Federico Bermúdez‐Rattoni

Universidad Nacional Autónoma de México

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Kioko Guzmán‐Ramos

Universidad Autónoma Metropolitana

Daniel Osorio‐Gómez

Universidad Nacional Autónoma de México

Martha L. Escobar

Universidad Nacional Autónoma de México

Marı́a Isabel Miranda

Universidad Nacional Autónoma de México

Israela Balderas

Universidad Nacional Autónoma de México

Victor Ramı́rez-Amaya

Instituto de Investigación Médica Mercedes y Martín Ferreyra

Carlos J. Rodríguez‐Ortiz

University of California, Irvine

Ranier Gutiérrez

Center for Research and Advanced Studies of the National Polytechnic Institute

Perla Moreno‐Castilla

Center for Research and Advanced Studies of the National Polytechnic Institute

Juan Fernández-Ruíz

Universidad Nacional Autónoma de México

Cooperative Institutions

Universidad Nacional Autónoma de México

160

Instituto Nacional de Cardiología

Center for Research and Advanced Studies of the National Polytechnic Institute

University of California, Irvine

Instituto Nacional de Neurología y Neurocirugía

University of California, Los Angeles

Instituto Politécnico Nacional

Centre National de la Recherche Scientifique

Universidad Autónoma Metropolitana

Autonomous University of Queretaro

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Differential involvement of glutamatergic and catecholaminergic activity within the amygdala during taste aversion retrieval on memory expression and updating

Behavioural Brain Research (2016)

Daniel Osorio‐Gómez Kioko Guzmán‐Ramos Federico Bermúdez‐Rattoni

Taste aversion

Microdialysis

Ifenprodil

10.1016/j.bbr.2016.03.038

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Citations (17)

Photostimulation of Locus Coeruleus CA1 catecholaminergic terminals reversed spatial memory impairment in an Alzheimer's disease mouse model.

Research Square (Research Square) (2025)

Donovan K. Gálvez-Márquez Oscar Urrego-Morales Luis F. Rodríguez-Durán Federico Bermúdez‐Rattoni

Abstract Rationale One of the earliest changes associated with Alzheimer's disease (AD) is the loss of catecholaminergic terminals in the cortex and hippocampus originating from the Locus Coeruleus (LC). This decline leads to reduced catecholaminergic neurotransmitters in the hippocampus, affecting synaptic plasticity and spatial memory. However, it is unclear whether restoring catecholaminergic transmission in the terminals from the LC may alleviate the spatial memory deficits associated with AD. Objectives This study investigates how optogenetic stimulation of catecholaminergic projections from the locus coeruleus to the hippocampal CA1 region may enhance spatial memory and alleviate synaptic plasticity deficits associated with Alzheimer's disease. Methods We conducted experiments using a 12-month-old 3xTg-AD mouse model (AD-TH), which expresses Cre recombinase under the control of the tyrosine hydroxylase (TH) gene. This model allowed us to photostimulate the terminals from the locus coeruleus in the hippocampal CA1 region before performing two different spatial memory tasks and inducing long-term potentiation (LTP). Results Optogenetic stimulation successfully reversed the impairment of spatial memory retrieval in aging AD-TH mice. Furthermore, this stimulation restored catecholaminergic neurotransmitter levels in the hippocampus and enhanced synaptic plasticity, as demonstrated by an LTP protocol. Conclusions These findings indicate that the catecholaminergic circuitry from the locus coeruleus (LC) to the hippocampal CA1 region plays a crucial role in disrupting synaptic plasticity and contributing to the spatial memory deficits seen in the early stages of AD. This study highlights the potential therapeutic benefits of targeting LC catecholaminergic neurons to improve cognitive function in patients with AD.

Locus coeruleus

Photostimulation

Memory Impairment

10.21203/rs.3.rs-5868268/v1

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Spatial Memory Impairment is Associated with Intraneural Amyloid-β Immunoreactivity and Dysfunctional Arc Expression in the Hippocampal-CA3 Region of a Transgenic Mouse Model of Alzheimer’s Disease

Journal of Alzheimer s Disease (2016)

Jean‐Pascal Morin Giovanni Cerón-Solano Giovanna Velázquez-Campos Gustavo Pacheco‐López Federico Bermúdez‐Rattoni

Dysfunction of synaptic communication in cortical and hippocampal networks has been suggested as one of the neuropathological hallmarks of the early stages of Alzheimer's disease (AD). Also, several lines of evidence have linked disrupted levels of activity-regulated cytoskeletal associated protein (Arc), an immediate early gene product that plays a central role in synaptic plasticity, with AD "synaptopathy". The mapping of Arc expression patterns in brain networks has been extensively used as a marker of memory-relevant neuronal activity history. Here we evaluated basal and behavior-induced Arc expression in hippocampal networks of the 3xTg-AD mouse model of AD. The basal percentage of Arc-expressing cells in 10-month-old 3xTg-AD mice was higher than wild type in CA3 (4.88% versus 1.77% , respectively) but similar in CA1 (1.75% versus 2.75% ). Noteworthy, this difference was not observed at 3 months of age. Furthermore, although a Morris water maze test probe induced a steep (∼4-fold) increment in the percentage of Arc+ cells in the CA3 region of the 10-month-old wild-type group, no such increment was observed in age-matched 3xTg-AD, whereas the amount of Arc+ cells in CA1 increased in both groups. Further, we detected that CA3 neurons with amyloid-β were much more likely to express Arc protein under basal conditions. We propose that in 3xTg-AD mice, intraneuronal amyloid-β expression in CA3 could increase unspecific neuronal activation and subsequent Arc protein expression, which might impair further memory-stabilizing processes.

