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Article ; Online: The Influence of Environmental Enrichment on Affective and Neural Consequences of Social Isolation Across Development.

Akinbo, Oreoluwa I / McNeal, Neal / Hylin, Michael / Hite, Natalee / Dagner, Ashley / Grippo, Angela J

2022 Volume 3, Issue 4, Page(s) 713–733

Abstract: Social stress is associated with depression and anxiety, physiological disruptions, and altered brain morphology in central stress circuitry across development. Environmental enrichment strategies may improve responses to social stress. Socially ... ...

Abstract	Social stress is associated with depression and anxiety, physiological disruptions, and altered brain morphology in central stress circuitry across development. Environmental enrichment strategies may improve responses to social stress. Socially monogamous prairie voles exhibit analogous social and emotion-related behaviors to humans, with potential translational insight into interactions of social stress, age, and environmental enrichment. This study explored the effects of social isolation and environmental enrichment on behaviors related to depression and anxiety, physiological indicators of stress, and dendritic structural changes in amygdala and hippocampal subregions in young adult and aging prairie voles. Forty-nine male prairie voles were assigned to one of six groups divided by age (young adult vs. aging), social structure (paired vs. isolated), and housing environment (enriched vs. non-enriched). Following 4 weeks of these conditions, behaviors related to depression and anxiety were investigated in the forced swim test and elevated plus maze, body and adrenal weights were evaluated, and dendritic morphology analyses were conducted in hippocampus and amygdala subregions. Environmental enrichment decreased immobility duration in the forced swim test, increased open arm exploration in the elevated plus maze, and reduced adrenal/body weight ratio in aging and young adult prairie voles. Age and social isolation influenced dendritic morphology in the basolateral amygdala. Age, but not social isolation, influenced dendritic morphology in the hippocampal dentate gyrus. Environmental enrichment did not influence dendritic morphology in either brain region. These data may inform interventions to reduce the effects of social stressors and age-related central changes associated with affective behavioral consequences in humans.
Language	English
Publishing date	2022-10-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2978299-5
ISSN	2662-205X ; 2662-2041
ISSN (online)	2662-205X
ISSN	2662-2041
DOI	10.1007/s42761-022-00131-8
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Article ; Online: Morphological changes in the basolateral amygdala and behavioral disruptions associated with social isolation.

Hylin, Michael J / Tang Watanasriyakul, W / Hite, Natalee / McNeal, Neal / Grippo, Angela J

Behavioural brain research

2021 Volume 416, Page(s) 113572

Abstract: Social isolation and the disruption of established social bonds contribute to several physical and psychological health issues. Animal models are a useful tool for investigating consequences of social stress, including social isolation. The current study ...

Abstract	Social isolation and the disruption of established social bonds contribute to several physical and psychological health issues. Animal models are a useful tool for investigating consequences of social stress, including social isolation. The current study examined morphological changes in the basolateral amygdala (BLA) and affect-related behavioral and endocrine changes due to prolonged social isolation, using the translational prairie vole model (Microtus ochrogaster). Adult male prairie voles were either socially paired (control) or isolated from a same-sex sibling for 4 weeks. Following this 4-week period, a subset of animals (n = 6 per condition) underwent a series of behavioral tasks to assess affective, social, and stress-coping behaviors. Plasma was collected following the last behavioral task for stressor-induced endocrine assays. Brains were collected from a separate subset of animals (n = 10 per condition) following the 4-week social housing period for dendritic structure analyses in the BLA. Social isolation was associated with depressive- and anxiety-like behaviors, as well as elevated oxytocin reactivity following a social stressor. Social isolation was also associated with altered amount of dendritic material in the BLA, with an increase in spine density. These results provide further evidence that social isolation may lead to the development of affective disorders. Dysfunction in the oxytocin system and BLA remodeling may mediate these behavioral changes. Further research will promote an understanding of the connections between oxytocin function and structural changes in the BLA in the context of social stress. This research can facilitate novel treatments for alleviating or preventing behavioral and physiological consequences of social stressors in humans.
MeSH term(s)	Animals ; Arvicolinae/physiology ; Basolateral Nuclear Complex/drug effects ; Behavior, Animal/physiology ; Corticosterone/blood ; Dendrites ; Male ; Neurosecretory Systems/drug effects ; Oxytocin/pharmacology ; Social Isolation/psychology ; Stress, Psychological/physiopathology ; Task Performance and Analysis
Chemical Substances	Oxytocin (50-56-6) ; Corticosterone (W980KJ009P)
Language	English
Publishing date	2021-09-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2021.113572
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Article ; Online: Understanding the Mechanisms of Recovery and/or Compensation following Injury.

