Communication: The Nervous and Endocrine Systems

(D. Facey, S. Wellens, B. Weeks, K. Tatro, M. Fitzgibbons, D. Koehler, R. Pouliot, R. Bailey )

(presented by Saint Michael's College, Colchester, VT, USA.)

 

The Nervous System

The nervous system collects and processes information, analyzes it, and generates coordinated output to control complex behaviors. The nervous system also is partly responsible for homeostasis. It works in conjunction with the endocrine system by employing nerve impulses and by responding rapidly to stimuli to adjust body processes.

 

What is the general organization of the Nervous System?

The nervous system is broken down into two major systems the Central Nervous System and the Peripheral Nervous System. These two systems are in control of sensory input, integration, and motor output. The Central Nervous system is made up of mainly the brain and spinal cord. The CNS is in control of the input from sensory receptors from the chemical and electrical signals sent from the PNS. The CNS takes the information and integrates it, then sends out the necessary motor output to the effector cells of the body.

The PNS is divided into two systems as well, the Somatic Nervous System, and the Autonomic Nervous System. The SNS consists of sensory neurons that send information from cutaneous and special sensor receptors in the head, body wall, and extremities to the CNS where the information is integrated and sent back out via motor neurons to skeletal muscles. The sensory neurons convey input from receptors from senses like vision, hearing, taste, smell and others. They also convey input from proprioceptors and general somatic receptors (pain, temperature, and tactile sensations). Motor neurons innervate skeletal muscle and produce voluntary movement. The ANS sends information from sensory neurons to viscera of the CNS. In the ANS the CNS sends information through motor neurons to smooth muscles, cardiac muscles and glands. The ANS is controlled by the hypothalamus and medulla oblongata of the brain, which regulate the smooth muscle, cardiac muscle, and specific glands.

The output portion of the autonomic nervous system further breaks down into two divisions, the sympathetic and parasympathetic. The parasympathetic division is the energy control center; it regulates energy through conservation and restoration. The sympathetic division is in charge of the flight of fight responses of the body. It is in charge of the excitatory processes of the body. This division is in charge of the usage of energy.

In summary, the nervous system has three overlapping functions. These functions are sensory input, integration, and motor output. Input is the conduction of signals from sensory receptors to integration centers of the nervous system. Integrating the information requires that the sensations triggered by environmental stimulation of receptors be interpreted and associated with appropriate responses of the body. Motor output is the conduction of signals from the brain or other processing center of the nervous system to effector cells. Effector cells are the muscle cells or gland cells that actually perform the body’s responses to stimuli.

 

What are neurons?

Neurons come in a variety of sizes and shapes, but they all have basically the same functional regions. Signals from other neurons or sensory cells are received on the dendrites and cell body (soma) and cause localized changes in membrane polarization. The electrical changes spread across the cell body and are combined at the axon hillock, located at the base of the axon. This is the region responsible for generating action potentials, which then travel quickly along the axon and its branches to the terminal knobs - small swollen areas at the end of the axon branches. Here the neuron interfaces with other cells at junctions called synapses through which signals are transmitted. Neurons that bring signals to the central nervous system (the brain and spinal cord) are referred to as sensory neurons, whereas those that carry signals from the central nervous system to the rest of the body are called motor neurons. Within the central nervous system there are also small, highly branched interneurons that help neurons communicate with one another. The axons of some vertebrate neurons have a fatty myelin sheath formed by supporting Schwann cells. This sheath helps support the fine axon and also increases the conduction velocity of nerve impulses (action potentials) - (see question below).

 

What are the supporting cells and what are their functions?

The supporting cells outnumber neurons tenfold to fiftyfold in the nervous system. They are essential for the structural integrity of the nervous system and for the normal functioning of neurons. They provide intimate structure and perhaps metabolic support for neurons.

There are different types in the body. Oligodendrocytes, are located in the CNS. Schwann cells of the peripheral nervous system wrap each axon in an insulating myelin sheath, which contributes to assuring reliable and rapid transmission of action potentials.

Although some glial cells have voltage-gated ion channels in their membranes, glial cells generally do not produce action potentials and their role in the nervous system has long been a puzzle. One suggestion has been that glial cells help to regulate the concentration of K+ and the pH in the extracellular fluid of the nervous system. Glial cell membranes are highly permeable to K+ and adjacent glial cells are often electrically coupled by junctions that allow K+ to flow between them. This flux permits glial cells to take up and redistribute extracellular K+, which otherwise could build up to high concentrations in narrow extracellular spaces following activity in neurons. Glial cells also may take up neurotransmitter molecules from the extracellular space, thereby limiting the amount of time a neurotransmitter could be active at synapses.

 

What is electrochemical equilibrium?

