Reproductive Hormonal Regulation

Now we continue with the reproductive system by focusing on the male system. And in particular, we're interested in contrasting what we've learned about the female control of the production of gametes to what occurs in the male system. Now I mentioned early on how the timing of events in the gametogenesis differs between males and females. Whereas females contain... The cells that ultimately produce the eggs, all of the cells that one will have in a lifetime, are within the ovaries upon birth, so that embryonic development includes the creation of these replicated cells that will then undergo meiosis 1 and meiosis 2 once a month that begins at puberty. In the male system, we have something very different in terms of timing. So there are a number of mitotic divisions during embryonic development, and those freeze upon birth and resume at puberty. So all through adulthood, we have mitotic divisions producing lots of germ cells that then each of which produce four sperm. So the timing of gametogenesis differs with gender, and that brings us to the question that we're focused on in this lecture, which is how... does the control of gametogenesis differ? Okay, what is it about the hormonal control in males that contrasts that in females? Now, all the details of our previous lecture on the female gametogenesis produces oscillations in luteinizing hormone and follicle stimulating hormone that looks something like this. So this is highly schematized. Because between puberty and menopause, there are many, many more of these cycles. But this is to indicate how you have these LH surges at ovulation and oscillations and follicle-stimulating hormone as well. And those serve to shepherd each of those oocytes, the cells that produce ultimately what becomes the egg. They shepherd them through one at a time. the process of producing the egg that ovulates and then makes its way through the fallopian tubes. Now prior to these events, that is during childhood up until puberty, there are none of these monthly oscillations. There is instead a much more long-term variation in follicle stimulating hormone and luteinizing hormone. Now I mentioned how in the luteal phase, so this is after ovulation, that the brain centers, the hypothalamus and the anterior pituitary, are inhibited by estrogens and progesterone. And that is what occurs during childhood. So this negative feedback loop explains how the brain responds to estrogen and progesterone. And that's what maintains FSH and LH at a low concentration. Okay, so this is what the control diagram looks like at this point in time, childhood. Now, over the course of embryonic development, and I should say between birth and the end of infancy, there are oscillations in these hormones that I... I'm not going to explain right now, but they're related to stimulating the production of those replicated cells. So there is another sort of similar surge that occurs up to six months. And then we have this low level maintained for this negative feedback loop in infancy. OK, so the details of these oscillations are outside our current scope. but they are related to what occurs in the cells up above. Now, during menopause at 50 years old, females cease to become fertile. The production of estrogen and progesterone in the ovaries halts because essentially the fecal and granulosa cells are removed from the equation. what occurs is essentially a release of the effects. of those cells. So instead of producing estrogens and progesterone, those concentrations go down. And as a consequence, the negative feedback that occurs during the luteal phase ceases to be present. And if we don't have negative feedback on these brain centers, then that causes FSH and LH to increase. And so after menopause, menopause itself can be associated with a variety of symptoms like hot flashes and there are these hormonal changes that trigger other secondary symptoms. And eventually we don't, we're not in a situation where a follicle stimulating hormone is stimulating the production of follicles any longer, but it remains at a high concentration. Okay, so all of this has echoes in the male reproductive system, but we'll see that the concentration and of hormones is quite different. In males, testosterone is an important hormone. It has influence on the development of sexual characteristics, secondary sexual characteristics like hair growth and other things, but it also is related to the production of gametes. And we see during embryonic development that this increase in plasma testosterone at very high levels occurs and is correlated with the mitotic divisions of the germ cells. Then we have during childhood, testosterone at a very low level and that is interrupted during puberty where we see a large increase in testosterone and then it's just maintained. And you can think of testosterone as being reflective of the situation in males where the goal of The yammy production is really to produce as many sperm as possible, and that is stimulated by this high concentration of testosterone that is maintained until senescence occurs very late in life. So this you can think of almost as being the sperm production curve because testosterone is stimulating all of those stages that I mentioned earlier, the mitotic divisions and then the two stages of meiosis that produce the spermatozoa. So let's consider the control that facilitates this increase and the implications of the increase in testosterone. So during puberty, we have that increase in testosterone that we see in red. Correlated with that event is changes in the same hormones that we saw in the release by the anterior pituitary in females, that is the luteinizing hormone. and the follicle-stimulating hormone. These were initially discovered in females, giving them their name. There are no follicles in males, but we see those same hormones in the male system, and they have a similar role as well. So if we focus in on the cross-section of a seminiferous tubule, then we can highlight two cells that are very similar to the roles played by the granulosa cells and the fecal cells in the female system. In the case of males, those two cell types are called the Leydig cells. They're responsible for secreting testosterone. So we're going to start to build our control system for males on the right. We've got the Leydig cells doing that function. The Leydig cells respond to luteinizing hormone that is secreted just like in females, by the anterior pituitary. The anterior pituitary is stimulated by a gonadotropin-releasing hormone that comes from the hypothalamus. Okay, so not only are these events correlated, but there's causation here. This luteinizing hormone increase drives the increase in testosterone because the luteinizing hormone stimulates the Leydig cells. Okay, so those are the superficial cells that we're concerned with. We also have another cell type that aids and you can think of as being sort of controllers of the gametogenesis. And in males we refer to gametogenesis as spermatogenesis because it's producing sperm. And that cell type is called the Sertoli cells. So the Sertoli cells are essentially support cells that regulate spermatogenesis and they respond to follicle stimulating hormone and testosterone. So luteinizing hormone I'm sorry, the Leydig cells are communicating with the Sertoli cells through the secretion of testosterone. Testosterone has a variety of effects on the body and so it's not just that interaction that testosterone is good for, but it does indeed stimulate the production of sperm, spermogenesis. All right, now this is the complete control system for puberty. All right, so when we have a change in testosterone, then it's just merely these events that are stimulating that. So you have a change in the exact initiation of the secretion of FSH and LH is a topic for another lecture. We're just going to take it for granted that something stimulates the anterior pituitary to begin this action. So the release of FSH and LH. Now, During adulthood, as we see in the graph up above, plasma testosterone is maintained. And whenever you have the maintenance of something, you should expect a negative feedback loop because we don't want just positive feedback that drive testosterone towards infinity. Instead, we see that it's maintained at a particular level, a set point, if you will. So the way that that negative feedback works is The Sertoli cells secrete a hormone called inhibin, which inhibits. And in particular, it has a negative feedback on the hypothalamus, similar to the way that estrogen plays that role in the female system. Testosterone does the same thing. So testosterone has a negative feedback on the Leydig cells. It also has a negative feedback on the hypothalamus, which has all these downstream effects as well. So FSH and LH, as not shown here, also level off over adulthood and maintain a stable concentration. Okay, so there are similar players from the female system with some important differences, and we do not see... the kind of complexity of monthly changes in the nature of the control system like you see in the female system, which is necessary in the case of females to control the production of individual eggs one at a time each month. And in this case, spermatogenesis is a constant signal which tells the germ cells to just continually produce sperm all through adulthood. Okay, so we return to the female system and we can see that this schematic provides the answer to our question that we set out to address. How does the control of gametogenesis differ? Well, it differs in these respects. It's not just in the timing of the events of mitotic and meiotic divisions, but how those are mediated by these hormones and the others that I've talked about. So whereas testosterone maintains a constant production. of spermatozoa throughout adulthood in males. In females, we have this monthly cycling that controls the production of individual eggs.

