Axonal damage and behavioral deficits in rats with repetitive exposure of the brain to laser-induced shock waves: Effects of inter-exposure time

2021 ◽  
Vol 749 ◽  
pp. 135722
Author(s):  
Kosuke Miyai ◽  
Satoko Kawauchi ◽  
Tamaki Kato ◽  
Tetsuo Yamamoto ◽  
Yasuo Mukai ◽  
...  
Keyword(s):  
Shock Waves ◽  
Exposure Time ◽  
Axonal Damage ◽  
Behavioral Deficits ◽  
Repetitive Exposure ◽  
The Brain

Steps toward recovery of function after hemilabyrinthectomy in frogs

1998 ◽  
Vol 119 (1) ◽  
pp. 27-33 ◽  
Author(s):  
Norbert Dieringer ◽  
Hans Straka
Keyword(s):  
Time Course ◽  
Recovery Of Function ◽  
Behavioral Deficits ◽  
Afferent Fibers ◽  
Vestibular Nuclear Complex ◽  
The Central Nervous System ◽  
Synaptic Changes ◽  
Necessary And Sufficient ◽  
The Brain

Removal of the labyrinthine organs on one side results in a number of severe postural and dynamic reflex deficits. Over time some of these behavioral deficits normalize again. At a chronic stage the brain of frogs exhibits a number of changes in vestibular and propriospinal circuits on the operated side that were studied in vitro. The onset of changes in the vestibular nuclear complex was delayed, became evident only after head posture had recovered by more than 50%, and was independent of the presence or absence of a degeneration of vestibular nerve afferent fibers. The time course of changes measured in the isolated spinal cord paralleled the time course of normalization of head and body posture. Results obtained after selective lesions of individual labyrinthine nerve branches show that unilateral inactivation of utricular afferent inputs is a necessary and sufficient condition to provoke postural deficits and propriospinal changes similar to those after the removal of all labyrinthine organs. The presence of multiple synaptic changes at distributed anatomic sites over different periods of time suggests that different parts of the central nervous system are involved in the normalization of different manifestations of the vestibular lesion syndrome. (Otolaryngol Head Neck Surg 1998;119:27–33.)

scholarly journals Repeated neonatal isoflurane exposures in the mouse induce apoptotic degenerative changes in the brain and relatively mild long-term behavioral deficits

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Susan E. Maloney ◽  
Carla M. Yuede ◽  
Catherine E. Creeley ◽  
Sasha L. Williams ◽  
Jacob N. Huffman ◽  
...  
Keyword(s):  
Degenerative Changes ◽  
Behavioral Deficits ◽  
The Brain

Simulations of focused shear shock waves in soft solids and the brain

2014 ◽  
Vol 136 (4) ◽  
pp. 2279-2280
Author(s):  
Bruno Giammarinaro ◽  
François Coulouvrat ◽  
Gianmarco Pinton
Keyword(s):  
Shock Waves ◽  
Soft Solids ◽  
The Brain

scholarly journals Mitochondria-Targeted Antioxidants as Potential Therapy for the Treatment of Traumatic Brain Injury

Antioxidants ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 124 ◽  
Author(s):  
Elena V. Stelmashook ◽  
Nickolay K. Isaev ◽  
Elisaveta E. Genrikhs ◽  
Svetlana V. Novikova
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cortical Lesion ◽  
Lesion Volume ◽  
Negative Effects ◽  
Behavioral Deficits ◽  
Secondary Damage ◽  
Long Time ◽  
The Brain ◽  
Brain Water

The aim of this article is to review the publications describing the use of mitochondria-targeted antioxidant therapy after traumatic brain injury (TBI). Recent works demonstrated that mitochondria-targeted antioxidants are very effective in reducing the negative effects associated with the development of secondary damage caused by TBI. Using various animal models of TBI, mitochondria-targeted antioxidants were shown to prevent cardiolipin oxidation in the brain and neuronal death, as well as to markedly reduce behavioral deficits and cortical lesion volume, brain water content, and DNA damage. In the future, not only a more detailed study of the mechanisms of action of various types of such antioxidants needs to be conducted, but also their therapeutic values and toxicological properties are to be determined. Moreover, the optimal therapeutic effect needs to be achieved in the shortest time possible from the onset of damage to the nervous tissue, since secondary brain damage in humans can develop for a long time, days and even months, depending on the severity of the damage.

scholarly journals Sox3 Is Required for Gonadal Function, but Not Sex Determination, in Males and Females