All living cells maintain some differences between the concentration of ions and other solutes inside and outside the cell. This is the purpose of a cell membrane in the first place - to help maintain differences between the inside and the outside. The combination of differences in the chemical concentrations of solutes and the distribution of the charges of the ions establishes an electrochemical gradient between the inside and outside of the cell membrane. If the chemical concentration gradients are offset by a difference in the distribution of electrical charges so that no net movement of ions takes place, we have a condition known as electrochemical equilibrium.

In this equilibrium condition any tendency of solutes to diffuse down their respective concentration gradients (from high to low concentration) is regulated by not only the difference in chemical concentration and by their electrical attraction to or repulsion by other charged molecules, but also their ability to pass through the cell membrane. Lipid soluble molecules can pass through the cell membrane. Molecules that are not lipid soluble must pass through channels in the membrane, and are therefore limited by the size and number of these channels.

When in electrochemical equilibrium, living cells have a net negative charge along the inside of the cell membrane. This is due primarily to the surplus of large negatively charged molecules, such as proteins, in the cytoplasm. These large molecules cannot diffuse down their concentration gradient and move to the outside of the cell because they are too big to pass through small channels in the cell membrane. The surplus of these large negatively charged ions inside the cell tends to repel other negatively charged ions, such as chloride, resulting in a higher concentration of these smaller negatively charged ions on the outside of the cell. Meanwhile, an ion pump actively transports positively charged sodium ions from the inside to the outside of the cell, creating a surplus of sodium ions outside the cell membrane. The ion pump does exchange some potassium (also positively charged) for the sodium, but it is an uneven exchange, with the amount of sodium leaving the cell exceeding the amount of potassium being brought in. Sodium and potassium ions are small enough to slowly diffuse down their chemical concentration gradients by passing through small channels in the cell membrane, but the ion pump keeps up with this slow leakage and maintains the electrochemical equilibrium. The result of all of this is that the ion pump maintains an equilibrium condition in which there is more sodium outside the cell, more potassium inside the cell, and the inside of the cell has a net negative charge with respect to the outside.

This balance between electrical and chemical gradients and the regulation of the passage of these ions back and forth is what distinguishes a living cell from an inert bag of ions. It also permits certain cells to respond to stimuli.

 

What is membrane potential? How is it related to an action potential?

The difference in electrical charge between the two sides of a cell membrane is known as the membrane potential. When a cell is not being stimulated, and is therefore "at rest", we refer to the membrane potential as the resting potential. If a cell becomes stimulated, perhaps by some mechanical or chemical disturbance, the permeability of the cell membrane can be momentarily affected resulting in a temporary change in the electrochemical balance. Most cells in an animal's body don't show much of a response to such a stimulus, other than to reestablish electrochemical equilibrium. Some cells, however, show a dramatic, active response at the level of the cell membrane that results in a momentary but striking reversal of charge distribution known as an action potential. This ability to generate action potentials is what makes certain cells excitable, and it is these excitable cells that are responsible for sensory, nerve, and muscle function.

Stimuli alter the permeability of the cell membrane by causing ion channels to open. For example, a slight stimulus may cause some sodium channels to open. With this route now available, sodium ions flow rapidly into the cell, driven by their own concentration gradient and the attraction of the excess negative ions. The sodium-potassium pump still is transporting some sodium out of the cell, but it is overwhelmed by this rapid influx of sodium ions. This results in a decrease in the electrical potential difference between the inside and the outside of the cell, so the membrane potential decreases (depolarization). If the sodium channels now close, the ion pump will reestablish electrochemical equilibrium.

In excitable cells, the sodium gates may not close right away, however. If the membrane potential becomes altered to a critical level, known as the "threshold potential", more sodium gates will open, thereby allowing even more sodium to flow into the cell even more rapidly. These sodium channels open in response to voltage change across the membrane. Therefore, they are referred to as voltage-regulated channels. As more sodium flows in, more sodium gates open, and so on. This example of positive feedback to rapidly allow more sodium into the cell is called the Hodgkin cycle. The net result of this rapid influx of sodium ions is that the inside of the cell has now become positive with respect to the outside. In this extremely depolarized condition the cell membrane cannot respond to another stimulus until its original polarity is reestablished. This extreme depolarization event is very brief, however, because the sodium gates close when the membrane potential reaches a certain point, preventing any further sodium influx. The cell membrane then "repolarizes" by opening potassium gates (also voltage-regulated) and allowing potassium ions to flow out, driven by their concentration gradient and the repulsion of the positively charged sodium ions that are now abundant inside the cell . The sodium-potassium pump could repolarize the membrane, but it would take too long to be biologically useful. This rapid repolarization of the cell membrane reestablishes the resting potential of the cell, and puts the cell in a condition where it now can respond to another stimulus. Gradually, the sodium-potassium exchange pump will move sodiums out and potassiums in, thereby reestablishing the original ion distribution.   This brief exchange of sodium and potassium ions only affects those ions immediately adjacent to the cell membrane.  It does not have a significant impact on the overall intracellular and extracellular concentration of sodium or potassium.

