Compensatory Ovarian Hypertrophy Research Articles

Differences in the ovulation rate of the right or left ovary in unilaterally ovariectomized rats: effect of ipsi- and contralateral vagus nerves on the remaining ovary.

The possible existence of peripheral asymmetry in the neuroendocrine mechanisms participating in the response of the ovary to gonadotrophins, and the participation of the vagus nerve, was investigated. At oestrus, the ovulation rate (number of ovulating/number of treated rats) of the left ovary in right unilaterally ovariectomized rats was lower than that in the right ovary in left unilaterally ovariectomized rats (42 vs 84%). No differences in the number of ova shed per ovulating animal nor in compensatory ovarian hypertrophy (COH) were observed. Bilateral section of the vagus nerve resulted in reduced COH only in those animals with the left ovary in situ (right unilaterally ovariectomized). Section of the left vagus nerve induced different effects depending upon which ovary was left in situ. When the left ovary was in situ an increase in ovulation rate, COH and number of ova shed was observed; however, when the right ovary was left in place the above three parameters decreased. Section of the right vagus nerve produced a decrease only in COH in both right and left unilaterally ovariectomized animals. It is concluded that in the unilaterally ovariectomized rat the right ovary seems more able to react to compensatory regulatory systems than does the left. The character of the information carried by the left and right vagus nerve is different.

Systematic studies invalidate the neonatally androgenized rat as a model for polycystic ovary disease.

As an adult, the neonatally androgenized (AZ) rat is anovulatory and exhibits follicular cysts. Thus, the AZ rat has been used as a model for polycystic ovary disease (PCO). However, its correlation with the human disease is not clear; so we have studied the AZ rat to determine its suitability as a PCO model. In Experiment I, reproductive hormones were measured at specific intervals between postnatal Days 15 and 90 in saline-treated and AZ rats. In Experiment II, AZ rats were treated with exogenous follicle-stimulating hormone (FSH) or subjected to unilateral ovariectomy (ULO) as analogies to therapies that have been used to treat human PCO. The results demonstrate that the luteinizing hormone (LH), FSH, testosterone (T), and estradiol (E2) concentrations of the AZ rat were not different from control values. Additionally, FSH therapy did not increase the E2 concentrations or the ovarian weight of the AZ rat. Furthermore, control and AZ rats exhibited similar post-ULO rises in FSH, but compensatory ovarian hypertrophy was not evident in the AZ rat. We conclude that 1) the hormonal and morphological patterns observed in the AZ rat do not correlate with those of PCO and 2) the androgenized rat does not provide an adequate model to study PCO.

Neuroendocrine and behavioral effects of intrathecal capsaicin in adult female rats

Neurol feedback from the gonads and the reproductive tract has an integral role in normal reproductive function in female rats. To further assess the role of sensory feedback in neuroendocrine control, the effects of an intrathecal injection of the neurotoxin, capsaicin (100–125 μg) into the lumbosacral region of the spinal cord on reproductive function was tested in female rats. In addition, the effects of capsaicin on the response to noxious heat and pressure were tested. Intrathecal capsaicin had no effect on estrous cycles, ovarian compensatory hypertrophy or female sexual behavior. However, capsaicin treated animals showed a dramatic reduction in fertility, relative to vehicle treated control rats and this was shown to be due to the reduced capacity of vaginal/cervical stimulation to produce pseudopregnancy. Consistent with a selective loss in the effectiveness of cervical stimulation, immobilization produced by vaginal probing was reduced in capsaicin treated rats, but this response slowly recovered across time in some animals. Similarly, the ability of vaginal probing to induce a lordotic response during estrogen treatment was reduced in the capsaicin treated animals. The capsaicin treated animals showed analgesia to noxious heat, as measured by the tail flick test, but showed a normal foot withdrawal in response to pressure. The analgesic effect of vaginal stimulation on noxious pressure was unaltered in the capsaicin treated rats. Finally, the neurotoxic effect of capsaicin was verified in terms of a quantitative reduction in substance P immunoreactivity in the dorsal horns of the lumbosacral region of the spinal cord of capsacin treated rats, relative to control animals. Estrogen treatment of ovariectomized rats quantitatively reduced substance P immunoreactivity in the spinal cord, an effect even more apparent in the capsaicin treated animals. These studies indicate that intrathecal capsaicin has an effect in adult female rats that is specific to the endocrine and behavioral consequences of vaginal stimulation. Whether substance P mediates any of the endocrine or behavioral effects of cervical stimulation remains to be established.

