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Development of the sexually dimorphic nucleus of the preoptic area and the influence of estrogen-like compounds

Neural Regeneration Research 2013年第29期8卷 2763-2774页

作者： Zhen He Sherry Ann Ferguson Li Cui Lazar John Greenfield merle gale paule Division of Neurotoxicology National Center for Toxicological ResearchFood and Drug Administration Department of Neurology University of Arkansas for Medical Sciences

One of the well-defined sexually dimorphic structures in the brain is the sexually dimorphic nucleus, a cluster of cells located in the preoptic area of the hypothalamus. The rodent sexually dimorphic nucleus of the preoptic area can be delineated histologically using conventional Nissl staining or immunohistochemically using calbindin D28K immunoreactivity. There is increasing use of the cal- bindin D28K-delineated neural cluster to define the sexually dimorphic nucleus of the preoptic area in rodents. Several mechanisms are proposed to underlie the processes that contribute to the sexual dimorphism （size difference） of the sexually dimorphic nucleus of the preoptic area. Recent evidence indicates that stem cell activity, including proliferation and migration presumably from the 3^rd ventricle stem cell niche, may play a critical role in the postnatal development of the sexually dimorphic nucleus of the preoptic area and its distinguishing sexually dimorphic feature： a signifi-cantly larger volume in males. Sex hormones and estrogen-like compounds can affect the size of the sexually dimorphic nucleus of the preoptic area. Despite considerable research, it remains un-clear whether estrogen-like compounds and/or sex hormones increase size of the sexually dimor-phic nucleus of the preoptic area via an increase in stem cell activity originating from the 3^rd ventricle stern cell niche.

关键词： neural regeneration review sexual orientation sexual behavior calbindin D28K estrogen-likecompound bisphenol A neural stem cells grants-supported paper neuroregeneration

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Pharmacological characterizationof synthetic cannabinoid MAM-2201：radioligand binding and abuse-related effects

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中国药理学与毒理学杂志 2017年第10期31卷 1016-1017页

作者： William E FANTEGROSSI Aaron JANOWSKY Amy J ESHLEMAN Lauren N RUSSELL Saki FUKUDA Jyoti GOGOI Cassandra PRIOLEAU Ambuja S BALE Srihari R TELLA merle G paule Takato HIRANITA Department of Pharmacology and Toxicology College of Medicine University of Arkansas for Medical Sciences AR 72207 Division of Neurotoxicology National Center for Toxicological Research Food and Drug Administration AR 72079 Departments of Psychiatry and Behavioral Neuroscience Oregon Health & Science University Portland OR 97239-3098 VA Portland Health Care System Portland OR 97239 Drug and Chemical Evaluation Section Drug Enforcement Administration

OBJECTIVE Over 30% of all new psychoactive substances identified by the UN Office on Drugs and Crime in 2016 were synthetic *** recent emergence of MAM-2201 on the illicit market is troubling because this drug has no precedent in either the scientific or patent literature,and appears to be a novel compound developed specifically as a "graymarket" drug of abuse bystructurally combining the known synthetic cannabinoids JWH-122 and *** is currently no published information regarding the pharmacology of *** The present studies characterized cannabinoid-like effects of MAM-2201 in vitro(interactions with cannabinoid type 1 receptors[CB1 Rs]) and in vivo(in mice and rats).RESULTS In a radioligand binding assay using [3 H]CP55,940 in HEK cell membranes transfected with the CB1 R,MAM-2201(K i=5.4 nmol·L^(-1)),had higher binding affinity than WIN 55,212-2(K i=80 nmol·L^(-1)),and D9-THC(K i=8.3 nmol·L^(-1)).The E max values for MAM-2201 and WIN 55,212-2 in an assay of agonist inhibition of forskolin-stimulated c AMP were 85%(EC50=0.45 nmol·L^(-1)) and 95%,respectively,as compared with the D9-THC E max of 74%.In mice,MAM-2201(0.003-1.0 mg·kg^(-1),IP) produced dose-dependent cannabimimetic effects which were both more potent and more effective than those of ***-2201 and D9-THC dose-dependently produced hypothermia:ED50=0.287 and 25.4 mg·kg^(-1),analgesia:ED50=0.125 and 29.4 mg·kg^(-1),and catalepsy:ED50=0.301 and18.9 mg·kg^(-1) in adult male CD1 ***,MAM-2201 also elicited convulsant effects at a dose of 1.0 mg·kg^(-1) in 8/8 murine *** rats,MAM-2201 produced dose-dependent D9-THC-like interoceptive effects in subjects trained to discriminate 3.0 mg·kg^(-1)(IP) D9-THC from *** MAM-2201 binds CB1 Rs with high affinity and agonist efficacy,and functions as a potent cannabinoid agonist in vivo across several complementary measures of cannabinoid activity in two rodent species.

关键词： cannabinoid CB1 receptor behavior abuse liability

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A common genetic mechanism underlying susceptibility to posttraumatic stress disorder

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World Journal of Neurology 2013年第3期3卷 14-24页

作者： Zhen He Li Cui Bei He Sherry A Ferguson merle G paule Division of Neurotoxicology National Center for Toxicological Research Food and Drug Administration Jefferson AR 72079-9502 United States Department of Neurology University of Arkansas for Medical Sciences Little Rock AR 72205 United States

We hypothesize that susceptibility to post-traumatic stress disorder(PTSD) may be determined in part by aberrant microtubule-associated protein tau expression in neurons of critical brain structures. The following lines of evidence support this hypothesis. First, epidemiologic data suggest the involvement of genetic factors in the susceptibility to PTSD. Second, the common features of both abnormal tau expression and PTSD include amygdalar and hippocampal atrophy, upregulation of norepinephrine biosynthetic capacity inthe surviving locus coeruleus neurons and dysfunction of N-methyl-D-aspartate-receptors. Finally, our experiments using r Tg4510 mice, a model that over-expresses human mutant tau and develops age-dependent tauopathy, demonstrate that these animals display circling behavior thought to be related to states of anxiety. To detect the potential molecular mechanisms underlying PTSD episodes, laser-assisted/capture microdissection can be used with microarray analysis as an alternative approach to identify changes in gene expression in excitatory and/or inhibitory neurons in critical brain structures(i.e., hippocampus and amygdala) in response to the onset of PTSD.

关键词： Amygdalar damage Anxiety behavior Microarrays Microdissection Microtubule-associated protein tau Post-traumatic stress disorder RNA quality

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