Hylin, Michael J / Kerr, Abigail L / Holden, Ryan

Neural plasticity

2017 Volume 2017, Page(s) 7125057

Abstract: Injury due to stroke and traumatic brain injury result in significant long-term effects upon behavioral functioning. One central question to rehabilitation research is whether the nature of behavioral improvement observed is due to recovery or the ... ...

Abstract	Injury due to stroke and traumatic brain injury result in significant long-term effects upon behavioral functioning. One central question to rehabilitation research is whether the nature of behavioral improvement observed is due to recovery or the development of compensatory mechanisms. The nature of functional improvement can be viewed from the perspective of behavioral changes or changes in neuroanatomical plasticity that follows. Research suggests that these changes correspond to each other in a bidirectional manner. Mechanisms surrounding phenomena like neural plasticity may offer an opportunity to explain how variables such as experience can impact improvement and influence the definition of recovery. What is more, the intensity of the rehabilitative experiences may influence the ability to recover function and support functional improvement of behavior. All of this impacts how researchers, clinicians, and medical professionals utilize rehabilitation.
MeSH term(s)	Animals ; Behavior, Animal ; Brain/physiopathology ; Brain Injuries, Traumatic/physiopathology ; Brain Injuries, Traumatic/rehabilitation ; Humans ; Neuronal Plasticity ; Recovery of Function ; Stroke/physiopathology ; Stroke Rehabilitation
Language	English
Publishing date	2017-04-20
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1454938-4
ISSN	1687-5443 ; 2090-5904 ; 0792-8483
ISSN (online)	1687-5443
ISSN	2090-5904 ; 0792-8483
DOI	10.1155/2017/7125057
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Article ; Online: Effects of nicotinamide on spatial memory and inflammation after juvenile traumatic brain injury.

Smith, Aidan C / Holden, Ryan C / Rasmussen, Sherry M / Hoane, Michael R / Hylin, Michael J

Behavioural brain research

2019 Volume 364, Page(s) 123–132

Abstract: Age is a consistent predictor of outcome following traumatic brain injury (TBI). Although children and adolescents have the highest rate of hospitalizations and long-term disabilities, few preclinical studies have attempted to model and treat TBI in this ...

Abstract	Age is a consistent predictor of outcome following traumatic brain injury (TBI). Although children and adolescents have the highest rate of hospitalizations and long-term disabilities, few preclinical studies have attempted to model and treat TBI in this population. Studies using nicotinamide (NAM), a soluble B-group vitamin, in older animals (3-6 months) have shown improved functional recovery in experimental models of TBI. The purpose of this study was two-fold: to examine the preclinical efficacy of NAM at different doses on behavioral outcomes in juvenile rats and examine the microglial response over time. Groups of juvenile rats (PND 28-60) were assigned to sham, NAM (125 mg/kg, 500 mg/kg, or 1000 mg/kg) or saline (1 mL/kg) and received unilateral cortical contusion injuries (CCI) and received injections at 15 min, 24 h, and 72 h after injury. Animals treated with NAM demonstrated no significant behavioral improvements over saline treatments. NAM treatments did however show slowed cortical loss and reduced microglia compared to saline treated animals. In summary, the preclinical efficacy of NAM as a treatment following CCI in juvenile animals differs from that previously documented in older rat models. While NAM treatments did reduce microglial activity and slowed progression of cortical loss, it did not reduce the total cortical volume lost nor did it improve behavioral outcomes. The findings of this study emphasize the need to examine potential treatments for TBI utilizing juvenile populations and may explain why so many treatments have failed in clinical trials.
MeSH term(s)	Age Factors ; Animals ; Brain Injuries, Traumatic/drug therapy ; Cerebral Cortex/drug effects ; Inflammation/drug therapy ; Male ; Maze Learning/drug effects ; Microglia/drug effects ; Models, Animal ; Motor Activity/drug effects ; Niacinamide/pharmacology ; Rats ; Rats, Sprague-Dawley ; Recovery of Function/drug effects ; Spatial Memory/drug effects
Chemical Substances	Niacinamide (25X51I8RD4)
Language	English
Publishing date	2019-02-13
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2019.02.024
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Zs.A 1599: Show issues

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Article ; Online: Metformin Reduces Repeat Mild Concussive Injury Pathophysiology.