Inhibitory Role of the Septum and Facilitory Role of the Preoptic Area in Regulating Ovarian Compensatory Hypertrophy in Rats

Inhibitory Role of the Septum and Facilitory Role of the Preoptic Area in Regulating Ovarian Compensatory Hypertrophy in Rats

Kainic acid lesioning of the preoptic area alters positive feedback of estrogen in prepubertal female rats.

Stereotaxic infusion of kainic acid (KA) was performed to induce intrinsic neural lesions of the preoptic area (POA) in 25-day-old female rats. After KA infusion, rats in Experiment 1 received 10 micrograms of estradiol benzoate (EB) administered subcutaneously to assess positive feedback of EB on release of luteinizing hormone (LH) from the pituitary gland. Rats were perfused for light microscopic (LM) or electron microscopic (EM) evaluation of the lesion site. Rats of Experiment 2 were allowed to develop until the appearance of vaginal opening (VO) after which time vaginal lavages were taken to monitor the cyclicity of the vaginal epithelium. At 50 days of age, the right ovary from each rat was removed, trimmed of fat, and weighed. At 60 days of age, the remaining ovary was removed to assess compensatory ovarian hypertrophy (COH). In Experiment 3, we investigated the effects of POA/KA-infusion on sexual behavior. Sex behavior tests were conducted at 48 h after EB during the dark phase of the light cycle. In Experiment 1, all the control and saline-infused rats exhibited the expected rise of plasma LH two days after estrogen injection while the POA/KA-infusion abolished the positive feedback effect of EB on LH release. Ultrastructural examination of the lesion site revealed that neurons were undergoing acute degeneration while axons and afferent terminals seen in the same fields of analysis were morphologically intact. Preoptic area/KA lesions caused a marked delay in the appearance of VO. Duration of this temporal delay in POA/KA-lesioned rats was approximately 4 days, or one vaginal cycle. The lesioned animals showed normal compensatory hypertrophy after unilateral ovariectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Ovarian compensatory hypertrophy following unilateral ovariectomy in the suckled sow.

The effects of unilateral ovariectomy on ovarian compensatory hypertrophy (OCH), endocrine profiles and the pituitary response to gonadotropin releasing hormone (GnRH) were studied in 46 multiparous suckled sows. On d 20 of lactation (d 0 of experiment), sows were subjected to sham ovariectomy (Sham; n = 23) or unilateral ovariectomy (ULO; n = 23). On d 1 (n = 16), 2 (n = 15) or 8 (n = 15) following initial surgery the remaining ovaries in both Sham and ULO sows were removed. Immediately following removal of the remaining ovaries, GnRH (10 micrograms) was administered to each sow. Peripheral blood samples were taken every 10 min for 80 min beginning 20 min prior to GnRH administration. No difference in ovarian weight was observed between ULO and Sham sows until d 8, when ovarian weight was greater (P less than .05) for the remaining ovary from ULO sows (3.96 +/- .21 vs 5.91 +/- .39 g). Ovarian follicular fluid weights from ULO sows were greater (P less than .05) than Sham sows on both d 2 and 8. On d 1, plasma concentrations of follicle stimulating hormone (FSH) were greater (P less than .05) in ULO sows than in Sham sows (2.9 +/- .2 vs 2.1 +/- .1 ng/ml). Plasma FSH concentrations, however, did not differ between Sham and ULO sows on either d 2 or 8. Ovarian venous concentrations of estradiol-17 beta were also greater (P less than .05) in ULO sows compared with Sham sows on d 2 but not d 8.

