The ovary responds to FSH and LH in a defined, sequential manner to produce follicular growth, ovulation, and corpus luteum formation. The cycle is designed to produce an optimal environment for pregnancy; if pregnancy does not occur, the cycle begins again.
In the early menstrual cycle the ovary produces estrogen, which is responsible for endometrial growth. Following ovulation, progesterone is also produced in significant quantities, which transforms the endometrium into a form ideal for implantation of the embryo. If no pregnancy occurs, the ovary ceases to produce estrogen and progesterone, the endometrium is sloughed, and the cycle begins again.
The reproductive process in women is a complex and highly evolved interaction of many components. The carefully orchestrated series of events that contributes to a normal ovulatory menstrual cycle requires precise timing and regulation of hormonal input from the central nervous system, the pituitary gland, and the ovary. This delicately balanced process can be disrupted easily and result in reproductive failure, which is a major clinical issue confronting gynecologists. To manage effectively such conditions, it is critical that gynecologists understand the normal physiology of the menstrual cycle. The anatomic structures, hormonal components, and interactions between the two play a vital role in the function of the reproductive system. Fitting together the various pieces of this intricate puzzle will provide “the big picture”: an overview of how the reproductive system of women is designed to function.
Neuroendocrinology represents facets of two traditional fields of medicine: endocrinology, which is the study of hormones (i.e., substances secreted into the bloodstream that have diverse actions at sites remote from the point of secretion), and neuroscience, which is the study of the action of neurons. The discovery of neurons that transmit impulses and secrete their products into the vascular system to function as hormones, a process known as neurosecretion, demonstrates that the two systems are intimately linked. For instance, the menstrual cycle is regulated through the feedback of hormones on the neural tissue of the central nervous system (CNS).
Hypothalamus The hypothalamus is a small neural structure situated at the base of the brain above the optic chiasm and below the third ventricle (Fig. 7.1). It is connected directly to the pituitary gland and is the part of the brain that is the source of many pituitary secretions. Anatomically, the hypothalamus is divided into three zones: periventricular (adjacent to the third ventricle), medial (primarily cell bodies), and lateral (primarily axonal). Each zone is further subdivided into structures known as nuclei, which represent locations of concentrations of similar types of neuronal cell bodies (Fig. 7.2).
The hypothalamus is not an isolated structure within the CNS; instead, it has multiple interconnections with other regions in the brain. In addition to the well-known pathways of hypothalamic output to the pituitary, there are numerous less well-characterized pathways of output to diverse regions of the brain, including the limbic system (amygdala and hippocampus), the thalamus, and the pons (1). Many of these pathways form feedback loops to areas supplying neural input to the hypothalamus.
Several levels of feedback to the hypothalamus exist and are known as the long, short, and ultrashort feedback loops. The long feedback loop is composed of endocrine input from
Figure 7.1 The hypothalamus and its neurologic connections to the pituitary.
Figure 7.2 The neuronal cell bodies of the hypothalamus.
circulating hormones, just as feedback of androgens and estrogens onto steroid receptors is present in the hypothalamus (2,3). Similarly, pituitary hormones may feed back to the hypothalamus and serve important regulatory functions in short-loop feedback. Finally, hypothalamic secretions may directly feed back to the hypothalamus itself in an ultrashort feedback loop.
The major secretory products of the hypothalamus are the pituitary-releasing factors (Fig. 7.3): 1.