Underwood, Erica L / Redell, John B / Maynard, Mark E / Kobori, Nobuhide / Hylin, Michael J / Hood, Kimberly N / West, Rebecca K / Zhao, Jing / Moore, Anthony N / Dash, Pramod K

eNeuro

2022 Volume 9, Issue 1

Abstract: Mild traumatic brain injury (mTBI) can initiate complex pathophysiological changes in the brain. Numerous cellular and molecular mechanisms underlying these pathologic changes are altered after injury, including those involved in energy utilization, ... ...

Abstract	Mild traumatic brain injury (mTBI) can initiate complex pathophysiological changes in the brain. Numerous cellular and molecular mechanisms underlying these pathologic changes are altered after injury, including those involved in energy utilization, excitotoxicity, ionic disturbances, and inflammation. It is thought that targeting multiple mechanisms may be necessary to produce meaningful reductions in brain pathology and to improve outcome. Previous studies have reported that the anti-diabetic drug metformin can also affect inflammatory, cell survival, and metabolic outcomes, possibly by acting on multiple targets and/or pathways. We therefore questioned whether metformin treatment can reduce pathology after repeat mild closed head injury (rmCHI) in male C57Bl/6 mice. We found that metformin, administered acutely after each head impact, resulted in markedly reduced white matter damage, astrogliosis, loss of hippocampal parvalbumin neurons, and improved mitochondrial function. In addition, both motor and cognitive functions were significantly improved when tested after discontinuation of the treatment. These studies suggest that metformin may be beneficial as a treatment for repeat concussion.
MeSH term(s)	Animals ; Brain ; Brain Concussion/drug therapy ; Disease Models, Animal ; Head Injuries, Closed ; Male ; Metformin/pharmacology ; Mice ; Mice, Inbred C57BL
Chemical Substances	Metformin (9100L32L2N)
Language	English
Publishing date	2022-01-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2800598-3
ISSN	2373-2822 ; 2373-2822
ISSN (online)	2373-2822
ISSN	2373-2822
DOI	10.1523/ENEURO.0421-21.2021
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Article ; Online: Enhanced presynaptic mitochondrial energy production is required for memory formation.

Underwood, Erica L / Redell, John B / Hood, Kimberly N / Maynard, Mark E / Hylin, Michael / Waxham, M Neal / Zhao, Jing / Moore, Anthony N / Dash, Pramod K

Scientific reports

2023 Volume 13, Issue 1, Page(s) 14431

Abstract: Some of the prominent features of long-term memory formation include protein synthesis, gene expression, enhanced neurotransmitter release, increased excitability, and formation of new synapses. As these processes are critically dependent on ... ...

Abstract	Some of the prominent features of long-term memory formation include protein synthesis, gene expression, enhanced neurotransmitter release, increased excitability, and formation of new synapses. As these processes are critically dependent on mitochondrial function, we hypothesized that increased mitochondrial respiration and dynamics would play a prominent role in memory formation. To address this possibility, we measured mitochondrial oxygen consumption (OCR) in hippocampal tissue punches from trained and untrained animals. Our results show that context fear training significantly increased basal, ATP synthesis-linked, and maximal OCR in the Shaffer collateral-CA1 synaptic region, but not in the CA1 cell body layer. These changes were recapitulated in synaptosomes isolated from the hippocampi of fear-trained animals. As dynamin-related protein 1 (Drp1) plays an important role in mitochondrial fission, we examined its role in the increased mitochondrial respiration observed after fear training. Drp1 inhibitors decreased the training-associated enhancement of OCR and impaired contextual fear memory, but did not alter the number of synaptosomes containing mitochondria. Taken together, our results show context fear training increases presynaptic mitochondria respiration, and that Drp-1 mediated enhanced energy production in CA1 pre-synaptic terminals is necessary for context fear memory that does not result from an increase in the number of synaptosomes containing mitochondria or an increase in mitochondrial mass within the synaptic layer.
MeSH term(s)	Animals ; Biological Transport ; Oxygen Consumption ; Synapses ; Memory Disorders ; Mitochondria
Language	English
Publishing date	2023-09-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-40877-0
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Article ; Online: The time-dependent and persistent effects of amphetamine treatment upon recovery from hemispatial neglect in rats.

