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Lopes, L. V.

Publications and source records attributed to Lopes, L. V..

7 recordsLinked to original sources

Reinforced Hippocampus-Accumbens pathway marks a shift towards cognitive decline in aging

Aging triggers early functional alterations in brain circuits that precede cognitive impairment, yet the underlying mechanisms remain unclear. Spatial navigation and memory, among the earliest affected, depend on hippocampus and downstream targets such as the nucleus accumbens (NAc), which integrates spatial and motivational information to guide goal-directed behaviors. Here we identify age-related, sex-dependent changes of the dorsal hippocampus-NAc (dHPC[->]NAc) pathway. Combining optogenetics with electrophysiology, chemogenetics, and behavioral analyses in mice, we show that aging shifts excitation-inhibition balance in dorsal CA1 toward pyramidal neuron hyperexcitability, strengthening hippocampal outputs. This selectively enhances synaptic drive onto D1 receptor-expressing medium spiny neurons and involves a previously unrecognized long-range parvalbumin-expressing glutamatergic projection. Reducing dHPC[->]NAc excitability improves memory in aged mice. In humans, fMRI reveals heightened posterior hippocampal activity and stronger pHPC-NAc coupling during navigation. Together, we uncover a targetable pathway acting in an intervention-sensitive window of aging to correct negative cognitive trajectories.

neuroscience↗

Chronic Circadian Disturbance Reshapes Hippocampal Connectivity and Cognitive Function

Circadian rhythms regulate a wide range of physiological and cognitive functions, yet the neural mechanisms linking circadian timing to memory remain poorly defined. Here, we identify a direct anatomical projection from the suprachiasmatic nucleus (SCN) to the dorsal hippocampus using complementary viral anterograde, retrograde, and monosynaptic tracing approaches, alongside established indirect pathways via septal and neuromodulatory regions. These findings revise prevailing models that restrict SCN influence on hippocampal function to polysynaptic routes. Functionally, chronic circadian disruption (CCD) induced region-specific metabolic alterations and widespread reorganization of brain-wide functional connectivity (FC). Hypometabolism emerged in the SCN, dentate gyrus, and perirhinal and entorhinal cortices, accompanied by loss of SCN- hippocampal connectivity and compensatory engagement of cortical and subcortical networks. In contrast, the serotonergic dorsal raphe nucleus showed selective hypermetabolism and increased connectivity with the SCN, prefrontal cortex, and hippocampus, suggesting altered neuromodulatory control under circadian misalignment. Behaviorally, CCD produced a selective impairment in object recognition memory, while spatial memory, working memory, cognitive flexibility, and hippocampal synaptic plasticity at the Schaffer collateral-CA1 synapse remained intact. Disrupted functional coupling within perirhinal-entorhinal- hippocampal and prefrontal-hippocampal circuits, together with altered SCN-medial septum- hippocampus connectivity, indicates that cognitive dysfunction arises from desynchronization of distributed brain networks rather than local synaptic failure. Together, these findings provide a new mechanistic framework linking circadian disruption to selective memory impairment and highlight network-level synchrony as a potential target for chronotherapeutic intervention.

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Auditory Gamma-Frequency Entrainment Abolishes Working Memory Deficits in a Rodent Model of Autism

Individuals on the autism spectrum often exhibit atypical responses to sensory stimuli and difficulties with behavioral regulation, reflecting altered functional patterns in core sensory-motor circuits. While impairments in higher cognitive functions are a hallmark of autism, they remain underexplored in rodent models compared to basic sensory-motor deficits. Furthermore, these sensory processing differences suggest the potential for using patterned auditory stimulation to modulate neural activity and mitigate symptoms. In this study, we investigated higher cognitive function in the valproic acid (VPA) rodent model of autism and evaluated whether auditory entrainment could ameliorate associated impairments. Pregnant dams received an intraperitoneal injection of VPA on embryonic day 12.5 (E12.5), and offspring were subsequently tested on a delayed non-match to place (DNMP) task to assess working memory. VPA-exposed animals showed significantly impaired performance and altered trial-by-trial learning dynamics, indicating deficits in working memory-based decision making. Notably, gamma-frequency auditory stimulation delivered during DNMP sessions led to increased gamma-frequency oscillations, and enhanced power in other bands (theta, beta) across brain regions, as assessed by LFP recordings in freely moving animals. More importantly, such stimulation eliminated the observed working memory impairments, enhancing performance both during and after entrainment. This provides strong evidence for the therapeutic potential of sensory entrainment in reversing autism-related cognitive deficits by modulating dysfunctional neural circuits.