Whereas females contain... The cells that ultimately produce the eggs, all of the cells that one will have in a lifetime, are within the ovaries upon birth, so that embryonic development includes the creation of these replicated cells that will then undergo meiosis 1 and meiosis 2 once a month that begins at puberty. In the male system, we have something very different in terms of timing.

So there are a number of mitotic divisions during embryonic development, and those freeze upon birth and resume at puberty. So all through adulthood, we have mitotic divisions producing lots of germ cells that then each of which produce four sperm. So the timing of gametogenesis differs with gender, and that brings us to the question that we're focused on in this lecture, which is how...

does the control of gametogenesis differ? Okay, what is it about the hormonal control in males that contrasts that in females? Now, all the details of our previous lecture on the female gametogenesis produces oscillations in luteinizing hormone and follicle stimulating hormone that looks something like this. So this is highly schematized. Because between puberty and menopause, there are many, many more of these cycles.

But this is to indicate how you have these LH surges at ovulation and oscillations and follicle-stimulating hormone as well. And those serve to shepherd each of those oocytes, the cells that produce ultimately what becomes the egg. They shepherd them through one at a time. the process of producing the egg that ovulates and then makes its way through the fallopian tubes. Now prior to these events, that is during childhood up until puberty, there are none of these monthly oscillations.

There is instead a much more long-term variation in follicle stimulating hormone and luteinizing hormone. Now I mentioned how in the luteal phase, so this is after ovulation, that the brain centers, the hypothalamus and the anterior pituitary, are inhibited by estrogens and progesterone. And that is what occurs during childhood.

So this negative feedback loop explains how the brain responds to estrogen and progesterone. And that's what maintains FSH and LH at a low concentration. Okay, so this is what the control diagram looks like at this point in time, childhood. Now, over the course of embryonic development, and I should say between birth and the end of infancy, there are oscillations in these hormones that I...

I'm not going to explain right now, but they're related to stimulating the production of those replicated cells. So there is another sort of similar surge that occurs up to six months. And then we have this low level maintained for this negative feedback loop in infancy. OK, so the details of these oscillations are outside our current scope.

but they are related to what occurs in the cells up above. Now, during menopause at 50 years old, females cease to become fertile. The production of estrogen and progesterone in the ovaries halts because essentially the fecal and granulosa cells are removed from the equation.

what occurs is essentially a release of the effects. of those cells. So instead of producing estrogens and progesterone, those concentrations go down.

