Lecture Outlines -

1.Ectotherms - we will deal here with ectotherms in warm/hot environments [pages 712-715]. The point that is essential to understanding these animals is that they live in environments [primarily deserts] where there is a great deal of energy, but little of it is in the form or chemical energy [food]. Thus, rather than 'burning-fuel' to maintain body temperatures these animals have become specialists at exchanging heat with their surrounding environment to maintain body temperature.

2.To understand how ectotherms maintain T_b refer to Fig. 17-6 on page 705.

a)In the morning these animals will come out of their burrows and find warm surfaces on rocks, trees or banks. They will orient to the sun to maximize heat uptake.

b)Internally, the animals will shunt blood to their sunny side thus acting as a radiation to maximize heat uptake.

c)when T_b is in the operational zone the animals will forage and carry out other daily routines.

d)during periods of the day when T_a exceeds the ideal range the animals will seek shade or even retreat to their burrows until the cooler afternoon.

e)in the late afternoon or evening when the animals can no longer maintain their operational T_b they will retreat to their burrows.

3.Cost/benefit of body temperature regulation.

a)benefit. The most obvious benefit for ectotherms is energy savings. Field measurements of rates of energy turnover show that endotherms expend 20 times the energy of an ectotherm of the same mass.

b)cost. The most obvious cost for ectotherms is that they can only regulate T_b during the daily period when there is sufficient energy available from their surrounding environment.

4.Heterotherms. A number of ectotherms generate large amounts of heat associated with locomotion. Rather than simply waste the heat a number of species have developed mechanisms for trapping it, thereby enabling them to regulate T_b either periodically or partially.

a)periodic regulation. A number of butterflies, bees, bumblebees, and nocturnal moths generate large amounts of heat associated with flight. These insects all have developed thoracic coverings of scales that act as insulation enabling the animals to trap this heat thereby regulating T_b during flight. A typical flight routine is [see fig. 17-18]:

i.preflight warmup during which muscles are worked isometrically to generate heat to warm the body to flight temperature.

ii.flight during which the heat produced by the flight muscles is used to maintain T_b.

iii.warm-weather flight-if ambient temperatures are high enough that the T_b begins to exceed the desired flight temperature the animal then shunts warm blood to the abdomen which acts as a radiator to dump the excess heat.

iv.post flight cooldown. Animals typically maintain T_b until they find a suitable site, burrow or crevice, where they will seek shelter until the next flight interval.

b)periodic regulation-Unique case #1: Have you ever been around a bee hive or seen one on film? There are two obvious features of these hives, almost continuous activity and a loud buzzing sound. Ever wonder why? It is actually an example of social-T_b-regulation. Even in the hives bees flap their wings nearly continuously. The activity produces a great deal of heat which is used to maintain hive temperature at a fairly constant level [about 35^o C at the core - where the queen resides]. During cold times the bees pack tightly to keep the heat in and during warm days they disperse more and even create wind currents with their wing beats to cool the hive. So the queen and her immediate surrounds see a temperature that is very closely regulated at around 35 ^oC.

c)periodic regulation-Unique case #2: Another animal has found a way to tap its unique physiology for temperature regulation. Indian pythons are in the constrictor family of snakes. They are massive lengths of muscle designed to constrict prey as large as humans, suffocating them in the process. The Indian python has modified this activity for another unique adaptation. When the female lays eggs she will circle the nest with her body. Via slow-periodic contractions she will generate heat which is used to maintain the temperature of the nest, essential for normal development of the young.

d)regional regulation. Some fish are continuous swimmers, they are open ocean animals that cover great distances. These animals have become so dependent on movement that they will suffocate if held stationary; they must swim! Obviously, swimming muscles are active all the time and heat production is continuous [see figs. 17-19 and 17-20]. Obviously fish do not have fur, feathers, fat insulation for trapping the heat. Since water is a great conductor of heat this poses a problem. These animals have developed a countercurrent exchange system in the circulation supplying the muscles which works as an excellent heat trap! The keys are as follows:

i.all blood in a fish must flow over the gills for gas exchange. These surfaces are also efficient at exchanging heat and so all arterial blood is at 4 ^oC, the temperature of the ocean.

ii.the arterial supply to the muscles consists of arteries running between and very close to veins carrying blood out of the muscles. The arterial blood begins at 4^oC while the venous blood leaving the muscles has been heated to 33 - 35 ^oC. As the venous blood passes close to the arterial blood heat exchange occurs; warming the arterial blood and cooling the venous blood. By the time the arterial blood reaches the muscle it is close to muscle temperature. Conversely, the venous blood has lost most of its excess heat, being cooled to near 4 ^oC. By this clever arrangement of blood vessels, the countercurrent system heat is trapped in the muscles keeping them warm. Some of this warm blood also is shunted to the brain thereby keeping brain temperature regulated as well.

