of increased cortisol, oxidative and inflammatory stress. These results are in line with the previous findings which suggest that neuronal integrity is essential for normal animal behavior [42–44]. Treating stressed animals with rutin resulted in an intact hippocampus with cell number and morphology similar to control animals.
Quercetin prevents chronic unpredictable stress induced behavioral dysfunction in mice by alleviating hippocampal oxidative and inflammatory stress
2017, Physiology and BehaviorCitation Excerpt :As expected, neurons of stressed animals were severely damaged, especially CA3 region of hippocampus and quercetin treatment rescued hippocampal neurons form stress mediated damage. These observations are in agreement with the previous findings which suggest that neuronal integrity is essential for normal animal behavior [48,49]. Integrity of hippocampal neurons observed in quercetin treated stressed animals may be attributed to its neuroprotective potential, since it is known to improve neuronal survival and sustain neuronal integrity during stressful conditions [31].
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Address correspondence and reprint requests to C. Bucherelli at Dipartimento di Scienze Fisiologiche, Università degli Studi di Firenze, Viale G. B. Morgagni 63, I-50134 Florence, Italy. Fax: 055-4379506. E-mail:[email protected].
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J. FieldH. W. MagounV. E. Hall