This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Antipyschotic medications are widely used for their FDA approved indications including schizophrenia and bipolar disorder. In addition, they are also used for other psychiatric disorders as augmenting agents. Antipsychotics are typically classified as typical or older agents like haloperidol, and atypical or newer agents like clozapine. There is ongoing scientific debate concerning the use of typical versus atypical agents regarding the benefits, side effects and their cost effectiveness, since atypical antipsychotics are more expensive. The efficacy of these medications is considered to be equivalent for the positive symptoms of schizophrenia. Atypical agents have better efficacy on the negative symptoms of schizophrenia. More importantly, the recent studies have shifted the focus of antipsychotic agents from its efficacy to its side effect burden on lipid and glucose metabolism. To our knowledge, there is no systematic study comparing the impact of all atypical agents on genomic expression profile in nervous or non-nervous tissues. While many other studies have approached the pharmacological genomic effects of these agents in the nervous system, there is a paucity of information addressing the genomics of metabolic effects of these agents in non-nervous tissues. Since the serum glucose and lipid levels are modulated by various peripheral tissues, it would be appropriate to study the effects of these agents on liver, skeletal and adipose tissues.

Agency
National Institute of Health (NIH)
Institute
National Center for Research Resources (NCRR)
Type
Exploratory Grants (P20)
Project #
5P20RR015567-07
Application #
7381113
Study Section
Special Emphasis Panel (ZRR1-RI-8 (02))
Project Start
2006-06-01
Project End
2007-05-31
Budget Start
2006-06-01
Budget End
2007-05-31
Support Year
7
Fiscal Year
2006
Total Cost
$16,798
Indirect Cost
Name
University of South Dakota
Department
Neurosciences
Type
Schools of Medicine
DUNS #
929930808
City
Vermillion
State
SD
Country
United States
Zip Code
57069
Burrell, Brian D (2017) Comparative biology of pain: What invertebrates can tell us about how nociception works. J Neurophysiol 117:1461-1473
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Smith, Justin P; Prince, Melissa A; Achua, Justin K et al. (2016) Intensity of anxiety is modified via complex integrative stress circuitries. Psychoneuroendocrinology 63:351-61
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Hahn, Elizabeth; Burrell, Brian (2015) Pentylenetetrazol-induced seizure-like behavior and neural hyperactivity in the medicinal leech. Invert Neurosci 15:177
Novick, Andrew M; Forster, Gina L; Hassell, James E et al. (2015) Increased dopamine transporter function as a mechanism for dopamine hypoactivity in the adult infralimbic medial prefrontal cortex following adolescent social stress. Neuropharmacology 97:194-200
Ranek, Mark J; Kost Jr, Curtis K; Hu, Chengjun et al. (2014) Muscarinic 2 receptors modulate cardiac proteasome function in a protein kinase G-dependent manner. J Mol Cell Cardiol 69:43-51
Watt, Michael J; Roberts, Christina L; Scholl, Jamie L et al. (2014) Decreased prefrontal cortex dopamine activity following adolescent social defeat in male rats: role of dopamine D2 receptors. Psychopharmacology (Berl) 231:1627-36

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