What are target cells in the endocrine system?

What are target cells in the endocrine system?

The endocrine system controls the functioning of our bodies. So does the nervous system. The two systems work in very different ways and they interact with each other. The two systems are sometimes referred to together as the neuroendocrine system. Hormones are chemical messengers that are released into the blood where they are transported to their targets throughout the body. The nervous system activates muscles and glands by means of an electrical signal (an action potential). The hormones released by the endocrine system affect the metabolism of their target cells. Responses to endocrine control are usually slower, but more prolonged than responses to nervous input.

Endocrine glands are ductless glands. They release their hormones directly into the blood. They include the following glands, and if we had time we’d look at them all, their hormones and functions of their hormones:

Pituitary Gland
Thyroid Gland
Parathyroid Glands
Adrenal Glands
The Gonads
Pineal Gland

There are two type of hormones, the water soluble amino acid based hormones and the lipid soluble steroids.
Most hormones are amino acid based hormones. They can range from simple modified amino acids to polypeptides to proteins.

The remainder are steroids, which are synthesized from cholesterol. Gonadal hormones and adrenocortical hormones are the only steroid ones.

Hormones circulate through out the body via the blood, contacting just about all cells. The “target” cells for a particular hormone have receptors, either on the cell membrane, or the case of lipid soluble hormones that can pass through the membrane, inside the cell. Only the cells that have the special receptors for that hormone will respond to exposure.

Hormone-receptor binding triggers the target cell to do what its supposed to. The extent of target cell activation is affected by: levels of hormone in the blood, the amount of receptors for that hormone, and the affinity of the receptor for the hormone.

Target cells may form more receptors in response to reduced exposure to a hormone (called “up-regulation”) or they may lose receptors in response to prolonged exposure (called “down-regulation”).

Hormones work by increasing or decreasing the rates at which target cells to what they do. So the effect of a hormone is directly related to the target cell, and different target cells may have different responses to the same hormone. Typically, hormones cause one or more of the following:

Changes in cell membrane permeability
Synthesis of proteins within a cell
Enzyme activation or deactivation
Induction of secretory activity
Stimulation of mitosis

So the hormone binds to the receptor, so what? How does that do anything? There are two major mechanisms, second-messenger mechanisms and direct gene activation, by which the hormone activates the target cell.

Direct Gene Activation. Steroid hormones pass through plasma membrane (they’re lipid soluble) and attach to receptor molecules that are inside the cell. This combination is now an activated “hormone-receptor complex” which binds to the chromatin (on another receptor site). This “turns on” the specific gene, that is, it initiates the process of transcription (which makes mRNA which is the beginning of protein synthesis). The synthesized protein could be anything. The point is, the presence of the hormone is what got it’s production started.

Second Messenger Systems are called that because the hormone (the 1st messenger) doesn’t enter the cell (too big, usually) but initiates production of a chemical messenger within the cell (second messenger). A molecule known as “cyclic AMP” is a good example of a second messenger, so we’ll talk about it.

Cyclic AMP does something inside the cell. It does a lot, but we’ll skip that for now. Levels of cyclic AMP in the cell are what matter. What happens is this:

The hormone binds to a receptor protein imbedded in the cell membrane.

A “G protein” is activated by this and detaches from the receptor protein. The “G protein” acts as a catalyst.

Whenever it finds an Adenylate Cyclase molecule embedded in the membrane it “tells” the adenylate cyclase molecule to make a cyclic AMP molecule from an ATP molecule.

The hormone is the first “messenger”. Cyclic AMP is the “second messenger”. The G protein is just called an intermediate.
(seems like messenger #2 to me. )

Not all G proteins are stimulatory. Some (resulting from different hormone-receptor combinations) can be inhibitory. In this way cytoplasmic levels of cyclic AMP can be adjusted by pairs of antagonistic hormones.

So what about this cyclic AMP? It diffuses throughout the cytoplasm of the cell, activating enzymes called protein kinases. There can be many different protein kinases in a cell. Protein kinases activate (or deactivate) all kinds of enzymes by phosphorylating them, that is they add phosphates to them.

This whole business is referred to as a “cascade” effect: One hormone molecule can set a G protein on its way to hooking up with many Adenylate Cyclases. These make many cyclic AMPs which go off and activate a whole bunch of different protein kinases which affect all kinds of cellular activity.

The concentration of hormones in the blood, or levels of hormones, reflect the rate of release and speed of inactivation of the hormone. Some are inactivated by destructive enzymes at the target cell, most are removed from the blood by the kidneys and liver.

The “half-life” of a hormone is a term used to describe its persistence in the blood stream. Usually they range from seconds to 30 minutes. Even though the hormone may be just about gone from the blood, some hormones have effects that last hours after blood levels are very low.

Hormones are released by glands when the glands have been stimulated. This stimulation can be humoral, neural, or hormonal.

Humoral stimuli – response to blood levels of ions or nutrients Ex: Ca++ and the release of PTH.

Neural Stimuli – nerve fibers stimulate hormone release from the gland. Ex: Sympathetic simulation of the adrenal medulla causes epinephrine release during stress.