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  1. Article ; Online: Electrophysiological field potential identification of an intact GABAergic system in mouse cortical slices.

    Voss, Logan J / Garcia, Violet

    Brain research

    2021  Volume 1756, Page(s) 147295

    Abstract: In brain slice experiments there's currently no validated electrophysiological method for differentiating viability between GABAergic and glutamatergic cell populations. Here we investigated the neurophysiology of high frequency field potential activity - ...

    Abstract In brain slice experiments there's currently no validated electrophysiological method for differentiating viability between GABAergic and glutamatergic cell populations. Here we investigated the neurophysiology of high frequency field potential activity - and its utility for probing the functional state of the GABAergic system in brain slices. Field potentials were recorded from mouse cortical slices exposed to 50 mM potassium ("elevated-K") and the induced high frequency (>20 Hz) response characterized pharmacologically. The elevated-K responses were also related to the high frequency activity imbedded in no-magnesium seizure-like events (SLE) from the same slices. The elevated-K response, comprising a transient burst of high frequency activity, was strongly GABA
    MeSH term(s) Action Potentials/drug effects ; Action Potentials/physiology ; Animals ; Brain/drug effects ; Brain/physiopathology ; Electrophysiological Phenomena/drug effects ; Mice, Inbred C57BL ; Neurons/drug effects ; Picrotoxin/pharmacology ; Seizures/drug therapy ; Seizures/physiopathology ; gamma-Aminobutyric Acid/pharmacology ; Mice
    Chemical Substances Picrotoxin (124-87-8) ; gamma-Aminobutyric Acid (56-12-2)
    Language English
    Publishing date 2021-01-28
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 1200-2
    ISSN 1872-6240 ; 0006-8993
    ISSN (online) 1872-6240
    ISSN 0006-8993
    DOI 10.1016/j.brainres.2021.147295
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Structural Preservation Does Not Ensure Function at Sensory Ia-Motoneuron Synapses following Peripheral Nerve Injury and Repair.

    Rotterman, Travis M / García, Violet V / Housley, Stephen N / Nardelli, Paul / Sierra, Rommy / Fix, Caitlin E / Cope, Timothy C

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2023  Volume 43, Issue 24, Page(s) 4390–4404

    Abstract: Injury that severs peripheral nerves often results in long-lasting motor behavioral deficits and in reorganization of related spinal motor circuitry, neither of which reverse even after nerve regeneration. Stretch areflexia and gait ataxia, for example, ... ...

    Abstract Injury that severs peripheral nerves often results in long-lasting motor behavioral deficits and in reorganization of related spinal motor circuitry, neither of which reverse even after nerve regeneration. Stretch areflexia and gait ataxia, for example, emerge from a combination of factors including degeneration of Ia-motoneuron synapses between peripherally damaged Ia muscle spindle afferents and motoneurons. Based on evidence that nerve injury acts via immune responses to induce synapse degeneration, we hypothesized that suppressing inflammatory responses would preserve Ia-motoneuron connectivity and aid in restoring normal function. We tested our hypothesis by administering the anti-inflammatory agent minocycline in male and female rats following axotomy of a peripheral nerve. The connectivity of Ia-motoneuron synapses was then assessed both structurally and functionally at different time points. We found that minocycline treatment overcame the physical loss of Ia contacts on motoneurons which are otherwise lost after axotomy. While necessary for functional recovery, synaptic preservation was not sufficient to overcome functional decline expressed as smaller than normal stretch-evoked synaptic potentials evoked monosynaptically at Ia-motoneuron connections and an absence of the stretch reflex. These findings demonstrate a limited capacity of minocycline to rescue normal sensorimotor behavior, illustrating that structural preservation of synaptic connectivity does not ensure normal synaptic function.
    MeSH term(s) Rats ; Male ; Female ; Animals ; Spinal Cord/physiology ; Peripheral Nerve Injuries ; Minocycline/pharmacology ; Minocycline/therapeutic use ; Motor Neurons/physiology ; Synapses/physiology ; Sensory Receptor Cells
    Chemical Substances Minocycline (FYY3R43WGO)
    Language English
    Publishing date 2023-05-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.0103-23.2023
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Effects of exercise on the sleep microarchitecture in the aging brain: A study on a sedentary sample.