2003 ◽  
Vol 23 (22) ◽  
pp. 8084-8091 ◽  
Author(s):  
Jeffrey Weiss ◽  
Joshua J. Meeks ◽  
Lisa Hurley ◽  
Gerald Raverot ◽  
Andrea Frassetto ◽  
...  
Keyword(s):  
Sex Determination ◽  
Targeted Mutagenesis ◽  
Seminiferous Tubules ◽  
Testis Weight ◽  
Behavioral Deficits ◽  
Hemizygous Male ◽  
Sperm Counts ◽  
Males And Females ◽  
The Brain ◽  
Cell Vacuolization

ABSTRACT Sox3 is expressed in developing gonads and in the brain. Evolutionary evidence suggests that the X-chromosomal Sox3 gene may be the ancestral precursor of Sry, a sex-determining gene, and Sox3 has been proposed to play a role in sex determination. However, patients with mutations in SOX3 exhibit normal gonadal determination but are mentally retarded and have short stature secondary to growth hormone (GH) deficiency. We used Cre-LoxP targeted mutagenesis to delete Sox3 from mice. Null mice of both sexes had no overt behavioral deficits and exhibited normal GH gene expression. Low body weight was observed for some mice; overgrowth and misalignment of the front teeth was observed consistently. Female Sox3 null mice (−/−) developed ovaries but had excess follicular atresia, ovulation of defective oocytes, and severely reduced fertility. Pituitary (luteinizing hormone and follicle-stimulating hormone) and uterine functions were normal in females. Hemizygous male null mice (−/Y) developed testes but were hypogonadal. Testis weight was reduced by 42%, and there was extensive Sertoli cell vacuolization, loss of germ cells, reduced sperm counts, and disruption of the seminiferous tubules. We conclude that Sox3 is not required for gonadal determination but is important for normal oocyte development and male testis differentiation and gametogenesis.

scholarly journals Chronic psychological stress and high-fat high-fructose diet disrupt metabolic and inflammatory gene networks in the brain, liver, and gut and promote behavioral deficits in mice

2017 ◽  
Vol 59 ◽  
pp. 158-172 ◽  
Author(s):  
Maria Elizabeth de Sousa Rodrigues ◽  
Mandakh Bekhbat ◽  
Madelyn C. Houser ◽  
Jianjun Chang ◽  
Douglas I. Walker ◽  
...  
Keyword(s):  
Psychological Stress ◽  
Gene Networks ◽  
High Fat ◽  
Behavioral Deficits ◽  
High Fructose Diet ◽  
Inflammatory Gene ◽  
High Fructose ◽  
The Brain

scholarly journals Reduction of cortical parvalbumin expressing GABAergic interneurons in a rodent hyperoxia model of preterm birth brain injury with deficits in social behavior and cognition

Development ◽  
2021 ◽  
Author(s):  
Till Scheuer ◽  
Elena auf dem Brinke ◽  
Sabine Grosser ◽  
Susanne A. Wolf ◽  
Daniele Mattei ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Psychiatric Symptoms ◽  
Autism Spectrum ◽  
Morphological Properties ◽  
Behavioral Deficits ◽  
Hyperactivity Disorder ◽  
Spectrum Disorders ◽  
The Brain ◽  
Psychiatric Problems ◽  
Behavior And Cognition

The inhibitory GABAergic system in the brain is involved in the etiology of various psychiatric problems, including autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and others. These disorders are influenced not only by genetic but also by environmental factors, such as preterm birth, although the mechanisms underlying are not known. In a translational hyperoxia model, exposing mice pups at age P5 to 80% oxygen for 48 hours to mimic a steep rise of oxygen exposure caused by preterm birth from in utero into room air, we documented a persistent reduction of cortical mature parvalbumin expressing interneurons until adulthood. Developmental delay of cortical myelin was observed together with decreased expression of oligodendroglial glial cell-derived neurotrophic factor (GDNF), a factor being involved in interneuronal development. Electrophysiological and morphological properties of remaining interneurons were unaffected. Behavioral deficits were observed for social interaction, learning, and attention. These results elucidate that neonatal oxidative stress can lead to decreased interneuron density and to psychiatric symptoms. The obtained cortical myelin deficit and decreased oligodendroglial GDNF expression indicate an impaired oligodendroglial-interneuronal interplay contributes to interneuronal damage.

