As the use of herbal medications continues to increase in America, the potential interaction between herbal and prescription medications necessitates the discovery of their mechanisms of action. The purpose of this study was to investigate the anxiolytic and antidepressant effects of curcumin, a compound from turmeric (Curcuma longa), and its effects on the benzodiazepine site of the γ-aminobutyric acid receptor A (GABAA) receptor. Utilizing a prospective, between-subjects group design, 55 male Sprague-Dawley rats were randomly assigned to 1 of the 5 intraperitoneally injected treatment groups: vehicle, curcumin, curcumin + flumazenil, midazolam, and midazolam + curcumin. Behavioral testing was performed using the elevated plus maze, open field test, and forced swim test. A 2-tailed multivariate analysis of variance and least significant difference post hoc tests were used for data analysis. In our models, curcumin did not demonstrate anxiolytic effects or changes in behavioral despair. An interaction of curcumin at the benzodiazepine site of the GABAA receptor was also not observed. Additional studies are recommended that examine the anxiolytic and antidepressant effects of curcumin through alternate dosing regimens, modulation of other subunits on the GABAA receptor, and interactions with other central nervous system neurotransmitter systems.

The aim of this research proposal was to investigate the effects of tetrahydropalmatine (THP) on gene expression in a post-traumatic stress disorder (PTSD) rodent model. Eighty male Sprague-Dawley rats were randomly assigned to the nonstressed groups or the 3-day restraint shock PTSD rodent model groups. There were four groups within the nonstressed rats (control, THP, midazolam, and midazolam with THP) and four groups within the stressed rats (control, THP, midazolam, and midazolam with THP). After injection the subjects were euthanized and the amygdala and hippocampus were sent for reverse transcriptase-polymerase chain reaction gene expression analysis. Of the genes interrogated, 17 genes in the amygdala and 18 genes in the hippocampus were found to have significant changes in gene expression and regulation. Significant transcriptional fold changes were found in important genes involved in dopamine, serotonin, acetylcholine, and gamma-aminobutyric acid neurotransmitter systems. The results provide quantifiable data demonstrating gene expression changes in PTSD-stressed and nonstressed rats receiving various treatments. These findings contribute important data to the limited molecular details pertaining to the neurobiology of PTSD.

The distribution and physiological role of the neuropeptide, arginine vasopressin (AVP), and its three receptor subtypes, V1a, V1b and V2, has been well described. A fourth AVP receptor, VACM-1, was recently discovered and appears to be a member of the cullin gene family. The objective of this research is to characterize VACM-1 receptor mRNA expression in the CNS as well as in various tissues and organs of the laboratory rat. Northern blotting of poly(A) + RNA from various tissues demonstrated the size of VACM-1 MRNA in the rat is approximately 6.3 kb. RT-PCR indicated the transcript is present in all twelve tissues examined: brainstem, cerebral cortex, cerebellum, hypothalamus, aorta, gastrointestinal tract, heart, kidney medulla, liver, lung, skeletal muscle, and spleen. Quantitative realtime PCR confirmed RT-PCR results that VACM-1 mRNA is in all organs and tissues and expression levels are similar in all tissues examined. The transcript encoding VACM-1, a novel AVP receptor, appears to be ubiquitously expressed in various tissues of the laboratory rat. VACM-1 shares some similarities with both V1 and V2 receptors, as it binds AVP analogues that independently recognized either of these receptors. Therefore, many functions ascribed to activation of the previously known AVP receptors could at least in part be mediated by VACM-1.