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Profile Detail

John Johnson

Associate Professor
Education

  • Postdoctoral Fellowship - Integrative Physiology Department and the Center for Neurosciences, University of Colorado at Boulder, 2002-05
  • PhD, Neuroscience, University of Colorado at Boulder, 2002
  • MA, Psychology, University of Colorado at Boulder, 1999
  • BS, Zoology, Michigan State University, 1995
Courses Taught

  • Advanced Human Physiology
  • Introduction to Neuroscience
Research Interests

yinyangI have broad interests in understanding the interactions between the nervous and immune systems, particularly with respect to alterations in behavior. It has only recently been appreciated that the nervous system and immune system communicate and influence one another. It is now recognized that products (e.g. cytokines) released by immune cells alter brain-mediated responses (e.g. behavioral, hormonal, and cognitive processes). For example, in response to foreign microorganisms cytokines are released by immune cells and stimulate brain-mediated physiological and behavioral responses, which are commonly referred to as sickness responses (e.g. fever, decreasing appetite, increasing sleep, amplifying pain, altering hormone levels, and impairing cognitive processes). 

Brain cytokine levels also increase when an organism is exposed to stressful events, during normal aging and during neurodegenerative diseases. It has been proposed that elevated brain cytokines may mediate some of the behavioral, cognitive, and emotional changes that are associated with these times. My laboratory is interested in understanding the regulation of brain cytokines, what role brain cytokines play in mediated various physiological/behavioral responses, and how the regulations/production of brain cytokines change with repeated stressor exposure.

Recent Abstracts

An Animal Model of Recurrent Depression: Sensitized Depression-like Behavior When Rats Re-exposed to Chronic Mild Stress

Jennifer Remus, Destiny Jamison, and John Johnson; Biological Sciences, Kent State University Kent, OH 44242

 

            Major depression is a debilitating disorder, characterized by feelings of worthlessness, persistent sadness and lack of motivation. Depression is also recognized to be a chronic, recurrent disorder with each episode of depression increasing the likelihood of another occurrence. The current study aimed to develop an animal model of recurrent depression in order to examine possible biological mechanisms responsible for this increased susceptibility. We hypothesized that animals with a prior depressive episode would be sensitized to future stressors, causing the animals to display depressive-like behaviors more rapidly or to a greater extent. Fisher rats (n=15) were exposed to chronic mild stress for 35 days or remained in their home cage as control animals during which animals showed a slow decrease in sucrose consumption. Following the 35 days, animals went through a 20 day recovery phase where no stressors were present and animal showed a steady increase in sucrose consumption back to baseline levels. At this time animals were re-exposed to chronic mild stress for 15 days. A rapid decline in sucrose consumption was observed. Linear regression lines were calculated for each animal’s sucrose consumption during the first and second stressor exposure and a paired t-test of the slope of each line revealed re-exposure to stress resulted in a significantly more rapid decline in sucrose consumption compared to that observed during the initial stressor exposure.

 

Repeated Stressor Exposure Regionally Sensitizes b-Adrenoceptor-Mediated Induction of Brain IL-1

Kristin Gabella, Veronica M. Porterfield, John D. Johnson

 

Chronic or repeated stressor exposure is associated with elevated brain cytokines, which are linked to poor health consequences including metabolic syndrome, heart disease, neurodegenerative conditions, cognitive decline, and depression.  During non-pathogenic times the production of brain cytokines, particularly IL-1, is largely mediated by beta-adrenergic receptors (b-ADRs).  Here, we tested the hypothesis that changes in b-ADR signaling following repeated stressor exposure favors increased brain cytokine production.  Fischer rats were exposed to repeated mild stressors or remained in their home cage.  Twenty-four hours after the last stressor animals were injected centrally with either saline or 10ug (1ug/ml) isoproterenol, a b-ADR agonist, via intra-cistera magna injections.  As previously demonstrated, isoproterenol stimulated widespread IL-1 protein production 2h later in control animals.  Interestingly, animals repeatedly exposed to stressors had similar basal cytokine levels but significantly greater IL-1 production in the hypothalamus and amygdala compared to controls, while levels were equal to controls in the hippocampus, prefrontal cortex, and brainstem.  These data demonstrate repeated stressor exposure cause regional changes in b-ADR signaling that favors greater brain cytokine production.  This is particularly interesting because to date only widespread priming of cytokine production to immunological stimuli has been reported following stressor exposure. These data indicate stressor exposure also primes cytokine production to stimuli that are not immunogens and this likely involves a different underlying mechanism to result in regional brain changes.