Brenneman, Miranda M / Hylin, Michael J / Corwin, James V

Behavioural brain research

2015 Volume 293, Page(s) 153–161

Abstract: Neglect is a neuropsychological disorder characterized by the failure to report or respond to stimuli presented to the side of the body opposite a brain lesion and occurs in approximately 40% of right hemisphere strokes. The need for effective therapies ... ...

Abstract	Neglect is a neuropsychological disorder characterized by the failure to report or respond to stimuli presented to the side of the body opposite a brain lesion and occurs in approximately 40% of right hemisphere strokes. The need for effective therapies to treat neglect in humans has led to the development of a rodent model. Unilateral destruction of medial agranular cortex (AGm), which is part of a cortical network for directed attention, produces severe multimodal neglect with deficits similar to those seen in humans. Amphetamines have previously been investigated for inducing plasticity and recovery of function following brain damage. Amphetamine treatment has been shown to produce recovery from visual, frontal, and sensorimotor cortex damage in animals and this recovery may be the result of axonal growth originating from the opposite, unlesioned hemisphere. The purpose of this study was to investigate whether amphetamine treatment would induce recovery from neglect produced by unilateral AGm destruction, the time frame in which amphetamine must be administered in order to be effective, and the permanence of recovery following treatment. The results indicated that subjects injected with 2mg/kg of d-amphetamine on days 0, 2, and 5 recovered in significantly fewer days than saline-treated controls, even when administration was delayed by 2 and 7 days. Additionally, these studies indicated that recovery persisted for at least 60 days suggesting that recovery is likely to be long term.
MeSH term(s)	Amphetamine/therapeutic use ; Analysis of Variance ; Animals ; Cerebral Cortex/injuries ; Disease Models, Animal ; Dopamine Agents/therapeutic use ; Functional Laterality/drug effects ; Impulsive Behavior/drug effects ; Male ; Orientation/drug effects ; Perceptual Disorders/chemically induced ; Perceptual Disorders/drug therapy ; Physical Stimulation ; Rats ; Rats, Long-Evans ; Recovery of Function/drug effects ; Recovery of Function/physiology ; Statistics, Nonparametric ; Time Factors
Chemical Substances	Dopamine Agents ; Amphetamine (CK833KGX7E)
Language	English
Publishing date	2015-10-15
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	449927-x
ISSN	1872-7549 ; 0166-4328
ISSN (online)	1872-7549
ISSN	0166-4328
DOI	10.1016/j.bbr.2015.07.032
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Zs.A 1599: Show issues

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Article ; Online: Effect of Disulfiram and Copper Plus Chemotherapy vs Chemotherapy Alone on Survival in Patients With Recurrent Glioblastoma: A Randomized Clinical Trial.

Werlenius, Katja / Kinhult, Sara / Solheim, Tora Skeidsvoll / Magelssen, Henriette / Löfgren, David / Mudaisi, Munila / Hylin, Sofia / Bartek, Jiri / Strandéus, Michael / Lindskog, Magnus / Rashid, Havyan Bahroz / Carstam, Louise / Gulati, Sasha / Solheim, Ole / Salvesen, Øyvind / Jakola, Asgeir Store

JAMA network open

2023 Volume 6, Issue 3, Page(s) e234149

Abstract: Importance: Disulfiram has demonstrated broad antitumoral effect in several preclinical studies. One of the proposed indications is for the treatment of glioblastoma.: Objective: To evaluate the efficacy and safety of disulfiram and copper as add-on ... ...

