Effect of Intraventricular Infusion of Catecholamines on Luteinizing Hormone Release in Ovariectomized and Ovariectomized, Steroid-Primed Rats

Abstract

This study examined alterations in episodic LH release in response to prolonged, slow infusions of dopamine (DA), norepinephrine (NE), or epinephrine (EPIN) into the third ventricle in adult, ovariectomized (OVX) rats, and the influence of priming with ovarian steroids on the LH response to the catecholamines. Unanesthetized rats with right atrial cannulae were bled continuously at slow rates for 1–1½ h prior to infusion, 1–1½ h during infusion, and up to 1 h afterwards. The amines were protected from oxidation by ascorbic acid, and infused in an artificial cerebrospinal fluid (CSF) vehicle (pH 7.29-7.33) into the third ventricle at a rate of 25–27 μl/h. Blood samples were analyzed for LH by radioimmunoassay. In unprimed, OVX rats, infusions of artificial CSF, as well as low doses of DA (2–4 μg/h) or NE (0.3–0.6 μg/h), had no effect on episodic LH release or mean blood LH levels. However, administration of 8.5 and l7μg DA/h, and 5.5 and 11 μg NE/h, resulted in a decrease in blood LH levels and, in most animals, prolonged intervals between peak blood LH levels during infusion or inhibitions which began rapidly and lasted for nearly the entire infusion period or longer. In contrast, infusion of 5.7 and 11.5 μg EPIN/h had no effect on blood LH levels in unprimed rats. In OVX rats primed 3 days prior to infusion with 50 μg estradiol benzoate and 25 mg progesterone (OEP), administration of CSF or the same doses of DA that previously inhibited episodic LH release had no effect on LH secretion. However, these steroids completely reversed the LH response to 11 μg NE/h, with increases in LH release occurring during infusion. EPIN, in doses ineffective in unprimed rats (5.7 and 11.5 μg/h), also caused elevations in blood LH levels in OEP rats. Finally, in rats primed with 5 μg estradiol benzoate/100 g b.w./day for the 2 days prior to infusion, none of the three neurotransmitters had any effect on LH release. These experiments indicate that in the absence of ovarian steroids intraventricular administration of DA can decrease mean blood LH levels and episodic LH release, and that this amine has no excitatory effect on LH release in steroid-primed rats. In contrast, NE and EPIN increased LH release in OEP rats, suggesting possible excitatory roles for both amines in the regulation of LH secretion. These data also indicate the critical importance of ovarian steroids in determining not only if a neurotransmitter (EPIN) can increase LH release, but also the direction in the LH response to a given neurotransmitter (NE). Finally, in addition to confirming the concept of an excitatory noradrenergic link in the regulation of LH release, studies in nonsteroid primed rats suggest the possible existence of noradrenergic receptors whose activation is subsequently inhibitory to episodic LH secretion.

Suppressive Action of Orexin A on Pulsatile Luteinizing Hormone Secretion Is Potentiated by a Low Dose of Estrogen in Ovariectomized Rats

“…It is therefore obvious that orexin A, as well as NPY, has a biphasic action on LH secretion depending on the endocrine status produced by estrogen. Further study including the biphasic action of noradrenaline [51]and angiotensin II [52], which was reported earlier, is needed to clarify the mechanism.…”

Effects of Diabetes and Estradiol on Norepinephrine Release in Female Rat Hypothalamus, Preoptic Area and Cortex

“…Hypothalamic NE neurotransmission is a critical component in the regulation of female rodent sexual behavior [18, 19, 20, 21]. Specifically, it is believed that an optimal level of released NE acts as a permissive factor by increasing the signal-to-noise ratio of specific synapses [46, 47].…”

“…NE release in the hypothalamus is temporally associated with the display of female reproductive behavior in rats [19]. Moreover, NE turnover and release in the hypothalamus and preoptic area (POA) are critical events for the regulation of luteinizing hormone release and thus of ovulation [20, 21]. Both the timing and magnitude of released hypothalamic NE is believed to be important for the neural regulation of reproductive behavior and the hypothalamic-pituitary-gonadal axis; either increases or decreases in hypothalamic NE release could interfere with the ability of NE to regulate these aspects of reproductive physiology.…”

Estradiol Enhances Prostaglandin E2Receptor Gene Expression in Luteinizing Hormone-Releasing Hormone (LHRH) Neurons and Facilitates the LHRH Response to PGE2by Activating a Glia-to-Neuron Signaling Pathway

“…Surprisingly, central administration of NE to ovariectomized rats or stimulation of a mesencephalic noradrenergic pathway in these animals suppresses LH release, in contrast to the increase seen in estrogen-primed rats (Gallo and Drouva, 1979;Leung et al, 1981Leung et al, , 1982. It is possible that in the absence of estrogen, NE no longer sets in motion stimulatory mechanisms but instead activates pathways inhibitory to LHRH secretion.…”