神经生物学

Spinal cord trauma causes acute hemorrhage and ischemia, which in turn initiate a cascade of secondary events resulting in cell death and loss of neural tissue at the site of impact. In contusion or compression injuries, the ensuing tissue damage can extend several segments rostral and caudal to ...

Spinal cord injury (SCI), by name alone, infers damage to structural elements of the spinal cord. The spinal white matter, composed of ascending (sensory) and descending (motor and autonomic) axonal tracts, and gray matter, which encompasses columns of neural cell bodies and glial cells, can be ...

This chapter introduces the chapters of Part VIII, which describe a variety of assessment methods to determine the outcomes after spinal cord injury (SCI) in animal models. The SCI community should be encouraged by the view that SCI has certain advantages for translation of therapies in humans ...

Motor function is a common deficit in patients who have experienced a traumatic brain injury (TBI). These deficits include difficulties with balance, increased dizziness, reductions in strength, and fine motor difficulties. Clinically relevant rodent models of TBI have utilized co ...

Assessment of neurologic deficit following traumatic brain injury (TBI) is integral to effective evaluation of injury severity, course, and recovery. Paradigms that involve training regimens can be difficult to employ and may not be feasible for short survival time points or simple mon ...

Free radical-induced oxidative damage to proteins and lipids is one of the most convincingly validated secondary injury mechanisms following traumatic brain injury or spinal cord injury. In particular, central nervous system (CNS) tissue is exquisitely sensitive to the process of l ...

The mechanical forces imparted on brain tissue during trauma trigger changes in proteins, membranes, DNA, and mRNA expression patterns of many different cell types, such as neurons, astrocytes, microglia, and oligodendrocytes. Biochemical and molecular biological assessments ...

This chapter briefly reviews electrophysiological applications in experimental models of traumatic brain injury (TBI). The review was restricted to studies where rodents were used in one of the more common in vivo models of TBI and where electrophysiological recordings were then con ...

Traumatic brain injury (TBI) is the leading cause of death in children and young adults. It is particularly worth noting that an estimated 7,500 soldiers have suffered TBI caused by improvised explosive device explosions in the Iraq war. TBI represents a significant socioeconomic burden. T ...

Traumatic brain and spinal cord injury manifests following structural compromise of the tissue, including neurons and their axons, glial cells, blood vessels and extracellular components, and subsequent secondary injury cascades. The degree of primary injury depends on the cell ...

Today’s cerebral vascular physiologists have a variety of techniques available to measure cerebral blood flow (CBF) and assess cerebral vascular reactivity. CBF measurement techniques can be grouped based on anatomical considerations (e.g., local, regional, global), number of me ...

This chapter reviews documented methods for tracking morphological damage across the neurovascular unit following experimental models of focal or diffuse traumatic brain injury. Sections within this chapter focus on the chronology of morphological change in specific compo ...

Traumatic brain injury (TBI) is a complex disease, altering numerous intracellular cascades which affect neuronal, vascular, and glial elements of the brain. Structural damage is coupled with cellular- and systems-level functional impairment. The array of assessments used in stat ...

Persistent neurogenesis occurs in discrete regions of the brain through neonatal to adult period, including the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) (J Comp Neurol 124:319–335, 1969) and the subventricular zone of the lateral ventricle (J Comp Neurol 137:433–458, 1 ...

Neurobehavioral assessment plays an important role in both adult and neonatal models of cerebral hypoxia–ischemia (NHI), since the final goal of such basic research is to identify new information leading towards novel approaches in human medical treatment. In animal NHI model, behavi ...

Neonatal hypoxic-ischemic (H-I) brain injury is a leading cause of perinatal mortality. Inflammation contributes substantially to the pathogenesis of perinatal H-I brain injury. The inflammatory response in neonatal H-I model could be assessed by measuring the expression of infl ...

Neonatal hypoxia–ischemia (HI) induces a series of intracellular signaling events, including destructive and protective mechanisms. The destructive events include neuronal membrane depolarization, excitotoxicity, free radical injury, overactivation of calcium- ...

Damages to the blood–brain barrier (BBB) and white matter (WM)/oligodendrocytes (OLs) are typical pathological findings in infants or animal models of neonatal hypoxia–ischemia (NHI). These injuries in turn produce severe neurological consequences, such as germinal matrix hem ...

Cell death in the immature brain can be studied in many ways using morphological and biochemical markers. Essential requirements for cell death and degeneration assessment techniques in the brain include sufficient sensitivity and the ability to differentiate between apoptotic ...

Focal cerebral ischemia is the commonest type of human strokes. Several animal models of focal brain ischemia have been developed to resemble human strokes closely. Infarct volume is an essential indicator of how severe the ischemic damage is 2,3,5-triphenyltetrazolium chloride (TTC) ...