Pediatric Neurologist
2 years of experience

Accepting new patients
Southeast Pasadena
14445 Olive View Dr
Sylmar, CA 91342
818-364-3233
Locations and availability (1)

Education ?

Medical School Score
Saint Louis University (2008) *
  • Currently 2 of 4 apples
Residency
UCLA Medical Center (2011) *
Fellowship
University of California - Ronald Reagan UCLA Medical Center *
Neurology with Special Qualifications in Child Neurology
* This information was reported to Vitals by the doctor or doctor's office.

Affiliations ?

Dr. Hartonian is affiliated with 1 hospitals.

Hospital Affilations

  • University of California - Ronald Reagan UCLA Medical Center *
  • Publications & Research

    Dr. Hartonian has contributed to 3 publications.
    Title Compensatory Changes in Cortical Cholinergic Innervation in the Rat Following an Immunotoxic Lesion.
    Date January 2006
    Journal Restorative Neurology and Neuroscience
    Excerpt

    PURPOSE: To investigate the plastic capacity of the cholinergic system in a partial animal model of Alzheimer's disease. METHODS: Rats received unilateral lesions of the horizontal diagonal band of Broca (HDB) using a cholinergic-specific toxin, 192 IgG-saporin. After the appropriate survival time (2, 4, 8, 12 and 24 weeks post-lesion) rats were sacrificed and the brains were prepared for histology. Immunocytochemical and morphometric techniques were employed to quantify the cholinergic neurons surviving the lesion and to measure the density of cortical cholinergic fibers. RESULTS: Cell counts revealed on average a 60% reduction in cholinergic neurons on the lesioned side, compared to the spared side. This cell loss was permanent, that is, there was no significant change in the amount of cell loss over time. In correlation with this cell loss, cholinergic fibers in the target area, the entorhinal cortex (EC), were also reduced such that the density of acetylcholinesterase (AChE)-stained fibers on the lesioned side was 44% of the spared side. The density of cholinergic fibers in the EC increased significantly between 2 and 12 weeks post-lesion (p=0.0216) but remained stable at that level by 24 weeks after the lesion. CONCLUSIONS: Following a cholinergic-specific lesion, a compensatory mechanism is activated in the basal forebrain cholinergic system, such that surviving neurons, projecting to the same target, extend their terminals to occupy the denervated area. It remains to be investigated whether these sprouts are able to establish proper synaptic connections and make a functional recovery in this particular system.

    Title Long-term Plastic Changes in Galanin Innervation in the Rat Basal Forebrain.
    Date April 2003
    Journal Neuroscience
    Excerpt

    Galanin immunoreactive fibers hyperinnervate remaining cholinergic basal forebrain neurons in Alzheimer's disease, perhaps exacerbating the cholinergic deficit. The purpose of our study is to determine whether a similar phenomenon occurs following intraparenchymal injection of 192 IgG-saporin, a specific cholinergic neurotoxin, within the nucleus of the horizontal limb of the diagonal band of Broca. Immunotoxic lesion produced on average a 31% reduction in cholinergic cell counts ipsilateral to the lesion, compared to the contralateral side. Increased galanin immunoreactivity, suggestive of increased fiber density, was observed within and adjacent to the lesion in 28 out of 36 rats, and this effect persisted across time up to 6 months (the longest time examined). We observed a parallel increase in the number of galanin positive neurons ipsilateral to the lesion, compared to the contralateral side. No correlative change could be detected in the number of galaninergic neurons in the amygdala or the bed nucleus of the stria terminalis. There was no statistically significant correlation between the extent of cholinergic cell loss and the increase in galanin immunoreactivity surrounding the lesion. Yet, since both of these changes persist over time, we suggest that galanin plasticity is triggered by neuronal damage. Our model can be useful to test the role that galanin plays in the regulation of acetylcholine and the efficacy of galanin inhibitors as potential therapeutic interventions in Alzheimer's disease.

    Title Molecular and Physiological Responses to Juvenile Traumatic Brain Injury: Focus on Growth and Metabolism.
    Date
    Journal Developmental Neuroscience
    Excerpt

    Traumatic brain injury (TBI), one of the most frequent causes of neurologic and neurobehavioral morbidity in the pediatric population, can result in lifelong challenges not only for patients, but also for their families. Survivors of a brain injury experienced during childhood - when the brain is undergoing a period of rapid development - frequently experience unique challenges as the consequences of their injuries are overlaid on normal developmental changes. Experimental studies have significantly advanced our understanding of the mechanisms and underlying molecular underpinnings of the injury response and recovery process following a TBI in the developing brain. In this paper, normal and TBI-related alterations in growth, development and metabolism are comprehensively reviewed in the postweanling/juvenile age range in the rat (postnatal days 21-60). As part of this review, TBI-related changes in gene expression are presented, with a focus on the injury-induced alterations related to cerebral growth and metabolism, and discussed in the context of existing literature related to physiological and behavioral responses to experimental TBI. Increasing evidence from the existing literature and from our own gene microarray data indicates that molecular responses related to growth, development and metabolism may play a particularly important role in the injury response and the recovery trajectory following developmental TBI. While gene expression analysis shows many of these changes occur at the level of transcription, a comprehensive review of other studies suggests that the control of metabolic substrates may preferentially be regulated through changes in transporters and enzymatic activity. The interrelation between cellular metabolism and activity-dependent neuroplasticity shows great promise as an area for future study for an optimal translation of experimental data to clinical TBI, with the ultimate goal of guiding therapeutic interventions.


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