Inhibin-like activity in ovarian venous serum after unilateral ovariectomy in prepubertal gilts.

To examine a role for inhibin in compensatory ovarian hypertrophy after unilateral ovariectomy (ULO) of prepubertal gilts, changes in inhibin activity in ovarian venous blood were estimated by bioassay. Three groups of 130-day-old gilts were unilaterally ovariectomized after collecting blood from an ipsilateral ovarian vein (Day O); blood samples were obtained from the remaining ovary on Day 2, 4, or 8. Coetaneous gilts underwent sham ovariectomy on Day 0, and venous blood was collected from both ovaries on Day 2, 4, or 8. An assay for inhibin activity, which measured inhibition of secretion of follicle-stimulating hormone (rFSH) by rat pituitary cells in culture, was validated for serum samples. Presumptive inhibin activity was always greater in ovarian venous serum than in peripheral serum samples. In the ULO groups, inhibin activity (in terms of a house reference preparation) in ovarian venous serum was 55 +/- 13 micrograms/ml (means +/- SE, n = 13) on Day 0, 251 +/- 79 (n = 5) on Day 2, 275 +/- 111 (n = 4) on Day 4, and 68 +/- 14 micrograms/ml (n = 4) on Day 8. The five-fold increases on Days 2 and 4 were significant (p less than 0.05). In contrast, no significant differences in inhibin activity were detected between ovarian venous serum (within gilts) or between Days 2, 4, and 8: 82 +/- 29, 73 +/- 30, and 99 +/- 48 micrograms/ml (n=4/day) in control groups. These results demonstrate that, in prepubertal gilts, the remaining ovary's response to ULO includes a major increase in release of inhibin-like activity.

The effects of vagotomy on compensatory ovarian hypertrophy and follicular activation after unilateral ovariectomy.

Following unilateral ovariectomy in the rat, the remaining ovary undergoes rapid compensatory changes including an increase in the number of antral follicles (follicular activation) and an increase in ovarian weight (compensatory ovarian hypertrophy). The ovary is innervated by the vagus nerve (Burden et al., 1983). In the present study, the effects of right and left cervical vagotomy and abdominal vagotomy on follicular activation and compensatory ovarian hypertrophy in the remaining right or left ovary were compared 15 days after unilateral ovariectomy. Neither right nor left cervical vagotomy affected compensatory ovarian hypertrophy of the right or left ovaries but abdominal vagotomy depressed compensatory ovarian hypertrophy in both the right and left ovaries. Left cervical vagotomy did not inhibit follicular activation, but right cervical vagotomy prevented follicular activation in the right but not left ovary. Also, abdominal vagotomy inhibited follicular activation in the right but not the left ovary. In animals with both ovaries which were subjected to the left or right cervical vagotomy or abdominal vagotomy follicular counts in both right and left ovaries were similar. Collectively, these data indicate that the vagus nerve participates in follicular activation after unilateral ovariectomy. The data also indicate that the right ovary is more dependent on vagal influences for follicular activation than the left ovary.

Differential effects of neurotoxic lesions on psychoneuroendocrine functions

The use of neurotoxic agents has provided new insight into the functions of the septal region. The psychoneuroendocrine effects of kainic acid (KA) lesions in the lateral septum (LS) have been confirmed, and we have compared the effects of these lesions to those following lesions of the medial septum (MS) and hippocampus (HP). In addition, the effects of the cytotoxin ibotenic acid (Ibo), have been studied. The alterations in psychoneuroendocrine functions resulting from the cytotoxic lesions have been compared to those from electrolytic septal lesions (DCLS) and sham operations. KA and Ibo lesions of the LS resulted in extensive bilateral loss of neurons in the LS; however, KALS lesions also resulted in cell loss in the CA3–CA4 cell regions of the HP. In contrast, KA and Ibo lesions of the MS did not produce any obvious cell loss in the MS. KA lesions of the HP produced extensive CA3–CA4 cell loss and a reduction in the size of the fornix and rostral septum. The behavioral and endocrine effects of these lesions were, relative to controls: the KALS group exhibited fewer percent days of vaginal estrus, increased ovarian compensatory hypertrophy (OCH), increased body weight (BWt), attenuation in the anorexic effects of estrogen, and decreased female sexual behavior. The KAMS group exhibited a transitory increase in BWt and increased male sexual behavior. IboLS group demonstrated a greater percent days of vaginal estrus and increased female sexual behavior whereas the IboMS group exhibited a decrease in OCH. The KAHP group exhibited a partial attenuation in the anorexic effects of estrogen on food intake and BWt gain. The DCLS group demonstrated increased female sexual behavior. These results indicate that the septal region is involved in both facilitatory and inhibitory modulation of a variety of estrogen responsive processes and further suggest that the MS and LS have different psychoneuroendocrine functions.

