Founded in 2001, the Department of Neurobiology at UMass Chan Medical School has evolved into a unique and integrated hub of investigators addressing fundamental problems in neurobiology, from single molecules to behavior, primarily using invertebrate model organisms. Combining cell biological, physiological and behavioral analyses with a critical interventionist angle afforded by cutting-edge genetic approaches, the Department aims to understand the complexity of brain development and function. This collection showcases journal articles and other publications co-authored by Neurobiology students. Use the “UMass Chan Affiliation” Filter by Category in the left sidebar to see the publications produced by a specific lab.

Read more about the Neurobiology collections


Contact escholarship@umassmed.edu with your questions.

Recently Published

  • Dopamine control of social novelty preference is constrained by an interpeduncular-tegmentum circuit

    Molas, Susanna; Freels, Timothy G; Zhao-Shea, Rubing; Lee, Timothy; Gimenez-Gomez, Pablo; Barbini, Melanie; Martin, Gilles E; Tapper, Andrew R (2024-04-03)
    Animals are inherently motivated to explore social novelty cues over familiar ones, resulting in a novelty preference (NP), although the behavioral and circuit bases underlying NP are unclear. Combining calcium and neurotransmitter sensors with fiber photometry and optogenetics in mice, we find that mesolimbic dopamine (DA) neurotransmission is strongly and predominantly activated by social novelty controlling bout length of interaction during NP, a response significantly reduced by familiarity. In contrast, interpeduncular nucleus (IPN) GABAergic neurons that project to the lateral dorsal tegmentum (LDTg) were inhibited by social novelty but activated during terminations with familiar social stimuli. Inhibition of this pathway during NP increased interaction and bout length with familiar social stimuli, while activation reduced interaction and bout length with novel social stimuli via decreasing DA neurotransmission. These data indicate interest towards novel social stimuli is encoded by mesolimbic DA which is dynamically regulated by an IPN→LDTg circuit to control NP.
  • The Sleepy Shrimp Is Caught by the Tide: Parhyale hawaiensis As a New Model Organism for Circatidal Rhythms

    Kwiatkowski, Erica R (2024-03-15)
    Biological rhythms allow organisms to time their physiologies to match environmental cycles. Circatidal rhythms are synchronized by tidal cycles along coastlines, and have a period of 12.4 or 24.8 hours (h). Little is known about their underlying molecular mechanisms, despite how essential they are for many marine species. We chose to utilize the crustacean Parhyale hawaiensis as they are amenable to genetic manipulation. I demonstrate that Parhyale exhibits robust circatidal rhythms of activity entrained by our artificial tidal regimen. These circatidal rhythms differ from those entrained by a 12h:12h light:dark cycle, in pattern and periodicity. To investigate if the circadian molecular clock is required for circatidal rhythms, we used CRISPR-Cas9 and generated a line of Parhyale carrying a null allele of the core circadian clock gene Bmal1. I show individuals lacking Bmal1 exhibit defects both in circadian behavior, as expected, but also in circatidal behavior, labeling Bmal1 the first circatidal clock gene. I then address how circatidal rhythms adapt to the three types of tidal cycle occurring on Earth, characterized by differing periodicities. I show that Parhyale can entrain to artificial regimens mimicking all types of tidal cycle, but as regimens got further from 12.4h in period, animals exhibited behavioral flexibility. Under these challenging tidal cycles, some animals exhibited 12.4h circatidal-like rhythms of behavior, while other had more 24h circadian-like patterns of activity, demonstrating that the interaction between circadian and circatidal cycles is quite complex. In summary, this work introduces Parhyale hawaiensis as a robust model organism to study circatidal rhythms.
  • Silencing Parkinson's risk allele Rit2 sex-specifically compromises motor function and dopamine neuron viability