The rapid depolarization and repolarization of the membrane of an excitable cell is called an "action potential", and it is important to understand this series of events in order to understand the events involved in the functioning of the nervous system.

 

How do neurons receive and integrate signals?

The reception of signals from other neurons or sensory cells causes a small change in the membrane potential at the site of the synapse. These changes in membrane potential are proportional to the intensity of the stimulus (graded potentials) and are referred to as postsynaptic potentials (PSPs) because they occur on the postsynaptic (receiving) membrane. These PSPs spread outward from the synapse and across the membrane of the dendrites and cell body. As they spread they may encounter and combine with PSPs from other synaptic junctions that also are being stimulated. (At any given moment a neuron may be receiving stimuli from many different sources.) The PSPs are continually being combined in the axon hillock, and if at any given moment the sum of all of the PSPs is sufficient to bring the membrane potential of the axon hillock to its threshold, an action potential is generated. If the summation of the PSPs fails to reach threshold, an action potential will not be generated.

 

Are all postsynaptic potentials excitatory?

No - postsynaptic potentials can be either excitatory (EPSPs) or inhibitory (IPSPs). EPSPs depolarize the postynaptic membrane, often by increasing the inward flow of sodium, thereby increasing the number of positive charged ions on the inside of the cell membrane. This results in a decrease in the voltage difference across the membrane, bringing the membrane potential of the axon hillock closer to threshold. This increases the likelihood that an action potential will be generated, which is why these depolarizing PSPs are called excitatory.

IPSPs, however, hyperpolarize the postsynaptic membrane, often by increasing the leakage of potassium ions out of the cell or increasing the flow of chloride ions into the cell. This increases the voltage difference across the membrane, and pushes the membrane potential further from the threshold voltage. This decreases the likelihood that an action potential will be generated, which is why these hyperpolarizing PSPs are called inhibitory.

 

How is an action potential generated and propagated along an axon?

The generation of an action potential involves the rapid depolarization and repolarization of the cell membrane. If an action potential is generated, the Hodgkin cycle assures that it is of maximal force, regardless of whether the sum of all PSPs greatly exceeded threshold or was just barely strong enough to reach threshold. This gives action potentials and "all-or-none" property. In other words, if threshold is reached or exceeded, the action potential will be maximal; if threshold is not reached an action potential will not be generated. There is no in-between at the level of the individual neuron. (Nerves are bundles of neurons and can show different levels of response because the individual neurons may exhibit different thresholds.)

If an action potential is generated at the axon hillock it now will spread quickly along the axon as a "wave" of depolarization. An important property of action potentials is that they do not lose intensity as they travel because they are regenerated as they move along the axon. This regeneration of the action potential occurs because the depolarization of one region of the axon depolarizes the adjacent region and brings it to its threshold, thereby generating another action potential. In axons that lack a fatty, insulating myelin sheath, this propagation of the action potential occurs continuously along the length of the axon. The opening and closing of the appropriate ion gates slows the signal down somewhat, but the signal's intensity does not diminish as it travels.

 

What is the role of a myelin sheath in action potential propagation?

Most vertebrate axons do have a myelin sheath, however, which helps the signal move more quickly by limiting action potential regeneration to the nodes of Ranvier. Action potentials can occur only where the axon cell membrane is in close contact with extracellular fluid. Therefore areas of the axon covered with a myelin sheath cannot regenerate action potentials. They can, however, rapidly conduct an electrical field to the next exposed section of axon membrane - the next node of Ranvier. Here the action potential is regenerated and transmitted further along the axon. Because fewer regeneration events take place, the signal moves more quickly than if the myelin were not present. The myelin sheath, then, increases the conduction velocity of an axon.

 

How does axon diameter affect the velocity of an action potential?

Another way to increase conduction velocity is to increase the diameter of an axon. As in electrical wires, there is some resistance to current flow along the periphery. Increasing the diameter of a wire increases the proportional cross-sectional area of the wire that is not in direct contact with the periphery, thereby decreasing the effect of peripheral resistance. In other words, more charge can flow quickly because proportionally less is slowed by peripheral resistance. Large diameter axons, therefore, can transmit action potentials faster than those with small diameters. Some invertebrates have very large diameter non-myelinated axons responsible for rapid reflexes. For example, the "giant axon" associated with the stellate ganglion of squid is responsible for the rapid contraction of the mantle which provides jet propulsion for squid escaping a predator.

Large diameter axons with myelin sheaths can transmit action potentials extremely fast. The Mauthner cells in fishes have among the highest conduction velocity known among the vertebrates (50 to 100 m/s). These large-diameter, myelinated neurons are responsible for the startle response that helps a fish rapidly curl its body and flick its tail, resulting in rapid movement away from a stimulus (think of this the next time that you tap on the side of an aquarium).