Effect of unilateral ovariectomy and injection of bovine follicular fluid on gonadotropin secretion and compensatory ovarian hypertrophy in prepuberal heifers.

A study was conducted to determine whether compensatory ovarian hypertrophy occurred in prepuberal heifers, and if so, could compensatory ovarian hypertrophy be prevented by injecting charcoal-extracted bovine follicular fluid (CFF). An additional objective was to determine the effect of CFF injections on follicle stimulating hormone (FSH) and luteinizing hormone (LH) concentrations following unilateral ovariectomy (ULO). Thirty-one prepuberal Angus, Hereford, and Angus X Hereford heifers were assigned by weight and breed to the following groups: Control-saline injections (C), unilateral ovariectomy-saline injections (ULO) and unilateral ovariectomy-CFF injections (ULO-CFF). In group C, a sham operation was performed on d 0 and both ovaries were removed on d 7. In groups ULO and ULO-CFF, either the right or left ovary was removed on d 0 and the remaining ovary was removed on d 7. From d 0 to 7, each heifer received an injection (iv, 7 ml/injection) of saline or CFF every 12 h. Jugular blood samples were collected immediately before each saline injection from d 0 to 7 and analyzed for FSH and LH. Unilateral ovariectomy increased ovarian (P less than .08) and follicular fluid (P less than .05) weights compared with groups C and ULO-CFF; however, lyophilized ovarian weight was similar (P greater than .05) for all groups. Injections of CFF blocked the increase in ovarian and follicular fluid weight following ULO. The total number of visible follicles per ovary was similar for all groups; however in the ULO group there was an increase (P less than .01) in those 5 to 6 mm and greater than or equal to 9 mm.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of follicular fluid treatment on follicle-stimulating hormone, luteinizing hormone and compensatory ovarian hypertrophy in prepuberal gilts.

Prepuberal 130-day-old gilts were treated with 10 ml of charcoal-stripped porcine serum (PS), whole porcine follicular fluid (WpFF) or charcoal-stripped pFF (CpFF) twice daily beginning the day before and continuing 8 days after unilateral ovariectomy (ULO). Follicle-stimulating hormone (FSH) declined for the first 14 h after ULO in WpFF and CpFF gilts and then by 24 h returned to values observed at or before ULO, whereas FSH was increased nearly twofold at 14 h in PS gilts. At 8 days after ULO the remaining ovaries from PS-treated gilts were heavier than ovaries from follicular fluid-treated gilts. In a second experiment, ovariectomized 130-day-old gilts were assigned to either a group infused with PS, a group infused with 5 ml CpFF, or a group infused with 10 ml Cpff at 18 and 2 h before a gonadotropin-releasing hormone (GnRH) challenge. Porcine follicular fluid had no effect on luteinizing hormone (LH) response to GnRH, depressed the FSH response to a 10-micrograms challenge of GnRH, but had no effect on FSH response to a 50-micrograms challenge of GnRH. In a third study, gilts were subjected to sham ovariectomy (Sham) or ULO at 130 days of age. GnRH (10 micrograms) was given on Days 1, 2 or 8 after surgery. The response to GnRH in ULO versus Sham gilts did not differ for FSH or LH on any day.(ABSTRACT TRUNCATED AT 250 WORDS)