neuroscience↗

Mapping functional traces of opioid memories in the rat brain

Addiction to psychoactive substances is a maladaptive learned behavior. Contexts surrounding drug use integrate this aberrant mnemonic process and hold strong relapse triggering ability. Here we asked where context and salience might be concurrently represented in the brain, and found circuitry hubs specific to morphine-related contextual information storage. Starting with a classical rodent morphine-conditioned place preference (CPP) apparatus, we developed a CPP protocol that allows stimuli presentation inside a magnetic resonance imaging scanner, to allow the investigation of whole brain activity during retrieval of drug-context paired associations, as well as resting state functional connectivity under the effect of morphine conditioning. Using fMRI we found context-specific responses to stimulus onset in multiple brain regions, namely limbic, sensory, and striatal. Furthermore, we found increased functional connectivity of lateral septum with regions within and beyond a proposed limbic network, and of the lateral habenula with hippocampal CA1 region, in response to repeated pairings of drug and context. Subsequent exposure to either morphine or saline-conditioned contexts led to significant, context-specific, functional interconnectivity among amygdala, lateral habenula, and lateral septum. Resting-state connectivity of the lateral habenula and amygdala, and that during saline-paired context presentation significantly predicted inter-individual CPP score differences. In sum, our findings show that drug- and saline-paired contexts form distinct memory traces in overlapping functional brain microcircuits, and intrinsic connectivity of habenula, septum, and amygdala likely influences the maladaptive contextual learning in response to opioids. We identify functional mechanisms involved in the acquisition and retrieval of drug-related memories that might be behind the relapse-triggering ability of opioid-associated sensory/contextual cues. Graphical abstractTo investigate the brain-wide regional activity underlying drug addiction Gomes-Ribeiro et al. have developed a rodent morphine-induced CPP (conditioned place preference) protocol whose contextual cues can be consistently presented inside an MRI apparatus. The authors found a common circuitry supporting the neural mechanisms responsible for memorizing an association between distinct contexts, and morphine or the absence thereof, that includes regions involved in affect, reward, contextual perception and memory, with subtle, intriguing, functional specificities ultimately underlying the storage of distinct, individual, CPP memory engrams across the different animals. Animals that are more prone to strong emotional responses (as measured by the baseline resting state amygdala and habenula functional connectivity), exhibit a kind of neural circuit priming effect, and thus develop stronger connectivity patterns in anticipation of stronger morphine addiction behavior. These findings could help to clarify the inter-individual sensitivity to opioids in humans, since despite responding positively to the effects of opioids, many humans do not develop an addiction. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=138 SRC="FIGDIR/small/552221v2_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@1cd4989org.highwire.dtl.DTLVardef@96c76corg.highwire.dtl.DTLVardef@feadd0org.highwire.dtl.DTLVardef@4547b6_HPS_FORMAT_FIGEXP M_FIG C_FIG

neuroscience↗

Age-dependent NMDA receptor function is regulated by the Amyloid Precursor Protein

N-methyl-D-aspartate receptors (NMDARs) are critical for the maturation and plasticity of glutamatergic synapses. In the hippocampus, NMDARs mainly contain GluN2A and/or GluN2B regulatory subunits. The amyloid precursor protein (APP) has emerged as a putative regulator of NMDARs, but the impact of this interaction to their function is largely unknown. By combining patch-clamp electrophysiology and molecular approaches, we unravel a dual mechanism by which APP controls GluN2B-NMDARs, depending on the life stage. We show that APP is highly abundant specifically at the postnatal postsynapse. It interacts with GluN2B-NMDARs, controlling its synaptic content and mediated currents, both in infant mice and primary neuronal cultures. Upon aging, the APP amyloidogenic derived C-terminal fragments, rather than APP full length, contribute to aberrant GluN2B-NMDAR currents. Accordingly, we found that the APP processing is increased upon aging, both in mice and human brain, and interfering with this mechanism normalized the aberrant currents. While the first mechanism might be essential for synaptic maturation during development, the latter could contribute to age-related synaptic impairments. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=99 SRC="FIGDIR/small/500736v1_ufig1.gif" ALT="Figure 1"> View larger version (20K): org.highwire.dtl.DTLVardef@1c4d540org.highwire.dtl.DTLVardef@18c7b67org.highwire.dtl.DTLVardef@1f9e482org.highwire.dtl.DTLVardef@109274f_HPS_FORMAT_FIGEXP M_FIG C_FIG In briefRajao-Saraiva et al. identified the APP full-length protein as a regulator of glutamatergic transmission in immature synapses, by controlling GluN2B synaptic content and mediated currents during postnatal development. Upon aging, the APP amyloidogenic derived C-terminal fragments, rather than APP full length, contribute to aberrant GluN2B-NMDAR currents. Our work highlights the importance of keeping APP processing under tight control, to ensure the normal functioning of glutamatergic synapses, being particularly relevant to understand age-related synaptic impairments and AD.

