Abstract
We examined whether N-methyl-D-aspartate (NMDA), amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) or trans-1-amino-1,3-cyclo-pentadicarboxylic acid (ACPD) increase intracavernous pressures when injected in the paraventricular nucleus of the hypothalamus. Sprague-Dawley rats weighing 250 to 300 gm. were anesthetized with pentobarbital and placed in a stereotaxic apparatus after catheterization of the carotid artery and insertion of a 25 gauge needle in the corpus cavernosum. Both catheters were coupled to pressure transducer systems. Electrical stimulations with glass tungsten microelectrodes and chemical injections with a 0.5 microl. syringe were done in the paraventricular nucleus. At the end of each experiment rats were perfused with saline and 10% formalin solutions. Brains slices 16 microm. thick were mounted and stained with cresyl violet to identify chemical and electrical stimulation sites. Electrical stimulations of the paraventricular nucleus increased intracavernous pressure from 15.5 +/- 5.7 to 50.02 +/- 20.4 cm. H2O in 10 rats (p <0.001) and decreased central pressure in 10 (p <0. 001). Intracavernous pressure increased from 17.2 +/- 5.26 to 60.6 +/- 14.36 cm. H2O with NMDA, 26.0 +/- 8.9 to 49.6 +/- 12.2 cm. H2O with AMPA and 18.0 +/- 2.3 to 41.0 +/- 22.68 cm. H2O with ACPD when injected in the paraventricular nucleus of 5 rats (analysis of variance 12.18, df 3, p <0.007). Mean delays and durations varied between 3.6 to 4.0 and 5.6 to 7.0, respectively, and were similar for all agonists (analysis of variance not significant). Glutamate receptor subtypes NMDA, ACPD and AMPA cause an increase in intracavernous pressure when injected in the paraventricular nucleus. Therefore, increases in intracavernous pressure following injection of glutamate must be initiated by the synergistic or additive effects of all of these receptor subtypes.
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