Psy137SexDiffAnimalModels

Da is a possible permissive factor for male sexual

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DA is a Possible Permissive Factor for Male Sexual Behavior Fig. 1. Effects of dopamine on steroid-primed pathways. Inhibitory GABAergic neurons (small black interneuron in top part of figure) prevent the full responsiveness of steroid-primed neurons (three horizontal neurons in top and bottom halves of figure). Dopamine (small black neuron in lower part of figure) may enhance the responsiveness of those neurons by inhibiting the GABAergic neurons, thereby disinhibiting the relevant output pathways. This increases the probability that a sexually relevant stimulus will elicit a sexual response. Black neurons are active; white neurons (open circles) are inactive. (From Hull et al. [37] , with permission.)
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DA in the MPOA as a function of Fig. 3. Extracellular dopamine in the MPOA of male rats during baseline, a precopulatory period (estrous female behind a perforated barrier), and three 6-min periods after the barrier was removed and the animals were free to copulate. All gonadally intact males and all castrates treated with testosterone propionate (200 μg/day) showed a significant increase in dopamine during the precopulatory period and during copulation; all of these animals did copulate. A total of nine of 14 oil-treated 1-week castrates also showed the precopulatory dopamine response and copulated after the barrier was removed. The remaining 1-week and all four 2-week oil-treated castrates failed to show the precopulatory dopamine response and failed to copulate; data from these two groups are combined. , P<0.05 compared to ϕ final baseline for intact males; , P<0.01 compared to final ϕϕ baseline for intact males; +, P<0.05 compared to final baseline for castrates treated with 200 μg testosterone propionate; *, P<0.05 compared to final baseline for 1-week vehicle-treated castrates that copulated; **, P<0.01 compared to final baseline for 1-week vehicle-treated castrates that copulated; #, P<0.05 compared to final baseline for vehicle-treated castrates that failed to copulate. (From Hull et al. [36], with permission.)
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NOS is necessary to induce DA release in the MPOA Fig. 6. Levels of extracellular dopamine in the MPOA of animals treated with an inhibitor of nitric oxide synthase (l-NAME) or its inactive isomer (d-NAME). l-NAME prevented the increase in dopamine release during copulation that was observed in animals treated with d-NAME. (From Lorrain et al. [49] , with permission.)
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Glutamate-Dopamine Interactions in mPOA during copulation. Model showing possible interactions between glutamate, nitric oxide (NO), and dopamine in the MPOA. (1) Glutamate (GLUT; gray hexagon) activates NMDA receptors, which opens calcium channels. (2) The resultant increase in intracellular calcium (gray diamonds) then activates calmodulin (CaM), (3) which in turn activates the enzyme NO synthase (NOS); this leads to an immediate production of NO. NOS links to the carboxy-terminal tail of the NMDA receptor, via a PSD-95 protein–protein interaction domain. Once synthesized, NO freely diffuses from cell to cell, (4) where it can alter activity in the presynaptic neurons. (5) Additionally, in dopamine-producing neurons, NO has been shown to inhibit the dopamine transporter (DAT) (6) and increase calcium-dependent and/or calcium-independent vesicular release. Therefore, increased NO in the MPOA, after glutamate release, would
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DA is a Possible Permissive Factor for Male Sexual Behavior...

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