 

How are nerve impulses carried across synapses?

When an action potential reaches the end of a neuron, the signal is transmitted to another cell, such as a muscle cell or another neuron. The area of signal transmission is called a synapse, and these come in two general varieties - electrical and chemical. In electrical synapses the presynaptic (transmitting) and postsynaptic (receiving) membranes are in direct contact with one another and small channels permit ions to flow through almost as if there was no barrier at all. Electrical synapses, therefore, transmit signals very rapidly.

Chemical synapses, which are more common, require the release of a chemical transmitter substance by the presynaptic membrane in order to stimulate the postsynaptic membrane. There are two types of chemical syapses - fast (direct) and slow (indirect). In both types, the arrival of the action potential at the presynaptic knob results in an opening of calcium channels on the presynaptic membrane. The resulting influx of calcium ions causes vesicles of transmitter substance to bind to the presynaptic membrane and release their contents.

In a fast chemical synapse, molecules of transmitter substance diffuse from the presynaptic membrane across the synaptic cleft and bind to receptor molecules on the postsynaptic membrane. These receptor proteins also form the ion channel, and the binding of the neurotransmitter directly alters the configuration of the proteins and opens the ion channels of the postsynaptic membrane.  (This is why these channels are referred to ligand-gated channels.) This allows molecules such as sodium to move across the membrane and alter its membrane potential, creating postsynaptic potentials.

In a slow chemical synapse, the binding of the neurotransmitter to a receptor on the cell membrane activates nearby G-proteins. This catalyzes a series of reactions that results in the release of another molecule (a second messenger) which binds to the proteins that form an ion channel. This alters the configuration of the channel, thereby opening it and allowing ions to flow through. This is an indirect, and therefore slower, mechanism because it requires a series of biochemical reactions. Transmission at slow chemical synapses is slower, longer lasting, and may be more widespread spatially than the rapid, localized and immediate response seen at fast chemical synapses. Both types of synapses may be found on the dendrites or soma of a receiving neuron, and the effects of slow synapses may play a role in modulating the effects of a fast synapse by altering the membrane potential of the postsynaptic membrane.

Molecules of transmitter substances in the synaptic cleft and those bound to receptor molecules on the postsynaptic membrane are quickly broken down by enzymes. This is important for two reasons. First, the resulting components are taken up by the presynaptic membrane and recycled to produce more transmitter substance. Second, the postsynaptic membrane must be relieved of the stimulation by the transmitter substance molecules so that it can reestablish its resting potential. If transmitter substance molecules remained bound to their receptor sites, the associated ion channels would remain open and the receiving cell could not function properly.

 

How do neurotoxins affect nerve function?

Understanding the cellular mechanisms of the nerve function helps us understand ways in which certain neurotoxins have their effects. Inhibition of proper nerve function can lead to death, often due to respiratory paralysis. Tetrodotoxin, the toxin from the viscera of puffer fish (Tetraodontiformes) binds to the extracellular surface of the proteins that make up sodium channels. This blocks the sodium channel, thereby inhibiting the proper function of neurons or other excitable cells. Saxitoxin, a paralytic shellfish toxin produced by some dinoflagellates responsible for "red tides", has the same specific effect as tetrodotoxin. The venom of the krait, one of the highly poisonous cobra snakes, contains alpha-bungarotoxin, which binds irreversibly to a particular group of neurotransmitter receptors, thereby inactivating them. The toxin responsible for botulism, which is produced by the bacterium Clostridium botulinum, prevents the release of an important group of neurotransmitters from their vesicles, thereby preventing neurotransmission.

 

The Endocrine System

The endocrine system is the internal system of the body that deals with chemical communication by means of hormones, the ductless glands that secrete the hormones, and those target cells that respond to hormones. The endocrine system functions in maintaining the basic functions of the body ranging from metabolism to growth. The endocrine system functions in long term behavior and works in conjunction with the nervous system in regulating internal functions and maintaining homeostasis.

What are hormones?

Hormones are the chemical messengers released by specialized endocrine cells or specialized nerve cells called neurosecretory cells. Hormones are released by the endocrine system glands into the body’s fluids, most often into the blood and transported throughout the body. Hormones are specified by their different chemical structures which can be classified into four categories…

Amines: are small molecules originating from amino acids. Examples of this are epineprine and thyroid hormones.

Prostaglandins:are cyclic unsaturated hydroxy fatty acids synthesized in membranes from 20 carbon fatty acid chains

Steroid hormones: are cyclic hydrocarbon derivatives synthesized in all instances from the precursor steroid cholesterol. Examples of this are testosterone and estrogen.

Peptide and Protein hormones: are the largest and most complex hormone. Example of this is insulin.