Recent Publications

Johnson, J.D., Zimomra, Z.R., Stewart, L.T.  Beta-Adrenergic Receptor Activation Primes Microglia Cytokine Production.  Journal of Neuroimmunology (2013) 254:161-164.

 

Porterfield, V.M., Gabella, K.M., Simmons, M.A., Johnson, J.D.  Repeated Stressor Exposure Regionally Enhances Beta-Adrenergic Receptor Mediated Brain IL-1b Production.

Brain, Behavior, and Immunity (2012) 26:1249-1255.

 

Campisi, J., Sharkey, C., Johnson, J.D., Asea, A.A., Maslanik, T., Bernstein-Hanley, I., Fleshner, M.  Stress-induced facilitation of host response to bacterial challenge is dependent on extracellular Hsp72 and independent of alpha beta T cells.  Stress (2012) 15(6):637-646

 

Camp, R.M., Remus, J.L., Kalburgi, S.N.,Porterfield, V.M.,Johnson, J.D. Fear Conditioning Can Contribute to Behavioral Changes Observed in a Repeated Stress Model  Behavioural Brain Research (2012) 233(2):536-544.

 

Zimomra, Z.R., Porterfield, V.M., Camp, R., Johnson, J.D. Time-Dependent Mediators of HPA Activation Following Peripheral E.coli Am.J.Physiol Regul Integr Comp Physiol (2011) Dec;301(6):R1648-57.

 

            Hains, L.E., Loram, L.C., Taylor, F., Strand, K., Weiseler, J.L., Barrientos, R., Young, J.J., Frank, M.G., Sobesky, J., Martin, T.J., Eisenach, J.C., Maier, S.F., Johnson, J.D., Fleshner, M., Watkins, L.R.  Immune Priming with prior Laparotomy or Corticosterone Potentiates Lipopolysaccharide-induced Fever and Sickness Behaviors.   Journal of Neuroimmunology (2011) Oct 28;239(1-2):53:60.

           

Porterfield, V.M., Zimomra, Z.R., Caldwell, E., Camp, R.M., Johnson, J.D.  Strain Differences in Restraint Stress Induced Brain Cytokines.   Neuroscience (2011) 188:48-54.

 

Fleshner, M., Kennedy, S.L., Johnson, J.D., Day, H.E.W., Greenwood, B.N.  Exercise and Stress Resistance: Neural-Immune Mechanisms.  The Neuroimmunological Basis of Behavior and Mental Disorders, (2009) Editors: Allan Siegel and Steven S. Zalcman

 

Johnson, J.D., Cortez, V., Kennedy, S.L., Foley, T.E., Hanson, H, Fleshner, M.  Role of Central b-Adrenergic Receptors in Regulating Proinflammatory Cytokine Responses to a Peripheral Bacterial Challenge.   Brain, Behavior, and Immunity (2008) 22:1078-1086.


Recent Grants

National Institute of Mental Health      

“Regulation of Brain IL-1 & Sickness Responses Following E.coli Challenge”

1/1/07 - 5/31/10

 

Ohio Board of Regents Research Incentive Program

“Development of an Interdisciplinary Translational Research Model to Study Depression in Laboratory Animals and Human Subjects”

6/15/09 – 6/14/11

 

Defense Advanced Research Projects Agency (DARPA)

“Targeting Stress Resilience Without Detriment to Adaptive Stress Response”

5/28/10-5/27/13
Scholarly, Creative & Professional Activities
Research Areas
  • Neuroimmune Interactions
  • Regulation of Brain Cytokines
  • Physiological & Pathological Consequences of Elevated Brain Cytokines
  • Stress, Immune, and Behavior
John Johnson
OFFICE
Department of Biological Sciences
CONTACT INFO
Phone: 330-672-3849
jjohns72@kent.edu
COURSES TEACHING
Spring 2014
  • BSCI 40195 - 017 St : Advanced Human Psysiology
  • BSCI 40196 - 015 Individual Investigation
  • BSCI 40600 - 016 Writing In Biological Sciences
  • BSCI 50195 - 018 St : Advanced Human Physiology
  • BMS 60791 - 003 Seminar In Neurobiology
  • BSCI 70195 - 018 St : Advanced Human Physiology
  • BMS 80199 - 005 Dissertation I
  • BSCI 80299 - 008 Dissertation Ii
Summer 2014
  • BMS 80299 - 018 Dissertation Ii
Fall 2014
  • BSCI 30520 - 001 Introduction To Neuroscience
  • BSCI 40600 - 004 Writing In Biological Sciences
  • BMS 60791 - 001 Sem : Research Methods In Neuro
  • BMS 70791 - 001 Sem : Research Methods
EXPERTISE