Articles by Lauren E. Frank in JoVE
Kemirgenler içinde Kurtarılabilir Stereotaksik Cerrahi Brenda M. Geiger1, Lauren E. Frank1, Angela D. Caldera-Siu1, Emmanuel N. Pothos1 1Department of Pharmacology and Experimental Therapeutics, Tufts University Hayvanların serbestçe hareket eden, farklı beyin bölgeleri ekstrasellüler nörotransmitter düzeylerinin izlenmesi nörotransmitter salınımı ve davranış arasındaki bağlantıyı irdeliyoruz. Ve bazal nörotransmisyon farmakolojik veya fizyolojik manipülasyonlar nasıl değiştirdiğini hakkında bilgi; in vivo mikrodiyaliz elektrokimyasal algılama ile birleştiğinde mükemmel anatomik ve kimyasal çözünürlük sağlar.
Kemirgen Yenidoğanlar İlköğretim grubuyla orta beyin dopamin Hücre Kültürleri Lauren E. Frank1, Angela D. Caldera-Siu1, Emmanuel N. Pothos1 1Department of Pharmacology and Experimental Therapeutics, Tufts University İlköğretim ayrışmış orta beyin dopamin hücre kültürleri dopamin nöronların presinaptik özellikleri çalışma için izin verir. Onlar gerçek zamanlı dopamin salınımını kinetik ve dopamin ekzositoz düzenleyicilerin protein / mRNA seviyeleri izlemek için kullanılabilir. Burada, biz kemirgen yenidoğanlarda bu kültürlerin nasıl oluşturmak göstermektedir.
Other articles by Lauren E. Frank on PubMed
Injections of the Selective Adenosine A2A Antagonist MSX-3 into the Nucleus Accumbens Core Attenuate the Locomotor Suppression Induced by Haloperidol in Rats Behavioural Brain Research. Mar, 2007 | Pubmed ID: 17223207 There is considerable evidence of interactions between adenosine A2A receptors and dopamine D2 receptors in striatal areas, and antagonists of the A2A receptor have been shown to reverse the motor effects of DA antagonists in animal models. The D2 antagonist haloperidol produces parkinsonism in humans, and also induces motor effects in rats, such as suppression of locomotion. The present experiments were conducted to study the ability of the adenosine A2A antagonist MSX-3 to reverse the locomotor effects of acute or subchronic administration of haloperidol in rats. Systemic (i.p.) injections of MSX-3 (2.5-10.0 mg/kg) were capable of attenuating the suppression of locomotion induced by either acute or repeated (i.e., 14 day) administration of 0.5 mg/kg haloperidol. Bilateral infusions of MSX-3 directly into the nucleus accumbens core (2.5 microg or 5.0 microg in 0.5 microl per side) produced a dose-related increase in locomotor activity in rats treated with 0.5 mg/kg haloperidol either acutely or repeatedly. There were no overall significant effects of MSX-3 infused directly into the dorsomedial nucleus accumbens shell or the ventrolateral neostriatum. These results indicate that antagonism of adenosine A2A receptors can attenuate the locomotor suppression produced by DA antagonism, and that this effect may be at least partially mediated by A2A receptors in the nucleus accumbens core. These studies suggest that adenosine and dopamine systems interact to modulate the locomotor and behavioral activation functions of nucleus accumbens core.
Evidence for Defective Mesolimbic Dopamine Exocytosis in Obesity-prone Rats FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology. Aug, 2008 | Pubmed ID: 18477764 The association between dietary obesity and mesolimbic systems that regulate hedonic aspects of feeding is currently unresolved. In the present study, we examined differences in baseline and stimulated central dopamine levels in obesity-prone (OP) and obesity-resistant (OR) rats. OP rats were hyperphagic and showed a 20% weight gain over OR rats at wk 15 of age, when fed a standard chow diet. This phenotype was associated with a 50% reduction in basal extracellular dopamine, as measured by a microdialysis probe in the nucleus accumbens, a projection site of the mesolimbic dopamine system that has been implicated in food reward. Similar defects were also observed in younger animals (4 wk old). In electrophysiology studies, electrically evoked dopamine release in slice preparations was significantly attenuated in OP rats, not only in the nucleus accumbens but also in additional terminal sites of dopamine neurons such as the accumbens shell, dorsal striatum, and medial prefrontal cortex, suggesting that there may be a widespread dysfunction in mechanisms regulating dopamine release in this obesity model. Moreover, dopamine impairment in OP rats was apparent at birth and associated with changes in expression of several factors regulating dopamine synthesis and release: vesicular monoamine transporter-2, tyrosine hydroxylase, dopamine transporter, and dopamine receptor-2 short-form. Taken together, these results suggest that an attenuated central dopamine system would reduce the hedonic response associated with feeding and induce compensatory hyperphagia, leading to obesity.