5.In sum: wherever circumstances shift the balance in favor of the benefits of T_b regulation it happens. However, where the costs exceed the benefits then T_b regulation is adjusted downward.

1.Endotherms: Organisms that produce a significant amount of heat metabolically to maintain body temperature (T_b) significantly higher than the surrounding temperature.

The authors of your text indicate that all mammals have similar and very constant temperatures. This is not the case. I better look at it is given in the following:

Body temperatures of mammals and birds

As you can see there is a broad range of body temperatures. In addition, within each species T_b varies on a daily cycle or a seasonal cycle. This is because of the offsetting balance between the considerable benefits of a relatively constant T_b weighed against the very high metabolic energy cost of maintaining that T_b constant.

2.Idealized relation of metabolic energy cost to regulate T_b against a variable T_a. This discussion is based on Fig. 17-21 and equation 17-7 (pg 719). Similar to regulating the temperature of your house, if temperature is to remain constant than the rate of heat production must equal the rate of heat loss!

--House example: As we move from summer to winter what happens? The outside temperature cools. To keep the house comfortable you make a series of adjustments. First, with moderate cooling you close windows, outside doors and close shades. What are you doing? You are in fact increasing the insulation or reducing the rate of heat flow. Once all of the insulation has been maximized if the outside temperature further cools you must increase the rate of heat production; the furnace comes on. This scenario is exactly what happens in endotherms and the patterns are shown in Fig 17-21.

Lets walk through the animal example (Fig. 17-21). Start with a reasonably warm temperature (summer). This may the at the point marked UCT. Notice the Metabolic rate of the animal is low (its at BMR in the Figure). As T_a is reduced what happens to metabolic heat production? Nothing! Why? Because the animal is increasing insulation and so body temperature remains the same without increasing heat production. This range of T_as is called the thermal neutral zone. How is insulation increased? Read through pages 718-719 for:

a)vasomotor responses-reduced blood flow to the skin so the warm blood does not lose as much heat.

b)postural changes-the animal may curl or cover exposed parts.

c)insulation adjustments-birds fluff their feathers, mammals fluff their fur.

At LCT (the lower critical temperature) notice that metabolic rate increases as T_a is further reduced! Why? The furnace is coming on because insulation is maximal! So the animal has no recourse except to increase the rate of metabolic heat production! This is called the zone of metabolic regulation.

Equation 17-7 explains the information shown in Fig. 17-21. In this equation

Q = C (T_b - T_a)

Where Q is the rate of heat loss and C is the animals thermal conductance (roughly the inverse of insulation). In the thermal neutral zone the animal is able to adjust C so as T_a is lowered (T_b - T_a) increases, Q does not change. Once C is minimal (insulation is maximal) then Q will increase as T_a is further reduced. Note also that by measuring Metabolic rate (an index of Q), T_b and T_a it is possible to calculate C for an organism. What would you guess the values of C to be for a tropical versus an arctic endotherm?

3.Endothermy in cold environments. An obvious challenge for endotherms is living in cold environments. A number of interesting adaptations to these conditions have been identified.

a)Thermogenesis: A number of endotherms have found ways to increase heat production to high levels. The two most prevalent are: i.shivering thermogenesis-in many birds and mammals cold exposure produces rapid/shallow contractions of antagonistic muscles (muscles that work against each other). The net effect is a large amount of heat production without movement.

ii.nonshivering thermogenesis-some mammals have developed a tissue called brown fat. In this specialized fat tissue lipids are metabolized without generating ATP, the energy is released directly as heat! The fat looks brown because it is inundated with blood vessels which carry the heat away to the core of the animal's body! Bats have large amounts of brown fat which the use to warm rapidly from bouts of torpor. Human infants also have brown fat which helps them to keep warm!