    Kearney, Patrick J; Zhang, Yuanxi; Liang, Marianna; Tan, Yanglan; Kahuno, Elizabeth; Conklin, Tucker L; Fagan, Rita R; Pavchinskiy, Rebecca G; Shaffer, Scott A; Yue, Zhenyu; et al. (2024-02-23)
    Parkinson's disease (PD) is the second most prevalent neurodegenerative disease and arises from dopamine (DA) neuron death selectively in the substantia nigra pars compacta (SNc). Rit2 is a reported PD risk allele, and recent single cell transcriptomic studies identified a major RIT2 cluster in PD DA neurons, potentially linking Rit2 expression loss to a PD patient cohort. However, it is still unknown whether Rit2 loss itself impacts DA neuron function and/or viability. Here we report that conditional Rit2 silencing in mouse DA neurons drove motor dysfunction that occurred earlier in males than females and was rescued at early stages by either inhibiting the DA transporter (DAT) or with L-DOPA treatment. Motor dysfunction was accompanied by decreased DA release, striatal DA content, phenotypic DAergic markers, DA neurons, and DAergic terminals, with increased pSer129-alpha synuclein and pSer935-LRRK2 expression. These results provide clear evidence that Rit2 loss is causal for SNc cell death and motor dysfunction, and reveal key sex-specific differences in the response to Rit2 loss.
  • Microglia-astrocyte crosstalk regulates synapse remodeling via Wnt signaling [preprint]

    Faust, Travis E; Lee, Yi-Han; O'Connor, Ciara; Boyle, Margaret A; Gunner, Georgia; Badimon, Ana; Ayata, Pinar; Schaefer, Anne; Schafer, Dorothy P (2024-02-09)
    Astrocytes and microglia are emerging key regulators of activity-dependent synapse remodeling that engulf and remove synapses in response to changes in neural activity. Yet, the degree to which these cells communicate to coordinate this process remains an open question. Here, we use whisker removal in postnatal mice to induce activity-dependent synapse removal in the barrel cortex. We show that astrocytes do not engulf synapses in this paradigm. Instead, astrocytes reduce their contact with synapses prior to microglia-mediated synapse engulfment. We further show that reduced astrocyte-contact with synapses is dependent on microglial CX3CL1-CX3CR1 signaling and release of Wnts from microglia following whisker removal. These results demonstrate an activity-dependent mechanism by which microglia instruct astrocyte-synapse interactions, which then provides a permissive environment for microglia to remove synapses. We further show that this mechanism is critical to remodel synapses in a changing sensory environment and this signaling is upregulated in several disease contexts.
  • Clocks at sea: the genome-editing tide is rising

    Kwiatkowski, Erica R; Rosenthal, Joshua J C; Emery, Patrick (2024-02-08)
    The coastline is a particularly challenging environment for its inhabitants. Not only do they have to cope with the solar day and the passing of seasons, but they must also deal with tides. In addition, many marine species track the phase of the moon, especially to coordinate reproduction. Marine animals show remarkable behavioral and physiological adaptability, using biological clocks to anticipate specific environmental cycles. Presently, we lack a basic understanding of the molecular mechanisms underlying circatidal and circalunar clocks. Recent advances in genome engineering and the development of genetically tractable marine model organisms are transforming how we study these timekeeping mechanisms and opening a novel era in marine chronobiology.
  • ATXN2 is a target of N-terminal proteolysis

    Chitre, Monika; Emery, Patrick (2023-12-21)
    Spinocerebellar ataxia 2 (SCA2) is a neurodegenerative disorder caused by the expansion of the poly-glutamine (polyQ) tract of Ataxin-2 (ATXN2). Other polyQ-containing proteins such as ATXN7 and huntingtin are associated with the development of neurodegenerative diseases when their N-terminal polyQ domains are expanded. Furthermore, they undergo proteolytic processing events that produce N-terminal fragments that include the polyQ stretch, which are implicated in pathogenesis. Interestingly, N-terminal ATXN2 fragments were reported in a brain extract from a SCA2 patient, but it is currently unknown whether an expanded polyQ domain contributes to ATXN2 proteolytic susceptibility. Here, we used transient expression in HEK293 cells to determine whether ATXN2 is a target for specific N-terminal proteolysis. We found that ATXN2 proteins with either normal or expanded polyQ stretches undergo proteolytic cleavage releasing an N-terminal polyQ-containing fragment. We identified a short amino acid sequence downstream of the polyQ domain that is necessary for N-terminal cleavage of full-length ATXN2 and sufficient to induce proteolysis of a heterologous protein. However, this sequence is not required for cleavage of a short ATXN2 isoform produced from an alternative start codon located just upstream of the CAG repeats encoding the polyQ domain. Our study extends our understanding of ATXN2 posttranslational regulation by revealing that this protein can be the target of specific proteolytic cleavage events releasing polyQ-containing products that are modulated by the N-terminal domain of ATXN2. N-terminal ATXN2 proteolysis of expanded polyQ domains might contribute to SCA2 pathology, as observed in other neurodegenerative disorders caused by polyQ domain expansion.
  • A neuronal coping mechanism linking stress-induced anxiety to motivation for reward

