Bryan Kolb

Publications (286) View all

• Article: Monte Carlo-based dose reconstruction in a rat model for scattered ionizing radiation investigations.

  Charles Kirkby, Esmaeel Ghasroddashti, Anna Kovalchuk, Bryan Kolb, Olga Kovalchuk
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  ABSTRACT: Abstract Purpose: In radiation biology, rats are often irradiated, but the precise dose distributions are often lacking, particularly in areas that receive scatter radiation. We used a non-dedicated set of resources to calculate detailed dose distributions, including doses to peripheral organs well outside of the primary field, in common rat exposure settings. Materials and Methods: We conducted a detailed dose reconstruction in a rat through an analog to the conventional human treatment planning process. The process consisted of: (i) characterizing source properties of an x-ray irradiator system, (ii) acquiring a computed tomography (CT) scan of a rat model, and (iii) using a Monte Carlo (MC) dose calculation engine to generate the dose distribution within the rat model. We considered cranial and liver irradiation scenarios where the rest of the body was protected by a lead shield. Organs of interest were the brain, liver and gonads. The study also included paired scenarios where the dose to adjacent, shielded rats was determined as a potential control for analysis of bystander effects. Results: We established the precise doses and dose distributions delivered to the peripheral organs in single and paired rats. Mean doses to non-targeted organs in irradiated rats ranged from 0.03 % - 0.1 % of the reference platform dose. Mean doses to the adjacent rat peripheral organs were consistent to within 10% those of the directly irradiated rat. Conclusions: This work provided details of dose distributions in rat models under common irradiation conditions and established an effective scenario for delivering only scattered radiation consistent with that in a directly irradiated rat.
  International Journal of Radiation Biology 04/2013; · 2.28 Impact Factor
• Source

  Available from: Monika Vinish

  Article: Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function

  Monika Vinish, Ahmed Elnabawi, Jean A. Milstein, Jesse S. Burke, Jonathan K. Kallevang, Kevin C. Turek, Carien S. Lansink, Istvan Merchenthaler, Aileen M. Bailey, Bryan Kolb, Joseph F. Cheer and Douglas O. Frost
  The International Journal of Neuropsychopharmacology 01/2013; · 4.58 Impact Factor
• Article: Olanzapine treatment of adolescent rats alters adult reward behaviour and nucleus accumbens function.

  Monika Vinish, Ahmed Elnabawi, Jean A Milstein, Jesse S Burke, Jonathan K Kallevang, Kevin C Turek, Carien S Lansink, Istvan Merchenthaler, Aileen M Bailey, Bryan Kolb, Joseph F Cheer, Douglas O Frost
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  ABSTRACT: Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug (APD) treatment. Most APDs are potent antagonists or partial agonists of dopamine (DA) D2 receptors; atypical APDs also have multiple serotonergic activities. DA and serotonin regulate many neurodevelopmental processes. Thus, early life APD treatment can, potentially, perturb these processes, causing long-term behavioural and neurobiological sequelae. We treated adolescent, male rats with olanzapine (Ola) on post-natal days 28-49, under dosing conditions that approximate those employed therapeutically in humans. As adults, they exhibited enhanced conditioned place preference for amphetamine, as compared to vehicle-treated rats. In the nucleus accumbens core, DA D1 receptor binding was reduced, D2 binding was increased and DA release evoked by electrical stimulation of the ventral tegmental area was reduced. Thus, adolescent Ola treatment enduringly alters a key behavioural response to rewarding stimuli and modifies DAergic neurotransmission in the nucleus accumbens. The persistence of these changes suggests that even limited periods of early life Ola treatment may induce enduring changes in other reward-related behaviours and in behavioural and neurobiological responses to therapeutic and illicit psychotropic drugs. These results underscore the importance of improved understanding of the enduring sequelae of paediatric APD treatment as a basis for weighing the benefits and risks of adolescent APD therapy, especially prophylactic treatment in high-risk, asymptomatic patients.
  The International Journal of Neuropsychopharmacology 01/2013; · 4.58 Impact Factor
• Article: Olanzapine treatment of adolescent rats causes enduring specific memory impairments and alters cortical development and function.

  Jean A Milstein, Ahmed Elnabawi, Monika Vinish, Thomas Swanson, Jennifer K Enos, Aileen M Bailey, Bryan Kolb, Douglas O Frost
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  ABSTRACT: Antipsychotic drugs are increasingly used in children and adolescents to treat a variety of psychiatric disorders. However, little is known about the long-term effects of early life antipsychotic drug treatment. Most antipsychotic drugs are potent antagonists or partial agonists of dopamine D2 receptors; atypical antipsychotic drugs also antagonize type 2A serotonin receptors. Dopamine and serotonin regulate many neurodevelopmental processes. Thus, early life antipsychotic drug treatment can, potentially, perturb these processes, causing long-term behavioral- and neurobiological impairments. Here, we treated adolescent, male rats with olanzapine on post-natal days 28-49. As adults, they exhibited impaired working memory, but normal spatial memory, as compared to vehicle-treated control rats. They also showed a deficit in extinction of fear conditioning. Measures of motor activity and skill, habituation to an open field, and affect were normal. In the orbital- and medial prefrontal cortices, parietal cortex, nucleus accumbens core and dentate gyrus, adolescent olanzapine treatment altered the developmental dynamics and mature values of dendritic spine density in a region-specific manner. Measures of motor activity and skill, habituation to an open field, and affect were normal. In the orbital- and medial prefrontal cortices, D1 binding was reduced and binding of GABA(A) receptors with open Cl(-) channels was increased. In medial prefrontal cortex, D2 binding was also increased. The persistence of these changes underscores the importance of improved understanding of the enduring sequelae of pediatric APD treatment as a basis for weighing the benefits and risks of adolescent antipsychotic drug therapy, especially prophylactic treatment in high risk, asymptomatic patients. The long-term changes in neurotransmitter receptor binding and neural circuitry induced by adolescent APD treatment may also cause enduring changes in behavioral- and neurobiological responses to other therapeutic- or illicit psychotropic drugs.
  PLoS ONE 01/2013; 8(2):e57308. · 4.09 Impact Factor
• Source

  Available from: Robbin Gibb

  Article: Principles of neuroplasticity and behavior.

  Bryan Kolb, Robbin Gibb
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  ABSTRACT: Behavioral neuroscience spent much of the twentieth century seeking the fundamental rules of cerebral organization. One underlying assumption of much of that work was that there is constancy in cerebral organization and function, both between and within mammalian species (e.g., Kaas, 2006). One unexpected principle to emerge, however, was that although there is much constancy in cerebral functioning, there is remarkable variability as well. This variability reflects the brain's capacity to alter its structure and function in reaction to environmental diversity, thus reflecting a capacity that is often referred to as brain plasticity. Although this term is now commonly used in psychology and neuroscience, it is not easily defined and is used to refer to changes at many levels in the nervous system ranging from molecular events, such as changes in gene expression, to behavior (e.g., Shaw & McEachem, 2001). The relationship between molecular or cellular changes and behavior is by no means clear and is plagued by the problems inherent in inferring causation from correlation. Nonetheless, we believe that it is possible to identify some general principles of brain plasticity and behavior. As we do so we will attempt to link these principles to potential clinical implications. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
  10/2012;