Hormones drive the endocrine system and without them the body could not function. Hormones are the communicators of the endocrine system and are responsible for maintaining and controlling cellular activity.

 

How do hormones function?

Hormones regulate bodily functions and are specific in what responses they elicit. As hormones are released into the bloodstream they can only initiate responses in target cells, which are specifically equipped to respond. Each hormone due to its chemical structure is recognized by those target cells with receptors compatible with their structure. Once a hormone is released, the first step is the specific binding of the chemical signal to a hormone receptor, a protein within the target cell or built into the plasma membrane. The receptor molecule is essential to a hormones function. The receptor molecule translates the hormone and enables the target cell to respond to the hormones chemical signal. The meeting of the hormone with the receptor cell initiates responses from the target cell. These responses vary according to target cell and lipid solubility.

Hormones are either lipid-soluble or lipid-insoluble, depending on their biochemical structure.  The lipid solubility of the hormone determines the mechanism by which it can affect its target cell.

Lipid-soluble hormones are able to penetrate through the cell membrane and bind to receptors located inside the cell. Such hormones diffuse across the plasma membrane and target those receptor cells found within the cytoplasm. Lipid-soluble hormones target the cytoplasmic receptors which readily diffuse into the nucleus and act on the DNA, inhibiting and stimulating certain proteins. DNA function is of great influence over the cellular activities of the body and therefore such hormonal-DNA interaction can have effects as long as hours and in some cases days. Two known types of lipid soluble hormones are steroids and thyroid hormones. Both travel over long courses of time via the bloodstream and both directly effect DNA functions.

Those hormones which are lipid-insoluble are unable to penetrate through the plasma membrane and function with their target cells in a much different and complex manner. Lipid-insoluble hormones must bind with cell-surface receptors which follow a different path involving a second messenger. The hormone's inability to penetrate the membrane requires a second messenger which translates the outer message and functions within the cell.

Once a lipid-insoluble hormone binds with a cell surface receptor, its’ signal is translated into the cell by specific secondary messengers. There are three known and accepted secondary messengers which vary in structure and function, but all three carry out the external signal internally. The three known secondary messengers are (1) cyclic nucleotide compounds (cNMPs), cAMP, and cGMP; (2) inositol phospholipids; and (3) Ca2+ ions. After a hormone binds with a receptor molecule it via a transducer protein sends the hormones signal through the membrane. The protein receptor initiates the formation of a second messenger, whether it be it be cAMP or an inositol phospholipid, which then binds to an internal regulator. The internal regulator controls the target cells’ response to the hormone's signal.

Each different type of secondary messenger evokes different responses by those cells they affect. cAMP has wide range of tissues it targets and those responses it elicits. cAMP pathways can increase the heart rate and force a contraction in a heart, it can decrease lipid breakdown in fat cells, and it can stimulate resorption of water in a kidney. An inositol phospholipid pathway can initiate breakdown of liver glycogen and DNA synthesis in fibroblasts. Ca2+ pathways are linked to initiating responses in striated muscles most notably contraction. These responses, however, are short lived responses; much shorter then those by lipid soluble affected cells. Although the cellular mechanisms of hormones vary according to solubility and first and second messengers, such hormones function in eliciting responses from their target cells.

Hormones more or less function as a stimulant, promoting an action in a target cell which can be magnified in stimulating organs or even systems. Hormone stimulation varies from growth and metabolic functions to ova and sperm production.

 

How are signals transmitted by the endocrine system?

There are two ways in which the endocrine system affects the rest of the organism. The first method of transmission, is called local signaling. This is when regulators are released by a gland or cell into the interstitial fluids and are absorbed by nearby cells. The second method of transmission is called long distance signaling. Long distance signaling takes place when an endocrine cell or neurosecretory cell releases hormones into the bloodstream. Once in the bloodstream the hormones travel to the receptor cell. When they reach their destination the receptor cell integrates the signal and reacts to its design.

 

What are growth factors in the endocrine system?

Growth factors affect the development of new cells. There are specific hormones that correspond with the development of specific cells. For example, epidermal growth factor is required to grow epithelial cells. The rate of growth can also be affected, for example an experiment on fetal mice was done to see if rate of growth of skin would change with an influx of hormones. It was found that by injecting the fetal mice with EGF that skin developed faster.

 

What is the role of the hypothalamus and pituitary gland?

The hypothalamus and pituitary gland are two parts of the brain that have important roles in integrating the nervous and endocrine system. The hypothalamus is found in the lower part of the brain in the midbrain where it functions in receiving messages from nerves and integrating that into endocrine gland responses. The hypothalamus is more or less the communication link between the nervous system and the endocrine system. The hypothalamus regulates the secretion of various hormones by controlling the main hormonal gland the pituitary gland

The pituitary gland releases hormones that control many of the endocrine system's functions. The pituitary gland releases hormones when signaled by the hypothalamus. The pituitary gland has numerous functions which are performed by its’ two parts. Pituitary’s two separate parts are essential to the production of many hormones but, their function in relation to the hypothalamus and endocrine system vary greatly.