    Klenowski, Paul M; Zhao-Shea, Rubing; Freels, Timothy G; Molas, Susanna; Zinter, Max; M'Angale, Peter; Xiao, Cong; Martinez-Núñez, Leonora; Thomson, Travis; Tapper, Andrew R (2023-12-06)
    Stress coping involves innate and active motivational behaviors that reduce anxiety under stressful situations. However, the neuronal bases directly linking stress, anxiety, and motivation are largely unknown. Here, we show that acute stressors activate mouse GABAergic neurons in the interpeduncular nucleus (IPN). Stress-coping behavior including self-grooming and reward behavior including sucrose consumption inherently reduced IPN GABAergic neuron activity. Optogenetic silencing of IPN GABAergic neuron activation during acute stress episodes mimicked coping strategies and alleviated anxiety-like behavior. In a mouse model of stress-enhanced motivation for sucrose seeking, photoinhibition of IPN GABAergic neurons reduced stress-induced motivation for sucrose, whereas photoactivation of IPN GABAergic neurons or excitatory inputs from medial habenula potentiated sucrose seeking. Single-cell sequencing, fiber photometry, and optogenetic experiments revealed that stress-activated IPN GABAergic neurons that drive motivated sucrose seeking express somatostatin. Together, these data suggest that stress induces innate behaviors and motivates reward seeking to oppose IPN neuronal activation as an anxiolytic stress-coping mechanism.
  • The homeodomain transcriptional regulator DVE-1 directs a program for synapse elimination during circuit remodeling

    Alexander, Kellianne D; Ramachandran, Shankar; Biswas, Kasturi; Lambert, Christopher M; Russell, Julia; Oliver, Devyn B; Armstrong, William; Rettler, Monika; Liu, Samuel; Doitsidou, Maria; et al. (2023-11-18)
    The elimination of synapses during circuit remodeling is critical for brain maturation; however, the molecular mechanisms directing synapse elimination and its timing remain elusive. We show that the transcriptional regulator DVE-1, which shares homology with special AT-rich sequence-binding (SATB) family members previously implicated in human neurodevelopmental disorders, directs the elimination of juvenile synaptic inputs onto remodeling C. elegans GABAergic neurons. Juvenile acetylcholine receptor clusters and apposing presynaptic sites are eliminated during the maturation of wild-type GABAergic neurons but persist into adulthood in dve-1 mutants, producing heightened motor connectivity. DVE-1 localization to GABAergic nuclei is required for synapse elimination, consistent with DVE-1 regulation of transcription. Pathway analysis of putative DVE-1 target genes, proteasome inhibitor, and genetic experiments implicate the ubiquitin-proteasome system in synapse elimination. Together, our findings define a previously unappreciated role for a SATB family member in directing synapse elimination during circuit remodeling, likely through transcriptional regulation of protein degradation processes.
  • PARP knockdown promotes synapse reformation after axon injury [preprint]

    Belew, Micah Y; Huang, Wenjia; Florman, Jeremy T; Alkema, Mark J; Byrne, Alexandra B (2023-11-05)
    Injured nervous systems are often incapable of self-repairing, resulting in permanent loss of function and disability. To restore function, a severed axon must not only regenerate, but must also reform synapses with target cells. Together, these processes beget functional axon regeneration. Progress has been made towards a mechanistic understanding of axon regeneration. However, the molecular mechanisms that determine whether and how synapses are formed by a regenerated motor axon are not well understood. Using a combination of in vivo laser axotomy, genetics, and high-resolution imaging, we find that poly (ADP-ribose) polymerases (PARPs) inhibit synapse reformation in regenerating axons. As a result, regenerated parp(-) axons regain more function than regenerated wild-type axons, even though both have reached their target cells. We find that PARPs regulate both axon regeneration and synapse reformation in coordination with proteolytic calpain CLP-4. These results indicate approaches to functionally repair the injured nervous system must specifically target synapse reformation, in addition to other components of the injury response.
  • Lipofuscin-like autofluorescence within microglia and its impact on studying microglial engulfment