Further evidence for hypothalamic asymmetry in endocrine control of the ovary

Nance D.M., M. Bhargava and G.A. Myatt. Further evidence for hypothalamic asymmetry in endocrine control of the ovary. BRAIN RES BULL 13(5) 651–655, 1984.—The differential release of FSH and LH associated with hemigonadectomy (hemi-x) of prepubertal male rats can be blocked by unilateral hypothalamic deafferentation located on the side ipsilateral, but not contralateral, to the hemi-x. Also, ovarian compensatory hypertrophy (OCH) in prepubertal female rats can be blocked by ipsilateral, but not contralateral, hypothalamic hemi-islands. Both these endocrine phenomenon are limited to knife cuts on a particular side of the brain. These results suggest that there are neural connections with the gonads which are involved in endocrine regulation and that hypothalamic control of the endocrine system may be asymmetrically organized. In support of this, the present study shows that in adult female rats, unilateral injections of the excitotoxin kainic acid (1.0 μg in 1.0 μl) into the retrochiasmatic area of the hypothalamus can block OCH if the injections are located on the side ipsilateral to the hemi-x. This phenomenon was more apparent if the lesions and hemi-x were located on the right side. In addition, neither hemi-x nor kainic acid injections alone had any effect on vaginal cycles, whereas the combination of these two treatments reduced the incidence of estrus. However, these effects on vaginal cycles were not specifically associated with lesions or hemi-x on a particular side, thus excluding this as an explanation of the different endocrine effects of kainic acid on the two sides of the brain. These results support the evidence for a direct neural contribution to endocrine control and further suggest a functional difference in the two-halves of the hypothalamus in neuroendocrine regulation.

Hypothalamic laterality in regulating gonadotropic function: Unilateral hypothalamic lesion and ovarian compensatory hypertrophy

Regardless of the side of hemiovariectomy, unilateral lesion placed in the right-side medial anterior hypothalamus suppressed ovarian compensatory hypertrophy, but the lesion made in the left side failed to suppress it. This suggests the presence of a hypothalamic laterality in regulating gonadotropin secretion.

Effect of unilateral ovariectomy on compensatory ovarian hypertrophy, peripheral concentrations of follicle-stimulating hormone and luteinizing hormone, and ovarian venous concentrations of estradiol-17 beta in prepuberal gilts.

A study was designed to characterize the compensatory ovarian response to unilateral ovariectomy (ULO) in prepuberal gilts and to investigate further the mechanisms involved in compensatory ovarian hypertrophy (COH). Forty-eight crossbred gilts were sham ovariectomized (Sham) or unilaterally ovariectomized at 130 days of age (Day 0). Remaining ovaries in ULO gilts were removed and Sham gilts were bilaterally ovariectomized 2, 4 or 8 days later. A peripheral blood sample was taken before surgery and ovarian venous blood samples were taken before removal of each ovary. Serum estradiol-17 beta (E2) concentrations were determined. Mean wet and dry ovarian weights per ovary on Day 2 for ULO and Sham gilts were 3.4 versus 2.8 and 0.26 versus 0.24 g, respectively. Those weights on Days 4 and 8 were greater (P less than 0.01) for ULO than Sham gilts. Follicular fluid weight per ovary was greater (P less than 0.05) for ULO than Sham gilts on Days 2, 4 and 8. Ovarian venous E2 concentrations were greater (P less than 0.01) for ULO than for Sham gilts on Days 2 and 4 but were similar on Day 8. In a second experiment, 42 prepuberal gilts 130 days of-age were subjected to Sham (n = 18), ULO (n = 18) or bilateral ovariectomy (BLO; n = 6) to evaluate follicle-stimulating hormone (FSH) and luteinizing hormone (LH) secretion immediately after surgical treatment. Release of FSH within the first 24 h was greater for BLO than ULO and for ULO than Sham gilts.(ABSTRACT TRUNCATED AT 250 WORDS)

Follicle stimulating hormone secretion and compensatory ovarian hypertrophy in prepubertal ewes