The posterior pituitary is an extension of the brain and secretes two types of hormones, oxytocin and antidiuretic hormone(ADH), both of which are produced by the hypothalamus and released into the posterior pituitary. Neurosecretory cells in the hypothalamus produce oxytocin and ADH and are transported down an axon to the posterior pituitary where it is stored. The posterior pituitary releases these hormones when needed via the bloodstream and bind to their target cells. The posterior pituitaries hormones elicit specific responses from the kidneys, by means of ADH, and the mammary glands, by means of oxytocin. ADH acts directly on the ability of the kidneys to reabsorb water, whereas oxytocin causes mammary glands to release milk.

The anterior pituitary also relies on the hypothalamus to control and regulate its hormonal release, but in a less direct manner.  The release of hormones by the anterior pituitary is driven by neurosecretory cells located in the hypothalamus. When the hypothalamus receives a signal for the need of a hormone produced by the anterior pituitary, it sends releasing hormones through short portal vessels and into a second capillary network within the anterior pituitary, where it acts on a specific hormone. Besides releasing stimulatory hormones the hypothalamus also releases inhibiting hormones which prevent the release of certain hormones from the anterior pituitary. The anterior pituitary produces and releases several different hormones with many different functions. Its hormones range from growth hormones that act on bones, to prolactin which stimulates mammary glands. A unique function of those hormones released by the anterior posterior, is that some of them act on other endocrine glands and signal them to produce and release other hormones. Tropic hormones are responsible for this, such as thyroid stimulating hormone which stimulates the thyroid and its production of hormones.

 

What are pheromones and what is their function?

Pheromones are chemical signals that function as external communicators whereas hormones are internal. Pheromones communicate between separate individuals, not within one individual as hormones do. Pheromones are communicating chemicals that act between animals of the same species. Pheromones are dispersed into the environment and are used in attraction, defense, and marking territories. Pheromones play a great role in the insect world, but their importance in human interaction is disputed. Some scientist question the presence of chemical influence on human behavior while an entire industry, the fragrance industry, bases its existence on the appreciation for external scents. Pheromones most likely play a hidden role in the interaction of humans with each other.

 

How is the Endocrine System related to the Nervous System?

The nervous and endocrine systems are related in three main areas, structure, chemical, and function. The endocrine and nervous system work parallel with each other and in conjunction function in maintaining homeostasis, development and reproduction. Both systems are the communication links of the body and aid the body’s life systems to function correctly and in relation to each other.

Structurally many of the endocrine systems glands and tissues are rooted in the nervous system, Such glands as the hypothalamus and posterior pituitary are examples of nerve tissues that influence the function of a gland and it’s secretion of hormones. Not only does the hypothalamus secrete hormones into the bloodstream, but it regulates the release of hormones in the posterior pituitary gland. Those that are not made of nervous tissue once were. The adrenal medulla is derived from the same cells that produce certain ganglia.

Chemically both the endocrine and nervous system function in communication by means of the same transmitters but use them in different ways. Hormones are utilized by both systems in signaling an example of this can be seen in the use of Norepinephrine. Norepineprine functions as a neurotransmitter in the nervous system and as an adrenal hormone in the endocrine system.

Functionally the nervous and endocrine system work hand in hand acting in communicating and driving hormonal changes. They work in maintaing homeostasis and respond to changes inside and outside the body. Besides functioning in similar manners they work in conjunction. An example of this can be seen in a mothers release of milk. When a baby sucks the nipple of its mother, sensory cells in the nipple sends signals to the hypothalmus, which then responds by releaing oxytocin from the posterior pituitary. The oxytocin is released into the bloodstream where it moves to its’ target cell, a mammary gland. The mammary gland then responds to the hormones signal by releasing milk through the nipple. Besides working in conjunction with each other, both systems affect one another. The adrenal medulla is under control the control of nerve cells, but the nervous systems development is under the control of the endocrine system.

 

What is growth hormone?

Growth hormone (GH) is a peptide hormone produced by the anterior lobe of the pituitary gland in response to GH-releasing hormone from the hypothalamus. Release of growth hormone is inhibited bysomatostatin, which also is produced by the hypothalamus.  GH enhances the metabolism of fats for energy. It also enhances amino acid uptake and protein synthesis, which help in growth of cartilage and bone.  Secretion of growth hormone is increased by exercise, stress, lowered blood glucose, and by insulin.

 

What are the hormones that influence our attitudes and behaviors?

There are many hormones that in one way or another effect attitude and behavior, but in the interest ot time and space, this section will mostly discuss the gonadal, placenta, and thyroid hormones.

