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              <text>&lt;a href="http://doi.org/10.1016/j.neuroscience.2008.04.051" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/j.neuroscience.2008.04.051&lt;/a&gt;</text>
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              <text>1488–1496</text>
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              <text>4</text>
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              <text>154</text>
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                <text>Differences in reserpine-induced striatal dopamine output and content between female and male mice: implications for sex differences in vesicular monoamine transporter 2 function.</text>
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              <elementText elementTextId="46297">
                <text>Neuroscience</text>
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                <text>2008</text>
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                <text>2008-07</text>
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                <text>*Sex Characteristics; Adrenergic Uptake Inhibitors/*pharmacology; Animals; Chromatography; Corpus Striatum/drug effects/*metabolism; Dopamine/*metabolism; Female; High Pressure Liquid; Male; Mice; Orchiectomy; Ovariectomy; Reserpine/*pharmacology; Vesicular Monoamine Transport Proteins/*metabolism</text>
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                <text>Dluzen D E; Bhatt S; McDermott J L</text>
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                <text>In this report a series of six in vitro experiments in which reserpine-evoked dopamine output and two in vivo experiments in which the effects of reserpine injections upon dopamine content from striatal tissue of female and male mice were performed as a means to assess possible sex differences in vesicular monoamine transporter 2 (VMAT2) function. Significantly greater amounts of dopamine were obtained from striatal tissue of female mice in response to either a brief (experiment 1) or continuous (experiment 2) infusion of reserpine. Similarly, reserpine-evoked dopamine output from striatal tissue of gonadectomized females was significantly greater that that of gonadectomized males (experiment 3). When reserpine-evoked dopamine responses were compared directly between intact versus gonadectomized females (experiment 4) or males (experiment 5) no statistically significant differences were obtained. Finally, comparisons of gonadectomized females treated or not with estrogen revealed no statistically significant differences in reserpine-evoked dopamine output (experiment 6). Injections of reserpine produced significantly greater depletions of striatal dopamine content within intact female versus male mice (experiment 7). Dopamine contents of gonadectomized females treated or not with estrogen did not differ following treatment with reserpine, but were significantly greater than that of gonadectomized males (experiment 8). Taken together, these results show that female striatal tissue is more responsive to reserpine-evoked dopamine output, and this sex difference appears to be estrogen independent. Similarly, the dopamine depleting effects of reserpine are greater in intact female mice, however, gonadectomy reverses this effect in an estrogen independent manner. The data suggest that female mice may have a greater amount/activity of VMAT2 function as revealed by the increased responsiveness to the VMAT2 blocking drug, reserpine. Such differences in VMAT2 function may be related to the gender differences observed in conditions like Parkinson's disease and drug addiction.</text>
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                <text>&lt;a href="http://doi.org/10.1016/j.neuroscience.2008.04.051" target="_blank" rel="noreferrer noopener"&gt;10.1016/j.neuroscience.2008.04.051&lt;/a&gt;</text>
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        <name>*Sex Characteristics</name>
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        <name>Bhatt S</name>
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        <name>Reserpine/*pharmacology</name>
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        <name>Vesicular Monoamine Transport Proteins/*metabolism</name>
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              <text>&lt;a href="http://doi.org/10.1016/s0006-8993(97)01101-3" target="_blank" rel="noreferrer noopener"&gt;http://doi.org/10.1016/s0006-8993(97)01101-3&lt;/a&gt;</text>
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              <text>119–124</text>
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              <text>1</text>
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              <text>779</text>
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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Castration reduces olfactory bulb norepinephrine transporter function as indicated by responses to noradrenergic uptake blockers.</text>
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                <text>Brain research</text>
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                <text>1998</text>
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                <text>1998-01</text>
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                <text>*Symporters; Adrenergic Uptake Inhibitors/*pharmacology; Animals; Atomoxetine Hydrochloride; Carrier Proteins/*metabolism; Infusions; Isotonic Solutions; Male; Norepinephrine Plasma Membrane Transport Proteins; Norepinephrine/*metabolism; Olfactory Bulb/*metabolism; Orchiectomy; Parenteral; Propylamines/pharmacology; Rats; Sprague-Dawley; Testis/*physiology; Thiophenes/pharmacology</text>
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                <text>Shang Y; Dluzen D E</text>
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                <text>It has been demonstrated that castration alters the functioning of the olfactory bulb (OB)-norepinephrine (NE) system. In the present experiment, we examined one of the mechanisms by which castration modulates the OB-NE system by comparing NE uptake activity between intact and castrated male rats as studied using an in vitro superfusion technique. To accomplish this goal, NE output from the OB of intact and castrated male rats in response to infusion with two different drugs which alter NE uptake functions, tomoxetine and talsupram, were tested. Overall, NE outputs in response to tomoxetine were significantly higher in the castrated than in intact rats and both groups were significantly greater than non-infused controls. For the talsupram infusion group, NE outputs from the castrated, but not intact rats, were significantly greater than controls. No statistically significant differences were detected between the castrated and intact rats. These results demonstrate that castration alters the NE uptake activities in response to these noradrenergic uptake blockers and suggest that one mechanism by which castration alters OB-NE functioning is through reducing the uptake activity of NE within the OB. Such findings have important implications for olfactory-based learning and memory/recognition processes which are believed to involve the OB-NE system and are altered following castration.</text>
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                <text>&lt;a href="http://doi.org/10.1016/s0006-8993(97)01101-3" target="_blank" rel="noreferrer noopener"&gt;10.1016/s0006-8993(97)01101-3&lt;/a&gt;</text>
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