A study was conducted to determine the effect of unilateral ovariectomy (ULO) on follicle stimulating hormone (FSH) secretion and compensatory ovarian hypertrophy in prepubertal ewes. Thirty-three ewe lambs were allotted according to age and weight to a control (C) or ULO group. In the C group, a sham ovariectomy was performed on day 0 and both ovaries were removed on day 7. In the ULO group, one ovary was removed on day 0 and the remaining ovary was removed on day 7. Blood samples were collected from the jugular vein via venipuncture at 0, 6, 12 and 24 hours after the time of sham surgery or ULO (day 0). Subsequent samples were collected daily until day 7, and all samples were assayed for FSH and LH. Unilateral ovariectomy increased (P<0.01) ovarian weight and follicular fluid weight; however, lyophilized ovarian weight was similar for both groups. Within the ULO group, removal of the ovary having the largest follicle(s) did not prevent an increase in ovarian weight or follicular fluid weight of the remaining ovary. Unilateral ovariectomy had no effect on the total number of follicles (1 to 6 mm) per ovary; however, the number of large (5 to 6 mm) follicles per ovary was increased (P<0.05) following ULO. By 12 hours after ULO there was a transient increase (P<0.05) in the circulating concentrations of FSH. Circulating concentrations of luteinizing hormone (LH) were either low or undetectable in these prepubertal ewes and no LH response was observed following ULO. These results indicate that compensatory ovarian hypertrophy in ULO prepubertal ewes is accompanied by a transient rise in circulating FSH concentrations.

Effect of ovarian sympathectomy on follicular development during compensatory ovarian hypertrophy in the guinea-pig.

Selective ovarian sympathectomy was achieved by injecting 6-hydroxydopamine into a surgically closed periovarian bursa on Day 3 of the oestrous cycle (Day 1 = day of oestrus). Control ovaries had the periovarian bursa surgically closed and were injected with solvent. On Day 15 of the cycle, serum was collected for progesterone determination and ovaries were processed for morphometric analysis of follicles. In both control and sympathectomized ovaries remaining after unilateral ovariectomy on Day 3, there was an increase in ovarian weight and an increase in healthy preovulatory follicles (greater than 700 microns diam.). Sympathectomy of the ovary remaining after unilateral ovariectomy increased healthy follicles 510-700 microns diameter but decreased the total number of follicles per ovary. In animals bearing both ovaries, unilateral sympathectomy did not affect any of the characteristics measured. Serum progesterone concentrations were unaffected by any of the treatments. These results indicate that adrenergic nerves play a role in follicular dynamics in ovaries undergoing compensatory hypertrophy but are not necessary for compensatory increases in weight and number of preovulatory follicles.

Ethanol inhibition of compensatory ovarian hypertrophy in unilaterally ovariectomized rats.

The purpose of this study was to determine the effect of ethanol consumption on compensatory ovarian hypertrophy (COH) which occurs following unilateral ovariectomy. Holtzman rats, 40 days old, were either unilaterally ovariectomized or sham-ovariectomized. The rats were then placed into subgroups which would receive either an ad libitum chow and water diet, a liquid diet, or a liquid diet containing 5% ethanol. The animals were maintained on their respective diets for 11 days. The rats were killed at 51 days of age, and the ovaries and uteri were removed, weighed, and prepared for histological investigation. The results showed that uteri from ethanol-fed animals failed to develop epithelial glands and exhibited a condensed stroma in comparison to uteri from animals fed ad libitum or pair-fed to ethanol-fed rats. Also, rats that were fed ad libitum had a COH of 82 +/- 16% and rats that were pair-fed a liquid diet had 114 +/- 28% COH; rats that were fed the liquid diet containing ethanol did not experience compensatory ovarian hypertrophy (-3 +/- 10%). Histologically, the ovaries of rats fed ad libitum showed large numbers of corpora lutea and only a few mature ova. The histology of ovaries from pair-fed animals was similar to those from animals fed ad libitum. In contrast, the ovaries from the animals fed the ethanol diet had nearly twice as many mature ova but only one-fourth as many corpora lutea as the number seen in ovaries from the other groups. The data show that ethanol consumption inhibits COH by suppressing ovulation and the subsequent luteal formation.