Memory Impairment

Dysfunctional family

Amyloid (mycology)

Expression (computer science)

10.3233/jad-150975

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New Insights on Retrieval-Induced and Ongoing Memory Consolidation: Lessons from Arc

Neural Plasticity (2015)

Jean‐Pascal Morin Kioko Guzmán‐Ramos Federico Bermúdez‐Rattoni

The mainstream view on the neurobiological mechanisms underlying memory formation states that memory traces reside on the network of cells activated during initial acquisition that becomes active again upon retrieval (reactivation). These activation and reactivation processes have been called “conjunctive trace.” This process implies that singular molecular events must occur during acquisition, strengthening the connection between the implicated cells whose synchronous activity must underlie subsequent reactivations. The strongest experimental support for the conjunctive trace model comes from the study of immediate early genes such as c-fos, zif268, and activity-regulated cytoskeletal-associated protein. The expressions of these genes are reliably induced by behaviorally relevant neuronal activity and their products often play a central role in long-term memory formation. In this review, we propose that the peculiar characteristics of Arc protein, such as its optimal expression after ongoing experience or familiar behavior, together with its versatile and central functions in synaptic plasticity could explain how familiarization and recognition memories are stored and preserved in the mammalian brain.

Engram

TRACE (psycholinguistics)

Immediate early gene

Memory Formation

10.1155/2015/184083

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Citations (12)

The conditioned stimulus^unconditioned stimulus^feedback feeding sequence: Reply to Ellins, von Kluge, and Cramer (1990).

Behavioral Neuroscience (1990)

Mark D. Holder Federico Bermúdez‐Rattoni John García

Taste-potentiated noise aversions have been demonstrated in rats (Ellins, Cramer, & Whitmore, 1985; Ellins & von Kluge, 1987; Holder, Bermudez-Rattoni, & Garcia, 1988). However, these aversions are apparently less readily established than taste-potentiated odor aversions suggesting that all exteroceptive stimuli are not equally well potentiated by taste (Holder et al., 1988). Despite the claims of Ellins, von Kluge, and Cramer (1990), we replicated their findings and see no inconsistency between our findings and theirs. Both sets of results are explained by a common theory of conditioning (Garcia, 1989; Garcia & Holder, 1985).

Taste aversion

Stimulus (psychology)

10.1037//0735-7044.104.1.233

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Reversible Inactivation of Brain Circuits in Learning and Memory Research -- Neural Plasticity and Memory: From Genes to Brain Imaging

Federico Bermúdez‐Rattoni

Biological neural network

Neuronal Circuits

Brain research

Source

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Addictive agents and intracranial stimulation (ICS): Novel antagonists and agonists of morphine and pressing for ICS

Pharmacology Biochemistry and Behavior (1983)

Federico Bermúdez‐Rattoni Sara E. Cruz-Morales Larry D. Reid

10.1016/0091-3057(83)90022-9

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Citations (19)

Taste aversion memory reconsolidation is independent of its retrieval

Neurobiology of Learning and Memory (2012)

Carlos J. Rodríguez‐Ortiz Israela Balderas Paola Torre Federico Bermúdez‐Rattoni

Taste aversion

Anisomycin

Retrograde amnesia

10.1016/j.nlm.2012.08.002

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Citations (58)

Acetylcholine determination of microdialysates of fetal neocortex grafts that induce recovery of learning

Brain Research Protocols (1998)

Marı́a Isabel Miranda Federico Bermúdez‐Rattoni

Microdialysis

Neocortex

Choline

10.1016/s1385-299x(97)00046-9

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Citations (6)

Adrenal Medullary Grafts Restore Olfactory Deficits andCatecholamine Levels of 6‐OHDA Amygdala Lesioned Animals

Neural Plasticity (1993)

Juan Fernández-Ruíz Rubén González Guzmán Marı́a Dolores Martı́nez Marı́a Isabel Miranda Federico Bermúdez‐Rattoni

Aside from motor and cognitive deficits, Parkinson patients also manifest a little-studied olfactory deficit. Since in Parkinson's disease there is a dopamine depletion of the amygdala due to mesocorticolimbic system degeneration, we decided to test olfactory and taste performance of 6-OHDA amygdala lesioned rats, as well as the possible restoration of either function with adrenal medullary transplants. Two 6-OHDA lesioned groups and one control group were tested in the potentiation of odor by taste aversion paradigm. On taste aversion none of the groups showed any impairment. In contrast, the 6-OHDA lesioned rats showed a marked impairment in olfactory aversion. At this point, one of the lesioned groups received a bilateral adrenal medullary graft within the lesioned area. After two months, all groups were submitted again to the behavioral paradigm. Taste remained unaffected, but the lesioned only group did not recover either olfactory aversion or normal catecholamine levels. The grafted group, on the other hand, restored olfactory aversion and catecholamine levels. It can be concluded from this study that catecholamine depletion of the amygdala is sufficient to produce a selective olfactory deficit, not accompanied by taste impairments, and that such a deficit can be reversed by adrenal medullary transplants, which in turn restore catecholamine levels.

10.1155/np.1993.289

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Citations (5)