Abstract	Importance: Disulfiram has demonstrated broad antitumoral effect in several preclinical studies. One of the proposed indications is for the treatment of glioblastoma. Objective: To evaluate the efficacy and safety of disulfiram and copper as add-on to alkylating chemotherapy in patients with recurrent glioblastoma. Design, setting, and participants: This was a multicenter, open-label, randomized phase II/III clinical trial with parallel group design. Patients were recruited at 7 study sites in Sweden and 2 sites in Norway between January 2017 and November 2020. Eligible patients were 18 years or older, had a first recurrence of glioblastoma, and indication for treatment with alkylating chemotherapy. Patients were followed up until death or a maximum of 24 months. The date of final follow-up was January 15, 2021. Data analysis was performed from February to September 2022. Interventions: Patients were randomized 1:1 to receive either standard-of-care (SOC) alkylating chemotherapy alone, or SOC with the addition of disulfiram (400 mg daily) and copper (2.5 mg daily). Main outcomes and measures: The primary end point was survival at 6 months. Secondary end points included overall survival, progression-free survival, adverse events, and patient-reported quality of life. Results: Among the 88 patients randomized to either SOC (n = 45) or SOC plus disulfiram and copper (n = 43), 63 (72%) were male; the mean (SD) age was 55.4 (11.5) years. There was no significant difference between the study groups (SOC vs SOC plus disulfiram and copper) in 6 months survival (62% [26 of 42] vs 44% [19 of 43]; P = .10). Median overall survival was 8.2 months (95% CI, 5.4-10.2 months) with SOC and 5.5 months (95% CI, 3.9-9.3 months) with SOC plus disulfiram and copper, and median progression-free survival was 2.6 months (95% CI, 2.4-4.6 months) vs 2.3 months (95% CI, 1.7-2.6 months), respectively. More patients in the SOC plus disulfiram and copper group had adverse events grade 3 or higher (34% [14 of 41] vs 11% [5 of 44]; P = .02) and serious adverse events (41% [17 of 41] vs 16% [7 of 44]; P = .02), and 10 patients (24%) discontinued disulfiram treatment because of adverse effects. Conclusions and relevance: This randomized clinical trial found that among patients with recurrent glioblastoma, the addition of disulfiram and copper to chemotherapy, compared with chemotherapy alone, resulted in significantly increased toxic effects, but no significant difference in survival. These findings suggest that disulfiram and copper is without benefit in patients with recurrent glioblastoma. Trial registration: ClinicalTrials.gov Identifier: NCT02678975; EUDRACT Identifier: 2016-000167-16.
MeSH term(s)	Humans ; Male ; Middle Aged ; Female ; Glioblastoma/drug therapy ; Copper/therapeutic use ; Disulfiram/therapeutic use ; Quality of Life ; Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Chemical Substances	Copper (789U1901C5) ; Disulfiram (TR3MLJ1UAI)
Language	English
Publishing date	2023-03-01
Publishing country	United States
Document type	Randomized Controlled Trial ; Multicenter Study ; Clinical Trial, Phase II ; Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2574-3805
ISSN (online)	2574-3805
DOI	10.1001/jamanetworkopen.2023.4149
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Article ; Online: Post-Injury Administration of Galantamine Reduces Traumatic Brain Injury Pathology and Improves Outcome.

Zhao, Jing / Hylin, Michael J / Kobori, Nobuhide / Hood, Kimberly N / Moore, Anthony N / Dash, Pramod K

Journal of neurotrauma

2017 Volume 35, Issue 2, Page(s) 362–374

Abstract: Acetylcholine is an excitatory neurotransmitter in the central nervous system that plays a key role in cognitive function, including learning and memory. Previous studies have shown that experimental traumatic brain injury (TBI) reduces cholinergic ... ...