scholarly journals A Delayed Presentation of Diffuse Axonal Injury

2021 ◽  
Author(s):  
Meaghan Wunder ◽  
Kara Ruicci
Keyword(s):  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Neurological Status ◽  
Axonal Damage ◽  
Delayed Presentation ◽  
Post Injury ◽  
Current Case ◽  
Lower Leg Fracture ◽  
The Brain ◽  
Leg Fracture

Diffuse axonal injury is one of the most common and debilitating pathologies resulting from mechanical deformation of the brain.  The current case involves a 19-year-old female involved in a high velocity ski crash. The accident resulted in a right lower leg fracture, with no loss of consciousness or evidence of head trauma.  Approximately 6.5 hours after her admission, the neurological status of the patient deteriorated markedly, and magnetic resonance imaging findings were consistent with diffuse axonal injury.  This presentation illustrates a case of delayed diffuse axonal injury, a phenomenon not commonly described.  Diffuse axonal injury involves rapid inertial forces causing strain to brain tissue.  This strain results in various stages of diffuse axonal damage and inflammation.  This article highlights a case of delayed onset diffuse axonal injury, describes the progression of neural sequelae post-injury resulting in axonal damage and explores proposed therapeutic targets. 

Axonal injury in the optic nerve: a model simulating diffuse axonal injury in the brain

1989 ◽  
Vol 71 (2) ◽  
pp. 244-253 ◽  
Author(s):  
T. A. Gennarelli ◽  
L. E. Thibault ◽  
R. Tipperman ◽  
G. Tomei ◽  
R. Sergot ◽  
...  
Keyword(s):  
Brain Injury ◽  
Optic Nerve ◽  
Axonal Injury ◽  
Diffuse Axonal Injury ◽  
Nerve Fibers ◽  
Axonal Damage ◽  
Electron Microscopic ◽  
Axonal Swelling ◽  
Content Type ◽  
The Brain

✓ A new model of traumatic axonal injury has been developed by causing a single, rapid, controlled elongation (tensile strain) in the optic nerve of the albino guinea pig. Electron microscopy demonstrates axonal swelling, axolemmal blebs, and accumulation of organelles identical to those seen in human and experimental brain injury. Quantitative morphometric studies confirm that 17% of the optic nerve axons are injured without vascular disruption, and horseradish peroxidase (HRP) studies confirm alterations in rapid axoplasmic transport at the sites of injury. Since 95% to 98% of the optic nerve fibers are crossed, studies of the cell bodies and terminal fields of injured axons can be performed in this model. Glucose utilization was increased in the retina following injury, confirming electron microscopic changes of central chromatolysis in the ganglion cells and increased metabolic activity in reaction to axonal injury. Decreased activity at the superior colliculus was demonstrated by delayed HRP arrival after injury. The model is unique because it produces axonal damage that is morphologically identical to that seen in human brain injury and does so by delivering tissue strains of the same type and magnitude that cause axonal damage in the human. The model offers the possibility of improving the understanding of traumatic damage of central nervous system (CNS) axons because it creates reproducible axonal injury in a well-defined anatomical system that obviates many of the difficulties associated with studying the complex morphology of the brain.

scholarly journals Insight from animal models of environmentally driven epigenetic changes in the developing and adult brain

2016 ◽  
Vol 28 (4pt2) ◽  
pp. 1229-1243 ◽  
Author(s):  
Tiffany S. Doherty ◽  
Tania L. Roth
Keyword(s):  
Central Nervous System ◽  
Animal Models ◽  
Behavioral Outcomes ◽  
Adult Brain ◽  
Epigenetic Changes ◽  
Behavioral Deficits ◽  
The Central Nervous System ◽  
Brain And Behavior ◽  
And Behavior ◽  
The Brain

AbstractThe efforts of many neuroscientists are directed toward understanding the appreciable plasticity of the brain and behavior. In recent years, epigenetics has become a core of this focus as a prime mechanistic candidate for behavioral modifications. Animal models have been instrumental in advancing our understanding of environmentally driven changes to the epigenome in the developing and adult brain. This review focuses mainly on such discoveries driven by adverse environments along with their associated behavioral outcomes. While much of the evidence discussed focuses on epigenetics within the central nervous system, several peripheral studies in humans who have experienced significant adversity are also highlighted. As we continue to unravel the link between epigenetics and phenotype, discerning the complexity and specificity of epigenetic changes induced by environments is an important step toward understanding optimal development and how to prevent or ameliorate behavioral deficits bred by disruptive environments.

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