A variety of hormones are produced by the gonads and placenta. Estrogens, such as estradiol, function in the development and maintenance of the female reproductive tract, in the simulation of the mammary glands, in the development of secondary sex characteristics, and in the regulation of behavior. Androgens, such as testosterone, influence the development and maintenance of the male reproductive tract, secondary sex characteristics, and behavior.

There has been a great deal of interest in the relationship between hormones and behavior and it has been found that the natural variation in the amount of hormones present is correlated with variation in behavior. For example, during the female menstrual period the "average" female shows a decreased body temperature, decrease in food and water intake, decrease in body weight, and she becomes sexually receptive. These variations within the body cause the females behavior to change. It's been found that it can result in changing of mood, performance in cognitive tasks, sensory sensitivity, and sexual activity. Unfortunately, due to the possible implications of gender issues this research is controversial. The same can happen with males. Research has shown that there is some suggestion of a relationship between androgens, like testosterone, and dominance-related behavior. For example, men with high levels of testosterone are prone to be more competitive and have a higher level of aggression.

Thyroid hormones can also influence a person's mood due to the changes in the thyroid's activity. Little is known about the mechanisms by which thyroid hormones elevate mood, but it has a connection to the neural functions in the brain, which have influence over hormone releasal.

Many psychological disorder are directly related to certain impairments of brain functioning (chemical and hormonal imbalances), while others are more behaviorally orientated. Affective Disorders, for example, are those in which there is a disturbance of mood. One form of this disorder is depression which has been related to a number of hormones like melatonin and thyroid hormones.

Headaches, which can dramatically make a person irritable, snappy, and emotional can be another consequence of a hormone. During the female menstrual period, around ovulation time, estrogen rises to a peak. When estrogen is high a message goes out to produce a hormone called serotonin. This hormone makes the blood vessels in the brain narrow. This doesn't cause any pain, but when the estrogen, and hence serotonin, levels drop, blood vessels in the head begin to expand and put pressure on nerves. This causes the pain you feel when you have a headache.

 

What is Seasonal Affective Disoder, and how is it that one hormone can make some people's winter mood less than pleasant?

Seasonal Affective Disorder(SAD) is a seasonal disruption of mood that occurs during the winter months. Symptoms of it usually begin in the fall when the day light hours begin to shorten and last until the day light hours begin to lengthen again in the spring. Some symptoms of SAD are depression, tiredness, increased appetite (which can lead to weight gain), and irritability. The direct cause for this disorder is in connection to the hormone melatonin.

The pineal gland, which is located in the center of the brain, releases a hormone called melatonin. This hormone can accumulate in the hypothalamus where it can have an effect on long-term releasing factors influencing growth and reproductive development and also on circannual rhythms (seasonal timing).  SAD is influenced by the latter of those.  Very little melatonin is secreted in the daytime (light) and a great deal is produced at night (dark). Because the winter months have longer nights there is an extra production of melatonin.  Therefore, the level of melatonin in the body increases.  This production of melatonin influences our overall mood and causes SAD.  Unfortunately, there isn't any concrete information on the exact reasoning to how or why this happens, but there are plenty of ways in which people try to cure it. For example, artificial lighting.

There have been several experiments that demonstrate that changes in the level of melatonin in the bodies of seasonally breeding animals affect their reproductive cycle. Artificial lighting can prolong this breeding activity due to the decrease in melatonin.

 

Special Topic Paper: Osteoporosis - Prevention and Post-Diagnosis Treatment (by Bobby Bailey)

When we think of the disease osteoporosis, we often attribute it to getting old. Osteoporosis, however, is much more complex. Physiologically, the body undergoes a lot of changes through the process of aging that relate to it, but it is these processes that allow the world of medicine to find means to prevent and even sometimes treat osteoporosis.

Osteoporosis is a condition of aging in which the density of bones in the body begins to decrease. Although many people view bones as rather inactive tissues, they actually are constantly in a flux known as turnover. This is the process by which the bone is continually remodeled to produce new bone (Snow-Harter, 1993). Constant muscular and weight bearing strain on the surface of the bone causes tiny stresses. These stresses get attacked by osteoclasts, which bore into the stress on the surface of the bone. This begins the process of resorption, during which the small hole almost triples in size. The next phase is the beginning of reformation of the bone matrix. This occurs when osteoblasts migrate to the cavity caused by resorption. The osteoblasts are responsible for producing the matrix that composes the structure of the bone. Osteoblastic activity also triggers calcium formation, which completes the formation of the bone. If this continual process occurs under the right conditions, the bone can actually increase in mass and density (Snow-Hartet, 1993). If conditions are not right, osteoporosis is the end result. Improper conditions, which will be discussed later, lead to an imbalance of osteoclastic and osteoblastic activity. If the resorption of bone is greater than the reformation of the bone matrix, bone density decreases leading to the increased susceptibility to fractures and other bone related injuries. (Snow-Hartet, 1993)