neuroscience↗

Glycation modulates glutamatergic signalling and exacerbates Parkinson's disease-like phenotypes

Alpha-synuclein (aSyn) is assumed to be a central player in the pathogenesis of synucleinopathies due to its accumulation in typical protein aggregates in the brain. However, it is still unclear how it contributes to neurodegeneration. Type-2 diabetes mellitus is a risk factor for Parkinsons disease and, one common molecular alteration among these disorders is an age-associated increase in protein glycation. Thus, we hypothesized that glycation-induced dysfunction of neuronal pathways might be an underlying molecular cause of synucleinopathies. Here, we evaluated if increased brain glycation modulated motor and/or non-motor phenotypes in a mouse model of synucleinopathies. In addition, we dissected the specific impact of methylglyoxal (MGO, a glycating agent) in mice overexpressing aSyn in the brain, and unveiled the major molecular pathways altered. Age-matched (16 weeks old) male aSyn transgenic (Thy1-aSyn) or WT mice received a single dose of MGO or vehicle via intracerebroventricular (ICV) injection. Behavioural phenotypes were analysed 4 weeks post-treatment, and, at the end of the tests, biochemical and histological studies were conducted on brain tissue. We found that glycation potentiates motor dysfunction, assessed by vertical pole, rotarod and hindlimb clasping tests in Thy1-aSyn mice. In addition, it induces cognitive impairment (Y maze test), olfactory disturbances (block test), and colonic dysfunction. These behavioural changes were accompanied by the accumulation of aSyn in the midbrain, striatum, and prefrontal cortex, and by an overall increase in glycation in the midbrain and cerebellum. Furthermore, MGO induced neuronal and dopaminergic cell loss in the midbrain of Thy1-aSyn mice. Quantitative proteomic analysis revealed that, in Thy1-aSyn mice, MGO mainly impacts on glutamatergic proteins in the midbrain, but not in the prefrontal cortex, where it mainly affects the electron transport chain. Among the altered proteins in the midbrain, we found an upregulation of N-Methyl-D-Aspartate (NMDA) and -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptors levels, glutaminase, vesicle glutamate transporter (VGLUT), and the excitatory amino acid transporter (EAAT1), suggesting potentiation of glutamatergic signalling. Overall, we demonstrated that MGO-induced glycation accelerates Parkinsonian-like sensorimotor and cognitive alterations. The increase in glutamatergic-related proteins in the midbrain may represent a compensatory mechanism to the MGO-induced dopaminergic neurodegeneration. Our study sheds light into the enhanced vulnerability of the midbrain in Parkinsons disease-related synaptic dysfunction that, ultimately leads to cell loss, and provides molecular insight into the observation that glycation suppressors and anti-glutamatergic drugs hold promise as disease-modifying therapies for synucleinopathies.

neuroscience↗

Modeling human age-associated increase in Gadd45γ expression leads to spatial recognition memory impairments in young adult mice

Aging is associated with the progressive decay of cognitive function. Hippocampus-dependent processes, such as the formation of spatial memory, are particularly vulnerable to aging. Currently, the molecular mechanisms responsible for age-dependent cognitive decline are largely unknown. Here, we investigated the expression and function of the growth arrest DNA damage gamma (Gadd45{gamma}) during aging and cognition. We report that Gadd45{gamma} expression is increased in the hippocampus of aged humans and that Gadd45{gamma} overexpression in the young adult mouse hippocampus compromises cognition. Moreover, Gadd45{gamma} overexpression in hippocampal neurons disrupted CREB signaling and the expression of well-established activity-regulated genes. This work shows that Gadd45{gamma} expression is tightly controlled in the hippocampus and its disruption may be a mechanism contributing to age-related cognitive impairments observed in humans.

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