Luis F. Rodríguez-Durán

Universidad Nacional Autónoma de México

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Martha L. Escobar

Universidad Nacional Autónoma de México

Federico Bermúdez‐Rattoni

Universidad Nacional Autónoma de México

Kioko Guzmán‐Ramos

Universidad Autónoma Metropolitana

Araceli Martínez-Moreno

Universidad Nacional Autónoma de México

Donovan K. Gálvez-Márquez

Universidad Nacional Autónoma de México

Teresa Montiel

Universidad Nacional Autónoma de México

María E. Gonsebatt

Universidad Nacional Autónoma de México

Daniel Osorio‐Gómez

Universidad Nacional Autónoma de México

Verónica M. Rodríguez

Universidad Nacional Autónoma de México

Janikua Nelson-Mora

Universidad Nacional Autónoma de México

Cooperative Institutions

Universidad Nacional Autónoma de México

Instituto Nacional de Cardiología

Universidad Autónoma Metropolitana

New South Wales Department of Health

Instituto Nacional de Neurología y Neurocirugía

Center for Research and Advanced Studies of the National Polytechnic Institute

Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán

Centro de Investigación en Materiales Avanzados

Autonomous University of Queretaro

University of California, Irvine

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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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Citations (0)

Inhibition of hippocampal palmitoyl acyltransferase activity impairs spatial learning and memory consolidation

Neurobiology of Learning and Memory (2023)

Oscar Urrego-Morales Elvi Gil-Lievana Gerardo Ramírez-Mejía Luis F. Rodríguez-Durán Martha L. Escobar

Palmitoylation

10.1016/j.nlm.2023.107733

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Citations (2)

Palatable Hyper-Caloric Foods Impact on Neuronal Plasticity

Frontiers in Behavioral Neuroscience (2017)

Jean‐Pascal Morin Luis F. Rodríguez-Durán Kioko Guzmán‐Ramos Claudia Pérez-Cruz Guillaume Ferreira

Neural plasticity is an intrinsic and essential characteristic of the nervous system that allows animals "self-tuning" to adapt to their environment over their lifetime. Activity-dependent synaptic plasticity in the central nervous system is a form of neural plasticity that underlies learning and memory formation, as well as long-lasting, environmentally-induced maladaptive behaviors, such as drug addiction and overeating of palatable hyper-caloric (PHc) food. In western societies, the abundance of PHc foods has caused a dramatic increase in the incidence of overweight/obesity and related disorders. To this regard, it has been suggested that increased adiposity may be caused at least in part by behavioral changes in the affected individuals that are induced by the chronic consumption of PHc foods; some authors have even drawn attention to the similarity that exists between over-indulgent eating and drug addiction. Long-term misuse of certain dietary components has also been linked to chronic neuroimmune maladaptation that may predispose individuals to neurodegenerative conditions such as Alzheimer's disease. In this review article, we discuss recent evidence that shows how consumption of PHc food can cause maladaptive neural plasticity that converts short-term ingestive drives into compulsive behaviors. We also discuss the neural mechanisms of how chronic consumption of PHc foods may alter brain function and lead to cognitive impairments, focusing on prenatal, childhood and adolescence as vulnerable neurodevelopmental stages to dietary environmental insults. Finally, we outline a societal agenda for harnessing permissive obesogenic environments.

Caloric theory

10.3389/fnbeh.2017.00019

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Citations (68)

Dopaminergic neurotransmission dysfunction induced by amyloid-β transforms cortical long-term potentiation into long-term depression and produces memory impairment

Neurobiology of Aging (2016)

Perla Moreno‐Castilla Luis F. Rodríguez-Durán Kioko Guzmán‐Ramos Alejandro Barcenas-Femat Martha L. Escobar

Long-term depression

Depression

10.1016/j.neurobiolaging.2016.02.021

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Citations (72)

Conditioned taste aversion prevents the long-lasting BDNF-induced enhancement of synaptic transmission in the insular cortex: A metaplastic effect

Neurobiology of Learning and Memory (2016)

Alejandro Rivera-Olvera Luis F. Rodríguez-Durán Martha L. Escobar

Basolateral amygdala

10.1016/j.nlm.2016.01.014

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Citations (17)

Brain-derived neurotrophic factor into adult neocortex strengthens a taste aversion memory

Behavioural Brain Research (2015)

Araceli Martínez-Moreno Luis F. Rodríguez-Durán Martha L. Escobar

Neocortex

Taste aversion

Insular cortex

Engram

Trk receptor

10.1016/j.bbr.2015.09.034

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Citations (8)

Conditioned taste aversion modifies persistently the subsequent induction of neocortical long-term potentiation in vivo

Neurobiology of Learning and Memory (2011)

Luis F. Rodríguez-Durán Diana V. Castillo Minerva Moguel-González Martha L. Escobar

Anisomycin

Taste aversion

LTP induction

Basolateral amygdala

10.1016/j.nlm.2011.03.003

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Citations (40)

Spatial contextual recognition memory updating is modulated by dopamine release in the dorsal hippocampus from the locus coeruleus

Proceedings of the National Academy of Sciences (2022)

Donovan K. Gálvez-Márquez Mildred Salgado-Ménez Perla Moreno‐Castilla Luis F. Rodríguez-Durán Martha L. Escobar

Detecting novelty is critical to consolidate declarative memories, such as spatial contextual recognition memory. It has been shown that stored memories, when retrieved, are susceptible to modification, incorporating new information through an updating process. Catecholamine release in the hippocampal CA1 region consolidates an object location memory (OLM). This work hypothesized that spatial contextual memory updating could be changed by decreasing catecholamine release in the hippocampal CA1 terminals from the locus coeruleus (LC). In a mouse model expressing Cre-recombinase under the control of the tyrosine hydroxylase (TH) promoter, memory updating was impaired by photoinhibition of the CA1 catecholaminergic terminals from the LC (LC-CA1) but not from the ventral tegmental area (VTA-CA1). In vivo microdialysis confirmed that the extracellular concentration of both dopamine (DA) and noradrenaline (NA) decreased after photoinhibition of the LC-CA1 terminals (but not VTA-CA1) during the OLM update session. Furthermore, DA D1/D5 and beta-adrenergic receptor antagonists disrupted behavior, but only the former impaired memory updating. Finally, photoinhibition of LC-CA1 terminals suppressed long-term potentiation (LTP) induction in Schaffer’s collaterals as a plausible mechanism for memory updating. These data will help understand the underpinning mechanisms of DA in spatial contextual memory updating.

Locus coeruleus

10.1073/pnas.2208254119

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Citations (29)

Gestational exposure to inorganic arsenic (iAs3+) alters glutamate disposition in the mouse hippocampus and ionotropic glutamate receptor expression leading to memory impairment

Archives of Toxicology (2017)

Janikua Nelson-Mora Martha L. Escobar Luis F. Rodríguez-Durán Lourdes Massieu Teresa Montiel

10.1007/s00204-017-2111-x

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Citations (36)

NMDA receptor activation and PKC but not PKA lead to the modification of the long-term potentiation in the insular cortex induced by conditioned taste aversion: Differential role of kinases in metaplasticity

Behavioural Brain Research (2014)