Better knowledge of the causes of osteoporosis leads to better treatment and prevention. The medicinal treatments will be discussed but prevention is by far the most cost effective (Wood, 1992). The easiest method of osteoporosis prevention is by a continual and progressive regiment of weight bearing exercise. Among pre-menopausal women, exercise is a fantastic way to promote bone and overall health of the body. As was discussed before, the continual stress on the bone surface can lead to increased osteoblastic reformation of the bone matrix. Exercise can also help women who have gone through menopause. A study of 22 healthy post-menopausal women showed that those receiving estrogen therapy actually increased bone density and mass after 22 months of exercise. Lumbar spine bone density actually increased by 6.1 %. Women that were not put on a workout plan showed a loss of bone (Wood, 1992).

Calcium consumption above the RDA value of 800 mg for adults is recommended to prevent the onset of osteoporosis. This is increasingly important for elderly, post-menopausal women because they have a less efficient calcium uptake mechanism due to aging. More supplemental calcium is required to improve absorption of the mineral (Wood, 1992). Calcium can also be used for treatment after the onset of osteoporosis. It was observed that post-menopausal osteoporosis patients who received 1000 mg of supplemental calcium a day showed a 50% decrease in non-vertebral bone loss (Wood, 1992). Some evidence suggests that calcium supplementation can only benefit a female post-menopausal osteoporosis patient if she is already undergoing estrogen therapy because estrogen helps control the absorption of calcium. This argument continues but it is known that estrogen therapy for osteoporosis patients is an effective treatment for the crippling disease.

There is powerful evidence that estrogen replacement maintains bone mass and reduces the fracture risk of post-menopausal women (Snow-Harter, 1993). Supplemental estrogen during the early years of menopause is effective in decreasing osteoporosis-related injuries by upwards of 50% (Wood, 1992). This treatment also has been noted to work well for women who have well-established osteoporosis. Results show that it can increase bone mass by 3% by decreasing resorption and shifting the balance to the side of the more favorable reformation (Wood, 1992).

Another anti-resorptive hormone that aids in decreasing the adverse effects of osteoporosis is calcitonin. No evidence currently exists stating why the drug works well, but trials do suggest that it is an effective agent in ceasing bone loss in patients with high bone turnover. Unfortunately, the evidence of this drug’s effects is unclear plus it is a very expensive form of therapy.

Other drugs known for their anti-resorptive properties are bisphosphonates. These drugs bind to hydroxyapatite crystals in the bones and remain in the bone for many years (Wood, 1992). These drugs seem to be effective at inhibiting resorption. This is done when they get released from the bone surface, bind to the osteoclasts, and interfere with resorption of the bone. The downside of these drugs is that they cause irritation in the digestive system.

Other methods of treatment actually support the formation of bone instead of protecting them from degradation. Sodium fluoride has been shown to increase bone density in the spine by 8 percent/year and by 4 percent/year in the femur (Wood, 1992). Unfortunately there is no evidence proving that this increased density is the same as bone strength. The increased bone growth can be abnormal in structure and lead to mass that is not strong.

Growth Factors such as insulin growth factors I and II are being related to the increased success of osteoblasts. This increase in osteoblast efficiency leads to increased rates of bone formation. Unfortunately, like most new drugs, these growth factors have adverse side effects. One issue that is raised is the ability for the factor to couple with a bone-seeking compound that will successfully deliver the treatment to the site (Wood, 1992).

The nice thing about knowing how a disease attacks the body is being able to take steps to prevent it, and there are a lot of ways to deter osteoporosis. Science has shown that exercise is the cheapest and one of the most effective ways to prevent osteoporosis. If this is coupled with proper diet, calcium supplementation, and estrogen therapy, the characteristic loss of bone mass and density from osteoporosis can actually be reversed. The same theories that make prevention possible are being proven to make treatment possible. Supplements like estrogen and calcium are sometimes very effective in stopping resorption, which leads to bone loss. Other drugs like sodium fluoride are able to promote the formation of new bone matrix. However, many of the treatments are experimental and unproven to be reliable in a broad range of cases. There is hope though, and science and medicine is well on its way to developing treatments to ease the pain of over 1.5 million Americans a year (Wood, 1992). On the other hand, even if foolproof treatments did exist, the only way that they could be effective is if people were educated about the disease. Education and self responsibility is the key to catching this disease before it attacks and for fighting it off if it does.

References:

Snow-Harter, C., and R. Marcus. 1993. Exercise, Bone Mineral Density, and Osteoporosis. Exercise and Sports Science Review. 21: 351-381.

Wood, A., 1992. The Prevention and Treatment of Osteoporosis. The New England

Journal of Drug Therapy. 327: 620-626.