Abstract	Acetylcholine is an excitatory neurotransmitter in the central nervous system that plays a key role in cognitive function, including learning and memory. Previous studies have shown that experimental traumatic brain injury (TBI) reduces cholinergic neurotransmission, decreases evoked release of acetylcholine, and alters cholinergic receptor levels. Galantamine (U.S. Food and Drug Administration approved for the treatment of vascular dementia and Alzheimer's disease) has been shown to inhibit acetylcholinesterase activity and allosterically potentiate nicotinic receptor signaling. We investigated whether acute administration of galantamine can reduce TBI pathology and improve cognitive function tested days after the termination of the drug treatment. Post-injury administration of galantamine was found to decrease TBI-triggered blood-brain barrier (BBB) permeability (tested 24 h post-injury), attenuate the loss of both GABAergic and newborn neurons in the ipsilateral hippocampus, and improve hippocampal function (tested 10 days after termination of the drug treatment). Specifically, significant improvements in the Morris water maze, novel object recognition, and context-specific fear memory tasks were observed in injured animals treated with galantamine. Although messenger RNAs for both M1 (Nos2, TLR4, and IL-12ß) and M2 (Arg1, CCL17, and Mcr1) microglial phenotypes were elevated post-TBI, galantamine treatment did not alter microglial polarization tested 24 h and 6 days post-injury. Taken together, these findings support the further investigation of galantamine as a treatment for TBI.
MeSH term(s)	Animals ; Blood-Brain Barrier/drug effects ; Brain/drug effects ; Brain/pathology ; Brain Injuries, Traumatic/pathology ; Cholinesterase Inhibitors/pharmacology ; Cognition/drug effects ; Galantamine/pharmacology ; Male ; Neuroprotective Agents/pharmacology ; Rats ; Rats, Sprague-Dawley ; Recovery of Function
Chemical Substances	Cholinesterase Inhibitors ; Neuroprotective Agents ; Galantamine (0D3Q044KCA)
Language	English
Publishing date	2017-12-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2017.5102
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Zs.A 2016: Show issues

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Article ; Online: Endoplasmic Reticulum Stress Contributes to the Loss of Newborn Hippocampal Neurons after Traumatic Brain Injury.

Hood, Kimberly N / Zhao, Jing / Redell, John B / Hylin, Michael J / Harris, Brynn / Perez, Alec / Moore, Anthony N / Dash, Pramod K

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

2018 Volume 38, Issue 9, Page(s) 2372–2384

Abstract: Adult hippocampal neurogenesis has been shown to be required for certain types of cognitive function. For example, studies have shown that these neurons are critical for pattern separation, the ability to store similar experiences as distinct memories. ... ...

Abstract	Adult hippocampal neurogenesis has been shown to be required for certain types of cognitive function. For example, studies have shown that these neurons are critical for pattern separation, the ability to store similar experiences as distinct memories. Although traumatic brain injury (TBI) has been shown to cause the loss of newborn hippocampal neurons, the signaling pathway(s) that triggers their death is unknown. Endoplasmic reticulum (ER) stress activates the PERK-eIF2α pathway that acts to restore ER function and improve cell survival. However, unresolved/intense ER stress activates C/EBP homologous protein (CHOP), leading to cell death. We show that TBI causes the death of hippocampal newborn neurons via CHOP. Using CHOP KO mice, we show that loss of CHOP markedly reduces newborn neuron loss after TBI. Injured CHOP mice performed significantly better in a context fear discrimination task compared with injured wild-type mice. In contrast, the PERK inhibitor GSK2606414 exacerbated doublecortin cell loss and worsened contextual discrimination. Administration of guanabenz (which reduces ER stress) to injured male rats reduced the loss of newborn neurons and improved one-trial contextual fear memory. Interestingly, we also found that the surviving newborn neurons in brain-injured animals had dendritic loss, which was not observed in injured CHOP KO mice or in animals treated with guanabenz. These results indicate that ER stress plays a key role in the death of newborn neurons after TBI. Further, these findings indicate that ER stress can alter dendritic arbors, suggesting a role for ER stress in neuroplasticity and dendritic pathologies.
MeSH term(s)	Animals ; Brain Injuries, Traumatic/metabolism ; Brain Injuries, Traumatic/physiopathology ; Cell Death/physiology ; Endoplasmic Reticulum Stress/physiology ; Hippocampus/metabolism ; Hippocampus/physiopathology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurogenesis/physiology ; Neurons/metabolism ; Neurons/pathology ; Rats ; Rats, Sprague-Dawley ; Transcription Factor CHOP/metabolism
Chemical Substances	Transcription Factor CHOP (147336-12-7)
Language	English
Publishing date	2018-01-31
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.1756-17.2018
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