Further studies on the rat posterodorsal medial amygdala: dendritic spine density and effect of 8-OH-DPAT microinjection on male sexual behavior.

The rat posterodorsal medial amygdala (MePD) is a component of the neural network that modulates male sexual behavior. Dendritic spines were counted in Golgi-impregnated bitufted and stellate neurons and from cells located in the medial and lateral MePD subregions. It was also studied the effect of 8-OH-DPAT, a 5-HT1A receptor agonist, microinjected into the MePD on male sexual behavior. There were no significant differences in the dendritic spine density obtained from multipolar bitufted and stellate neurons (n = 48 cells in each group; p > 0.05) or in the data from the medial or the lateral MePD (n = 48 neurons per region; p > 0.05). Rats were stereotaxically microinjected into the MePD with saline (0.2 microl, n = 6) or 8-OH-DPAT (0.1 and 1.0 microg/0.2 microl, n = 6 and 5, respectively). Behavioral recordings prior to surgery and "non-target" microinjections served as additional control data. 8-OH-DPAT 1.0 microg decreased the latencies to intromission and ejaculation, the postejaculatory refractory period and the mount frequency when compared to control pre-surgery data (p < 0.05). When compared among groups, 8-OH-DPAT 1.0 microg promoted the highest percentage reduction in the postejaculatory refractory period. Saline and injections in the vicinity of MePD did not promote relevant effects on ejaculation (p > 0.05). Results indicate that a similar dendritic spine density can be found in morphologically different populations of MePD neurons and, 8-OH-DPAT can facilitate male sexual behavior by acting on postsynaptic 5-HT1A receptors in this brain area.

Dendritic spine density of posterodorsal medial amygdala neurons can be affected by gonadectomy and sex steroid manipulations in adult rats: a Golgi study.

The posterodorsal medial amygdala (MePD) is a sex steroid-responsive area in the rat brain. The dendritic spine density of Golgi-impregnated MePD neurons were studied in: (1) adult gonadectomized (GDX) males after a short or a longer postcastration period (8 and 90 days, respectively), compared to age-matched sham operated and to intact controls; (2) adult GDX females, which received oil, estradiol benzoate (EB) alone or EB and progesterone as substitutive therapy; and, (3) EB-treated GDX females that concomitantly received saline or LY235959, a competitive antagonist of NMDA receptors, to test a possible glutamatergic mediation on the estrogen-mediated increase in spine density in this brain area. Intact males showed a higher spine density than males studied 8 days after sham operation or those in both short- and long-term GDX groups (p<0.02), but not when compared to males at 90 days after sham operation (p=0.12). In females, dendritic spine density increased following EB injections when compared to the oil group (p=0.05), with an effect that was potentiated by progesterone (p<0.01). LY235959 was not able to block the stimulating effect of EB on dendritic spines of GDX females (p>0.2). These data provide novel evidence that MePD dendritic spines are affected by sex steroid manipulations in adult rats, GDX males had a specific spine density decrease after a long postcastration period, and estrogen (apparently independently of a NMDA receptor interaction) and progesterone have stimulatory effects on the number of dendritic spines in GDX females.