    Stillman, Jacob M; Mendes Lopes, Francisco; Lin, Jing-Ping; Hu, Kevin; Reich, Daniel S; Schafer, Dorothy P (2023-11-03)
    Engulfment of cellular material and proteins is a key function for microglia, a resident macrophage of the central nervous system (CNS). Among the techniques used to measure microglial engulfment, confocal light microscopy has been used the most extensively. Here, we show that autofluorescence (AF) likely due to lipofuscin (lipo-AF) and typically associated with aging, can also be detected within microglial lysosomes in the young mouse brain by light microscopy. This lipo-AF signal accumulates first within microglia and it occurs earliest in white versus gray matter. Importantly, in gray matter, lipo-AF signal can confound the interpretation of antibody-labeled synaptic material within microglia in young adult mice. We further show that there is an age-dependent accumulation of lipo-AF inside and outside of microglia, which is not affected by amyloid plaques. We finally implement a robust and cost-effective strategy to quench AF in mouse, marmoset, and human brain tissue.
  • Identifying new players in structural synaptic plasticity through dArc1 interrogation

    Xiao, Cong; M'Angale, P Githure; Wang, Shuhao; Lemieux, Adrienne; Thomson, Travis (2023-09-27)
    The formation, expansion, and pruning of synapses, known as structural synaptic plasticity, is needed for learning and memory, and perturbation of plasticity is associated with many neurological disorders and diseases. Previously, we observed that the Drosophila homolog of Activity-regulated cytoskeleton-associated protein (dArc1), forms a capsid-like structure, associates with its own mRNA, and is transported across synapses. We demonstrated that this transfer is needed for structural synaptic plasticity. To identify mRNAs that are modified by dArc1 in presynaptic neuron and postsynaptic muscle, we disrupted the expression of dArc1 and performed genomic analysis with deep sequencing. We found that dArc1 affects the expression of genes involved in metabolism, phagocytosis, and RNA-splicing. Through immunoprecipitation we also identified potential mRNA cargos of dArc1 capsids. This study suggests that dArc1 acts as a master regulator of plasticity by affecting several distinct and highly conserved cellular processes.
  • A comparative analysis of microglial inducible Cre lines

    Faust, Travis E; Feinberg, Philip A; O'Connor, Ciara; Kawaguchi, Riki; Chan, Andrew; Strasburger, Hayley; Frosch, Maximilian; Boyle, Margaret A; Masuda, Takahiro; Amann, Lukas; et al. (2023-08-26)
    Cre/loxP technology has revolutionized genetic studies and allowed for spatial and temporal control of gene expression in specific cell types. Microglial biology has particularly benefited because microglia historically have been difficult to transduce with virus or electroporation methods for gene delivery. Here, we investigate five of the most widely available microglial inducible Cre lines. We demonstrate varying degrees of recombination efficiency, cell-type specificity, and spontaneous recombination, depending on the Cre line and inter-loxP distance. We also establish best practice guidelines and protocols to measure recombination efficiency, particularly in microglia. There is increasing evidence that microglia are key regulators of neural circuits and major drivers of a broad range of neurological diseases. Reliable manipulation of their function in vivo is of utmost importance. Identifying caveats and benefits of all tools and implementing the most rigorous protocols are crucial to the growth of the field and the development of microglia-based therapeutics.
  • Distinct Th17 effector cytokines differentially promote microglial and blood-brain barrier inflammatory responses during post-infectious encephalitis [preprint]

    Wayne, Charlotte R; Bremner, Luca; Faust, Travis E; Durán-Laforet, Violeta; Ampatey, Nicole; Ho, Sarah J; Feinberg, Philip A; Arvanitis, Panos; Ciric, Bogoljub; Ruan, Chunsheng; et al. (2023-05-09)
    Group A Streptococcus (GAS) infections can cause neuropsychiatric sequelae in children due to post-infectious encephalitis. Multiple GAS infections induce migration of Th17 lymphocytes from the nose into the brain, which are critical for microglial activation, blood-brain barrier (BBB) and neural circuit impairment in a mouse disease model. How endothelial cells (ECs) and microglia respond to GAS infections, and which Th17-derived cytokines are essential for these responses are unknown. Using single-cell RNA sequencing and spatial transcriptomics, we found that ECs downregulate BBB genes and microglia upregulate interferon-response, chemokine and antigen-presentation genes after GAS infections. Several microglial-derived chemokines were elevated in patient sera. Administration of a neutralizing antibody against interleukin-17A (IL-17A), but not ablation of granulocyte-macrophage colony-stimulating factor (GM-CSF) in T cells, partially rescued BBB dysfunction and microglial expression of chemokine genes. Thus, IL-17A is critical for neuropsychiatric sequelae of GAS infections and may be targeted to treat these disorders.
  • TIR-1/SARM1 inhibits axon regeneration and promotes axon degeneration