And as a consequence, the negative feedback that occurs during the luteal phase ceases to be present. And if we don't have negative feedback on these brain centers, then that causes FSH and LH to increase. And so after menopause, menopause itself can be associated with a variety of symptoms like hot flashes and there are these hormonal changes that trigger other secondary symptoms. And eventually we don't, we're not in a situation where a follicle stimulating hormone is stimulating the production of follicles any longer, but it remains at a high concentration.

Okay, so all of this has echoes in the male reproductive system, but we'll see that the concentration and of hormones is quite different. In males, testosterone is an important hormone. It has influence on the development of sexual characteristics, secondary sexual characteristics like hair growth and other things, but it also is related to the production of gametes.

And we see during embryonic development that this increase in plasma testosterone at very high levels occurs and is correlated with the mitotic divisions of the germ cells. Then we have during childhood, testosterone at a very low level and that is interrupted during puberty where we see a large increase in testosterone and then it's just maintained. And you can think of testosterone as being reflective of the situation in males where the goal of The yammy production is really to produce as many sperm as possible, and that is stimulated by this high concentration of testosterone that is maintained until senescence occurs very late in life. So this you can think of almost as being the sperm production curve because testosterone is stimulating all of those stages that I mentioned earlier, the mitotic divisions and then the two stages of meiosis that produce the spermatozoa.

So let's consider the control that facilitates this increase and the implications of the increase in testosterone. So during puberty, we have that increase in testosterone that we see in red. Correlated with that event is changes in the same hormones that we saw in the release by the anterior pituitary in females, that is the luteinizing hormone. and the follicle-stimulating hormone. These were initially discovered in females, giving them their name.

There are no follicles in males, but we see those same hormones in the male system, and they have a similar role as well. So if we focus in on the cross-section of a seminiferous tubule, then we can highlight two cells that are very similar to the roles played by the granulosa cells and the fecal cells in the female system. In the case of males, those two cell types are called the Leydig cells. They're responsible for secreting testosterone.

So we're going to start to build our control system for males on the right. We've got the Leydig cells doing that function. The Leydig cells respond to luteinizing hormone that is secreted just like in females, by the anterior pituitary. The anterior pituitary is stimulated by a gonadotropin-releasing hormone that comes from the hypothalamus.

Okay, so not only are these events correlated, but there's causation here. This luteinizing hormone increase drives the increase in testosterone because the luteinizing hormone stimulates the Leydig cells. Okay, so those are the superficial cells that we're concerned with. We also have another cell type that aids and you can think of as being sort of controllers of the gametogenesis. And in males we refer to gametogenesis as spermatogenesis because it's producing sperm.

And that cell type is called the Sertoli cells. So the Sertoli cells are essentially support cells that regulate spermatogenesis and they respond to follicle stimulating hormone and testosterone. So luteinizing hormone I'm sorry, the Leydig cells are communicating with the Sertoli cells through the secretion of testosterone.

Testosterone has a variety of effects on the body and so it's not just that interaction that testosterone is good for, but it does indeed stimulate the production of sperm, spermogenesis. All right, now this is the complete control system for puberty. All right, so when we have a change in testosterone, then it's just merely these events that are stimulating that.

So you have a change in the exact initiation of the secretion of FSH and LH is a topic for another lecture. We're just going to take it for granted that something stimulates the anterior pituitary to begin this action. So the release of FSH and LH. Now, During adulthood, as we see in the graph up above, plasma testosterone is maintained. And whenever you have the maintenance of something, you should expect a negative feedback loop because we don't want just positive feedback that drive testosterone towards infinity.

Instead, we see that it's maintained at a particular level, a set point, if you will. So the way that that negative feedback works is The Sertoli cells secrete a hormone called inhibin, which inhibits. And in particular, it has a negative feedback on the hypothalamus, similar to the way that estrogen plays that role in the female system.

Testosterone does the same thing. So testosterone has a negative feedback on the Leydig cells. It also has a negative feedback on the hypothalamus, which has all these downstream effects as well.

So FSH and LH, as not shown here, also level off over adulthood and maintain a stable concentration. Okay, so there are similar players from the female system with some important differences, and we do not see... the kind of complexity of monthly changes in the nature of the control system like you see in the female system, which is necessary in the case of females to control the production of individual eggs one at a time each month.

And in this case, spermatogenesis is a constant signal which tells the germ cells to just continually produce sperm all through adulthood. Okay, so we return to the female system and we can see that this schematic provides the answer to our question that we set out to address. How does the control of gametogenesis differ?

Well, it differs in these respects. It's not just in the timing of the events of mitotic and meiotic divisions, but how those are mediated by these hormones and the others that I've talked about. So whereas testosterone maintains a constant production. of spermatozoa throughout adulthood in males. In females, we have this monthly cycling that controls the production of individual eggs.

Transcript for:Reproductive Hormonal Regulation

Transcript for:
Reproductive Hormonal Regulation