UCLA Neuroscience Program Ph.D. Admissions Neuroscience Faculty UCLA and Beyond  



Christopher Giza
Developmental Traumatic Brain Injury and Neuroplasticity

Work: http://neurosurgery.ucla.edu/Faculty/Giza/Faculty_Giza.html

Mailing Address:
Division of Neurosurgery
Office Address:
Division of Pediatric Neurology
Phone Numbers:
310-206-3480 Research only
310-825-6196 Clinical (Patient-related)

Selected Publications:

Giza CC, Prins ML Is being plastic fantastic? Mechanisms of impaired plasticity following developmental traumatic brain injury. Developmental Neuroscience 2006; 28(4-5): 364-379.
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Prins ML, Giza CC Induction of monocarboxylate transporter-2 expression and ketone transport following traumatic brain injury in juvenile and adult rats. Developmental Neuroscience 2006; 28(4-5): 447-56.
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Giza CC, Santa Maria NS, and Hovda DA. N-methyl-D-aspartate receptor subunit changes following traumatic injury to the developing brain. Journal of Neurotrauma 2006; 23(6): 950-61.
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Gurkoff GG, Giza CC and Hovda DA. Lateral fluid percussion injury in the developing rat causes an acute, mild behavioral dysfunction in the absence of significant cell death. Brain Research 2006; 1077(1): 24-36.
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Giza, CC. Better Never Than Late: Lasting Effects of Pediatric Traumatic Brain Injury. Indian Journal of Neurotrauma 2006; 3(1): 19-26.
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Madikians A and Giza CC. A Clinician's Guide to the Pathophysiology of Traumatic Brain Injury. Indian Journal of Neurotrauma 2006; 3(1): 9-17.
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Giza CC, Griesbach GS and Hovda DA. Experience-Dependent Behavioral Plasticity is Disturbed Following Traumatic Injury to the Immature Brain.. Behavioral Brain Research 2005; 157(1): 11-22.
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Bhidayashiri R, Waters M and Giza CC. Neurological Differential Diagnosis: A Prioritized Approach. 2005; .
Bhidayasiri R and Giza CC. Images in Pediatric Neurosurgery - Subdural hematoma and retinal hemorrhages in an infant: accidental or non-accidental injury?. Pediatric Neurosurgery 2004; 40(3): 147-8.
Osteen CL, Giza CC and Hovda DA. Injury-induced alterations in NMDA receptor subunit composition contribute to prolonged 45calcium accumulation following lateral fluid percussion.. Neuroscience 2004; 128(2): 305-322.
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Zanier ER, Lee SM, Vespa P, Giza CC and Hovda DA. Increased hippocampal CA3 vulnerability to low level glutamate analogue following lateral fluid percussion injury.. Journal of Neurotrauma 2003; 20(5): 409-420.
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Ip EY, Giza CC, Griesbach G and Hovda DA. Effects of enriched environment and fluid percussion injury on dendritic arborization within the cerebral cortex of the developing rat.. Journal of Neurotrauma 2002; 19(5): 573-85.
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Giza CC, Prins ML, Hovda DA, Herschman HR and Feldman JD. Genes preferentially induced by depolarization after concussive brain injury: Effects of age and injury severity.. Journal of Neurotrauma 2002; 19(4): 387-402.
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Donnelly TJ and Giza CC. Differential Diagnosis Mnemonics. 2001; .
Giza CC and Hovda DA. The Neurometabolic Cascade of Concussion.. Journal of Athletic Training 2001; 36(3): 228-235.
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Fineman I, Giza CC, Nahed B, Lee SM and Hovda DA. Inhibition of neocortical plasticity during development by moderate concussive brain injury.. Journal of Neurotrauma 2000; 17(9): 739-49.
Rabizadeh S, Ye X, Wang JJL, Sperandio S, Wang, JJL, Ellerby HM, Ellerby LM, Giza CC, Andrusiak RL, Frankowski H, Yaron Y, Moayeri NN, Rovelli G, Evans CJ, Butcher LL, Nolan GP, Assa-Munt N, and Bredesen DE. Neurotrophin dependence domain: A domain required for the mediation of apoptosis by the p75 neurotrophin receptor. Journal of Molecular Neuroscience 2000; 15: 215-229.
Research Interest:

Areas of research interest and active investigation include developmental TBI and its pathophysiology. Ongoing studies include those examining impaired neurotransmission, altered developmental plasticity, acute alterations in metabolism, morphological injury, vulnerability to secondary insults and behavioral impairments. Basic research into post-traumatic brain activation, molecular signaling and experience-dependent plasticity are fundamental parts of the laboratory program. We are currently investigating the response of molecular signaling molecules after developmental TBI, and how post-injury environment may modulate the molecular and neuroplastic potential of the immature brain. Specifically, there appears to be an impairment of excitatory neurotransmission and activity-dependent neurotrophin expression that represent mechanisms underlying the injury-induced impairment of brain plasticity. Another basic research area spans the terrain between acute neuronal injury and delayed plasticity. Using induction of post-traumatic seizures as a secondary injury, we are studying the vulnerability of the injured immature brain. By conducting long-term behavioral, electrophysiological and morphological assessments of these subjects, we also gain insight into aberrant neuronal sprouting and epileptogenesis following TBI. In addition to the basic science approach to the problem of pediatric TBI, the group is currently engaged in establishing a translational/clinical program. This will be designed to capture physiological monitoring and imaging data from the acute hospitalization, with standardized outpatient clinic followup. One area of clinical investigation already underway is the study of neuropsychological function, anatomical imaging, functional brain mapping and white matter tract morphology across time in normal developing control children and in children recovering following moderate to severe TBI. A second clinical area under development will be the correlation of acute physiological variables (such as intracranial pressure, cerebral perfusion, magnetic resonance spectroscopy, acute white matter lesions, and early secondary insults) with neurological and behavioral outcomes. One important goal of the group is to translate research findings between laboratory and clinical arenas to gain better mechanistic insight into the physiological distinctions of pediatric TBI, and to better understand and to eventually facilitate how the developing brain recovers from TBI.