    Czech, Victoria L; O'Connor, Lauren C; Philippon, Brendan; Norman, Emily; Byrne, Alexandra B (2023-04-21)
    Growth and destruction are central components of the neuronal injury response. Injured axons that are capable of repair, including axons in the mammalian peripheral nervous system and in many invertebrate animals, often regenerate and degenerate on either side of the injury. Here we show that TIR-1/dSarm/SARM1, a key regulator of axon degeneration, also inhibits regeneration of injured motor axons. The increased regeneration in tir-1 mutants is not a secondary consequence of its effects on degeneration, nor is it determined by the NADase activity of TIR-1. Rather, we found that TIR-1 functions cell-autonomously to regulate each of the seemingly opposite processes through distinct interactions with two MAP kinase pathways. On one side of the injury, TIR-1 inhibits axon regeneration by activating the NSY-1/ASK1 MAPK signaling cascade, while on the other side of the injury, TIR-1 simultaneously promotes axon degeneration by interacting with the DLK-1 mitogen-activated protein kinase (MAPK) signaling cascade. In parallel, we found that the ability to cell-intrinsically inhibit axon regeneration is conserved in human SARM1. Our finding that TIR-1/SARM1 regulates axon regeneration provides critical insight into how axons coordinate a multidimensional response to injury, consequently informing approaches to manipulate the response toward repair.
  • Intravital Imaging of Fluorescent Protein Expression in Mice with a Closed-Skull Traumatic Brain Injury and Cranial Window Using a Two-Photon Microscope

    Zhong, Jianjun; Gunner, Georgia; Henninger, Nils; Schafer, Dorothy P; Bosco, Daryl A (2023-04-21)
    The goal of this protocol is to demonstrate how to longitudinally visualize the expression and localization of a protein of interest within specific cell types of an animal's brain, upon exposure to exogenous stimuli. Here, the administration of a closed-skull traumatic brain injury (TBI) and simultaneous implantation of a cranial window for subsequent longitudinal intravital imaging in mice is shown. Mice are intracranially injected with an adeno-associated virus (AAV) expressing enhanced green fluorescent protein (EGFP) under a neuronal specific promoter. After 2 to 4 weeks, the mice are subjected to a repetitive TBI using a weight drop device over the AAV injection location. Within the same surgical session, the mice are implanted with a metal headpost and then a glass cranial window over the TBI impacting site. The expression and cellular localization of EGFP is examined using a two-photon microscope in the same brain region exposed to trauma over the course of months.
  • Gliotransmission and adenosine signaling promote axon regeneration

    Wang, Fei; Ruppell, Kendra Takle; Zhou, Songlin; Qu, Yun; Gong, Jiaxin; Shang, Ye; Wu, Jinglin; Liu, Xin; Diao, Wenlin; Li, Yi; et al. (2023-04-06)
    How glia control axon regeneration remains incompletely understood. Here, we investigate glial regulation of regenerative ability differences of closely related Drosophila larval sensory neuron subtypes. Axotomy elicits Ca2+ signals in ensheathing glia, which activates regenerative neurons through the gliotransmitter adenosine and mounts axon regenerative programs. However, non-regenerative neurons do not respond to glial stimulation or adenosine. Such neuronal subtype-specific responses result from specific expressions of adenosine receptors in regenerative neurons. Disrupting gliotransmission impedes axon regeneration of regenerative neurons, and ectopic adenosine receptor expression in non-regenerative neurons suffices to activate regenerative programs and induce axon regeneration. Furthermore, stimulating gliotransmission or activating the mammalian ortholog of Drosophila adenosine receptors in retinal ganglion cells (RGCs) promotes axon regrowth after optic nerve crush in adult mice. Altogether, our findings demonstrate that gliotransmission orchestrates neuronal subtype-specific axon regeneration in Drosophila and suggest that targeting gliotransmission or adenosine signaling is a strategy for mammalian central nervous system repair.
  • Behavioral circatidal rhythms require Bmal1 in Parhyale hawaiensis

