scholarly journals A novel role for dopamine signaling in the pathogenesis of bone loss from the atypical antipsychotic drug risperidone in female mice

Bone ◽  
2017 ◽  
Vol 103 ◽  
pp. 168-176 ◽  
Author(s):  
Katherine J. Motyl ◽  
Megan Beauchemin ◽  
Deborah Barlow ◽  
Phuong T. Le ◽  
Kenichi Nagano ◽  
...  
Keyword(s):  
Bone Loss ◽  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Atypical Antipsychotic Drug ◽  
Female Mice ◽  
Dopamine Signaling

scholarly journals Housing temperature influences atypical antipsychotic drug‐induced bone loss in female C57BL / 6J mice

JBMR Plus ◽  
2021 ◽  
Author(s):  
Roni F. Kunst ◽  
Audrie L. Langlais ◽  
Deborah Barlow ◽  
Karen L. Houseknecht ◽  
Katherine J. Motyl
Keyword(s):  
Bone Loss ◽  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Atypical Antipsychotic Drug ◽  
Drug Induced ◽  
Housing Temperature

ICI 204,636: A new and novel atypical antipsychotic drug

1990 ◽  
Vol 3 (1) ◽  
pp. 46
Author(s):  
J.B. Malick ◽  
B.M. Migler ◽  
A.I. Salama ◽  
J.M. Goldstein ◽  
C.F. Saller ◽  
...  
Keyword(s):  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Atypical Antipsychotic Drug ◽  
Ici 204,636

The atypical antipsychotic drug clozapine enhances chronic PCP-induced regulation of prefrontal cortex 5-HT2A receptors

2004 ◽  
Vol 47 (4) ◽  
pp. 527-537 ◽  
Author(s):  
Lucinda J. Steward ◽  
Matthew D. Kennedy ◽  
Brian J. Morris ◽  
Judith A. Pratt
Keyword(s):  
Prefrontal Cortex ◽  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Atypical Antipsychotic Drug

Psychopharmacology of olanzapine

1999 ◽  
Vol 174 (S38) ◽  
pp. 52-58 ◽  
Author(s):  
C. M. E. Stephenson ◽  
L. S. Pilowsky
Keyword(s):  
Side Effects ◽  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Therapeutic Efficacy ◽  
Atypical Antipsychotics ◽  
Extrapyramidal Side Effects ◽  
Atypical Antipsychotic Drug ◽  
Blood Monitoring

The development of atypical antipsychotics has revolutionised the treatment of schizophrenia, as well as providing new insights into its cause. The archetypal atypical antipsychotic is clozapine, which has therapeutic advantages over traditional antipsychotics, as well as a low potential for producing extrapyramidal side-effects (EPS) (Kane et al, 1988). However, clozapine causes agranulocytosis in 1% of patients, and there has consequently been a search for novel atypical antipsychotics, as efficacious as clozapine, but without the need for intensive blood monitoring. There has been much discussion of the definition and characteristics of an atypical antipsychotic drug, and an operational understanding seems to have been agreed upon, that atypical drugs have therapeutic efficacy in treating schizophrenia, without producing EPS (Deutch et al, 1991; Kerwin, 1994).

scholarly journals Atypical Antipsychotic Drug Olanzapine Deregulates Hepatic Lipid Metabolism and Aortic Inflammation and Aggravates Atherosclerosis

2018 ◽  
Vol 50 (4) ◽  
pp. 1216-1229 ◽  
Author(s):  
Chia-Hui Chen ◽  
Song-Kun Shyue ◽  
Chiao-Po Hsu ◽  
Tzong-Shyuan Lee
Keyword(s):  
Fatty Acids ◽  
Lipid Metabolism ◽  
Atypical Antipsychotic ◽  
Antipsychotic Drug ◽  
Free Cholesterol ◽  
Hepatic Lipid Metabolism ◽  
Atypical Antipsychotic Drug ◽  
In Vivo Models ◽  
Hepatic Lipid ◽  
Related Proteins

Background/Aims: Olanzapine, an atypical antipsychotic drug, has therapeutic effects for schizophrenia. However, clinical reports indicate that patients taking atypical antipsychotic drugs are at high risk of metabolic syndrome with unclear mechanisms. We investigated the effect of olanzapine on atherosclerosis and the mechanisms in apolipoprotein E-null (apoE-/-) mice. Methods: ApoE-/- mice were used as in vivo models. Western blot analysis was used to evaluate protein expression. Conventional assay kits were applied to assess the levels of cholesterol, triglycerides, free cholesterol, cholesteryl ester, fatty acids, glycerol, and cytokines. Results: Daily treatment with olanzapine (3 mg/kg body weight) for four weeks increased mean arterial blood pressure and the whitening of brown adipose tissue in mice. In addition, olanzapine impaired aortic cholesterol homeostasis and exacerbated hyperlipidemia and aortic inflammation, which accelerated atherosclerosis in mice. Moreover, lipid accumulation in liver, particularly total cholesterol, free cholesterol, fatty acids, and glycerol, was increased with olanzapine treatment in apoE-/- mice by upregulating the expression of de novo lipid synthesis-related proteins and downregulating that of cholesterol clearance- or very low-density lipoprotein secretion-related proteins. Conclusion: Olanzapine may exacerbate atherosclerosis by deregulating hepatic lipid metabolism and worsening hyperlipidemia and aortic inflammation.

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