    Cassim, Tuan Z / McGregor, Keith M / Nocera, Joe R / García, Violet V / Sinon, Christopher G / Kreuzer, Matthias / García, Paul S

    Frontiers in systems neuroscience

    2022  Volume 16, Page(s) 855107

    Abstract: Having a healthy sleep pattern plays a vital role in one's overall health. Sleep in the elderly is characterized by decreased slow-wave sleep and an increase of REM sleep. Furthermore, quantitative electroencephalographic (qEEG) studies have shown an age- ...

    Abstract Having a healthy sleep pattern plays a vital role in one's overall health. Sleep in the elderly is characterized by decreased slow-wave sleep and an increase of REM sleep. Furthermore, quantitative electroencephalographic (qEEG) studies have shown an age-related attenuation of total EEG power in sleep. However, exercise has been shown to improve sleep across all age groups. In this study, we used the Sleep Profiler™ EEG Sleep Monitor to observe EEG changes occurring during sleep following an aerobic exercise intervention. This study was done on older adults (
    Language English
    Publishing date 2022-10-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2453005-0
    ISSN 1662-5137
    ISSN 1662-5137
    DOI 10.3389/fnsys.2022.855107
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Spinal Motor Circuit Synaptic Plasticity after Peripheral Nerve Injury Depends on Microglia Activation and a CCR2 Mechanism.

    Rotterman, Travis M / Akhter, Erica T / Lane, Alicia R / MacPherson, Kathryn P / García, Violet V / Tansey, Malú G / Alvarez, Francisco J

    The Journal of neuroscience : the official journal of the Society for Neuroscience

    2019  Volume 39, Issue 18, Page(s) 3412–3433

    Abstract: Peripheral nerve injury results in persistent motor deficits, even after the nerve regenerates and muscles are reinnervated. This lack of functional recovery is partly explained by brain and spinal cord circuit alterations triggered by the injury, but ... ...

    Abstract Peripheral nerve injury results in persistent motor deficits, even after the nerve regenerates and muscles are reinnervated. This lack of functional recovery is partly explained by brain and spinal cord circuit alterations triggered by the injury, but the mechanisms are generally unknown. One example of this plasticity is the die-back in the spinal cord ventral horn of the projections of proprioceptive axons mediating the stretch reflex (Ia afferents). Consequently, Ia information about muscle length and dynamics is lost from ventral spinal circuits, degrading motor performance after nerve regeneration. Simultaneously, there is activation of microglia around the central projections of peripherally injured Ia afferents, suggesting a possible causal relationship between neuroinflammation and Ia axon removal. Therefore, we used mice (both sexes) that allow visualization of microglia (CX3CR1-GFP) and infiltrating peripheral myeloid cells (CCR2-RFP) and related changes in these cells to Ia synaptic losses (identified by VGLUT1 content) on retrogradely labeled motoneurons. Microgliosis around axotomized motoneurons starts and peaks within 2 weeks after nerve transection. Thereafter, this region becomes infiltrated by CCR2 cells, and VGLUT1 synapses are lost in parallel. Immunohistochemistry, flow cytometry, and genetic lineage tracing showed that infiltrating CCR2 cells include T cells, dendritic cells, and monocytes, the latter differentiating into tissue macrophages. VGLUT1 synapses were rescued after attenuating the ventral microglial reaction by removal of colony stimulating factor 1 from motoneurons or in CCR2 global KOs. Thus, both activation of ventral microglia and a CCR2-dependent mechanism are necessary for removal of VGLUT1 synapses and alterations in Ia-circuit function following nerve injuries.
    MeSH term(s) Animals ; Female ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Microglia/physiology ; Motor Neurons/physiology ; Myelitis/etiology ; Myelitis/physiopathology ; Neuronal Plasticity ; Peripheral Nerve Injuries/complications ; Peripheral Nerve Injuries/physiopathology ; Receptors, CCR2/physiology ; Sciatic Nerve/injuries ; Sciatic Nerve/physiopathology ; Spinal Cord/physiopathology ; Synapses/physiology
    Chemical Substances Ccr2 protein, mouse ; Receptors, CCR2
    Language English
    Publishing date 2019-03-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 604637-x
    ISSN 1529-2401 ; 0270-6474
    ISSN (online) 1529-2401
    ISSN 0270-6474
    DOI 10.1523/JNEUROSCI.2945-17.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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