    Kwiatkowski, Erica R; Schnytzer, Yisrael; Rosenthal, Joshua J C; Emery, Patrick (2023-03-19)
    Organisms living in the intertidal zone are exposed to a particularly challenging environment. In addition to daily changes in light intensity and seasonal changes in photoperiod and weather patterns, they experience dramatic oscillations in environmental conditions due to the tides. To anticipate tides, and thus optimize their behavior and physiology, animals occupying intertidal ecological niches have acquired circatidal clocks. Although the existence of these clocks has long been known, their underlying molecular components have proven difficult to identify, in large part because of the lack of an intertidal model organism amenable to genetic manipulation. In particular, the relationship between the circatidal and circadian molecular clocks, and the possibility of shared genetic components, has been a long-standing question. Here, we introduce the genetically tractable crustacean Parhyale hawaiensis as a system for the study of circatidal rhythms. First, we show that P. hawaiensis exhibits robust 12.4-h rhythms of locomotion that can be entrained to an artificial tidal regimen and are temperature compensated. Using CRISPR-Cas9 genome editing, we then demonstrate that the core circadian clock gene Bmal1 is required for circatidal rhythms. Our results thus demonstrate that Bmal1 is a molecular link between circatidal and circadian clocks and establish P. hawaiensis as a powerful system to study the molecular mechanisms underlying circatidal rhythms and their entrainment.
  • Lipofuscin-like autofluorescence within microglia and its impact on studying microglial engulfment [preprint]

    Stillman, Jacob M; Lopes, Francisco M; Lin, Jing-Ping; Hu, Kevin; Reich, Daniel S; Schafer, Dorothy P (2023-03-01)
    Engulfment of cellular material and proteins is a key function for microglia, a resident macrophage of the central nervous system (CNS). Among the techniques used to measure microglial engulfment, confocal light microscopy has been used the most extensively. Here, we show that autofluorescence (AF), likely due to lipofuscin and typically associated with aging, can also be detected within microglial lysosomes in the young mouse brain by light microscopy. This lipofuscin-AF signal accumulates first within microglia and increases with age, but it is not exacerbated by amyloid beta-related neurodegeneration. We further show that this lipofuscin-AF signal within microglia can confound the interpretation of antibody-labeled synaptic material within microglia in young adult mice. Finally, we implement a robust strategy to quench AF in mouse, marmoset, and human brain tissue.
  • The choroid plexus links innate immunity to CSF dysregulation in hydrocephalus

    Robert, Stephanie M; Reeves, Benjamin C; Kiziltug, Emre; Duy, Phan Q; Karimy, Jason K; Mansuri, M Shahid; Marlier, Arnaud; Allington, Garrett; Greenberg, Ana B W; DeSpenza, Tyrone; et al. (2023-02-16)
    The choroid plexus (ChP) is the blood-cerebrospinal fluid (CSF) barrier and the primary source of CSF. Acquired hydrocephalus, caused by brain infection or hemorrhage, lacks drug treatments due to obscure pathobiology. Our integrated, multi-omic investigation of post-infectious hydrocephalus (PIH) and post-hemorrhagic hydrocephalus (PHH) models revealed that lipopolysaccharide and blood breakdown products trigger highly similar TLR4-dependent immune responses at the ChP-CSF interface. The resulting CSF "cytokine storm", elicited from peripherally derived and border-associated ChP macrophages, causes increased CSF production from ChP epithelial cells via phospho-activation of the TNF-receptor-associated kinase SPAK, which serves as a regulatory scaffold of a multi-ion transporter protein complex. Genetic or pharmacological immunomodulation prevents PIH and PHH by antagonizing SPAK-dependent CSF hypersecretion. These results reveal the ChP as a dynamic, cellularly heterogeneous tissue with highly regulated immune-secretory capacity, expand our understanding of ChP immune-epithelial cell cross talk, and reframe PIH and PHH as related neuroimmune disorders vulnerable to small molecule pharmacotherapy.
  • Modulation of neuronal excitability by binge alcohol drinking

    Giménez-Gómez, Pablo; Le, Timmy; Martin, Gilles E (2023-02-14)
    Drug use poses a serious threat to health systems throughout the world. The number of consumers rises every year being alcohol the drug of abuse most consumed causing 3 million deaths (5.3% of all deaths) worldwide and 132.6 million disability-adjusted life years. In this review, we present an up-to-date summary about what is known regarding the global impact of binge alcohol drinking on brains and how it affects the development of cognitive functions, as well as the various preclinical models used to probe its effects on the neurobiology of the brain. This will be followed by a detailed report on the state of our current knowledge of the molecular and cellular mechanisms underlying the effects of binge drinking on neuronal excitability and synaptic plasticity, with an emphasis on brain regions of the meso-cortico limbic neurocircuitry.

View more