Dietary Arginine Deprivation and Delayed Puberty in the Female Rat

Dietary arginine deprivation was found to delay puberty in the female rat. Physiological pinealectomy by exposing to constant light suggests this gland is not involved in this delay. Compensatory ovarian hypertrophy (COH) was used to test the hypothalamic sensitivity to negative steroid feedback. COH occurred in hemiovariectomized immature rats ad libitum fed the control or arginine-deficient diet but failed to occur in hemiovariectomized, underfed, growth-matched control rats, which suggests that feed restriction and arginine deficiency do not exert identical effects on the hypothalamic-pituitary-gonadal axis. Puberty, as defined by vaginal opening, first ovulation and the initiation of estrous cycles, was advanced by a week in the immature female rat fed a control diet after treatment with estradiol benzoate, 0.05 μg/(100 g body weight · day) starting at 26 days of age. The time of first estrus and the first ovulation was not advanced in arginine-deficient rats by the same dosage of estrogen when administration began at 26 days of age. Treatment at an older age (40 or 54 days) or with a higher dosage [0.25 μg/(100 g body weight · day)] at 26 days of age did advance puberty. The failure of estrogen to induce vaginal cyclicity suggests an insufficient amount of endogenous estrogen to trigger a gonadotropin surge to cause the onset of puberty in the rat fed an arginine-deficient diet.

Psychoneuroendocrine effects of neurotoxic lesions in the septum and striatum of rats

The psychoneuroendocrine effects of electrolytic septal lesions were compared with neurotoxic lesions in the lateral septum or striatum of rats induced by 6-hydroxydopamine (6-OHDA) or kainic acid (KA). Lesion effects were examined in terms of changes in body weight (BWt) regulation, ovarian compensatory hypertrophy (OCH) and female sexual behavior. Septal injections of 6-OHDA selectively reduced septal levels of dopamine (DA) by 60% whereas striatal injections reduced striatal levels of DA by 77% and septal levels by 30%. Significant effects of these various lesions were relative to controls (1) KA lesions in the septum increased and 6-OHDA lesions in the striatum decreased BWt; (2) 6-OHDA lesions in the striatum reduced ovarian weight and KA lesions in the septum increased OCH; (3) electrolytic septal lesions increased and KA septal lesions decreased female sexual behavior; (4) the effects of estrogen on food intake and BWt were attenuated in KA septal lesioned rats. Since this experiment failed to show an inhibitory role for DA on lordotic behavior, in a second experiment brain levels of DA were depleted by 6-OHDA injections in the ventral tegmental area or substantia nigra. Levels of female sexual behavior for these animals were comparable to controls. Thus, decreases in brain levels of DA previously shown to associated with electrolytic septal lesions may not be causally related to the observed increase in lordotic behavior. Lateral septal damage induced by KA appears to modify a variety of estrogen-sensitive systems.

Compensatory ovarian hypertrophy in the long-term hemicastrate rat: size distribution of growing and atretic follicles.

In the intact rat, on estrus, the follicle-stimulating hormone (FSH) surge recruits nearly twice the correct number of follicles for ovulation, then, on metestrus, the excess follicles undergo atresia. In contrast, in the long-term hemicastrate rat, the FSH surge recruits fewer antral follicles on estrus, but there is little atresia on metestrus. To determine if fewer follicles are recruited by the FSH surge of long-term hemicastrates because the pool of follicles capable of responding to the FSH is smaller than in intact rats, preantral, antral, atretic, and healthy follicles were counted in ovaries of rats killed on each day of the estrous cycle. In general, there were only half as many healthy preantral follicles per rat in hemicastrates compared with intacts. There were an equal number of large antral follicles per rat in hemicastrates compared with intacts. Thus, compensatory hypertrophy did not extend to preantral follicles but was evident in large preovulatory follicles. These results suggest that fewer follicles are recruited on estrus in hemicastrate rats because fewer follicles are at the appropriate stage of development to respond to the FSH surge.