b)Countercurrent heat exchange: Animals in cold environments may have thick coats of feathers or fur for insulation over their bodies. But their limbs may be a tremendous source of heat loss (see fig 17-24). To prevent this loss arteries carrying warm blood from the body are surrounded by veins carrying cool blood from the extremity. Heat from the arteries passes to the venous blood and is carried back to the body rather than to the cool limb. This happens in humans as well. You can measure you core temperature (about 37 ^oC), your armpit (about 35^oC), the crook of your arm (elbow, about 32 ^oC) and closed palm of hand (28-30 ^oC).

c)High insulation = low conductanc: In predictably cold environments (arctic regions, water) endotherms add insulation. This is a double-edged sword; during times of heat production (exercise) these animals may have problems getting rid of the excess heat. Polar bears for example can run for only short distances, but seek a dip in the arctic ocean to dump heat. The insulation takes several forms: birds have feathers, mammals fur and aquatic forms of both groups typically add thick layers of fat called blubber.

d)limited heterothermy: another trick employed widely is to let T_b "drift" rather than keeping it 'constant.' Many birds allow T_b to fall 3 - 5 ^oC during the night in order to reduce metabolic cost. Many mammals follow this practice as well. Even in humans T_b may fall 1 - 2 degrees during sleep!

4. Endothermy in warm environments. When T_a exceeds T_b there is only one mechanism for dumping the excess heat and that is to employ evaporative cooling. Many animals pant (a rapid shallow breathing) which carries heat away from the buccal cavity as water vapor. Humans sweat. This is actually inefficient (keeps the surface temperature cool so increases heat uptake) but effective. Evaporative cooling is also dangerous as it 'costs' a great deal of water. Some animals avoid the water loss. In one example, camels, the animals allow T_b to cycle day/night accumulating heat during the day and dumping it via nonevaporative means at night! This saves the camel a great deal of water which is critical in their desert environment. Small mammals avoid the heat by retreating to burrows during the daylight hours.

Cold. Some ectotherms live in amazingly cold climates. In fact one species of fish lives at -1.5 ^oC. That's below the freezing point of water. And it spends its entire life at this temperature. Obviously it lives in: i.Antarctic waters, ii.marine waters [the freezing point of sea water is -1.8 ^oC. In addition, some animals actually freeze during their overwintering period. How do animals at these low temperatures survive? To understand this material you should be able to describe:

i.Preemptive ice crystal formation [see fig. 17-14].

ii.Antifreezes.

iii.Supercooling.

Dormancy: A state of lowered metabolism. Many endotherms find themselves in circumstances where their environment is cold at a time when food availability is low. So the demands for metabolic heat production are high, but the food to sustain the metabolic rates is suspect. One adaptation is to set back the thermostat; reduce body temperature and therefore the need for high rates of metabolic heat production. These activities take several forms and have been developed to a high degree in several species.

i.sleep-as mentioned above even during sleep T_b may drop from one to several degrees. In Australian aborigines for example limb temperature may fall to 15 ^oC. This saves the individual considerable energy. Recall also the bird examples.

ii.torpor-is a moderate reduction in core T_b, to as low as 12 - 15 ^oC for 8 - 10 hours at a time. These animals are still responsive, but sluggish. And the regulate their temperatures at the lower set points. Thus it is an organized way of conserving energy during periods of cold when feeding is not an option.

iii.hibernation-is an extreme reduction in core T_b, to as low as 0 - 5 ^oC for relatively long periods (up to two-three weeks at a time during an entire winter). Obviously this is a seasonal activity and takes considerable preparation. Marmots and a number of ground squirrels are hibernation specialists. This activity enables these animals to live in cold environments with long periods of food deprivation.

iv.winter sleep-Periods of moderate reductions in T_b to about 28 - 30 ^oC which may extend to a few weeks or even months. This activity is practiced in some large mammals, especially bear. These animals are too large to incur larger drops in T_b because the cost and effort of rewarming their large mass is too great. These animals reduce energy cost, but remain functionally active. Most significantly cubs are born during this 'sleep' and nurse for extended periods before the mother wakes. It enables the mother to direct her limited resources to caring for her new born cubs.

September 20, 2006 Membrane potentials. This chapter focuses on membrane potentials in neurons, but you should remember that all living cells have a membrane potential of some kind! Also, I will not present the material in the same order it appears in the chapter. The following notes attempt to follow the lecture rather than the text.

1.The resting potential. Pg 131-132]. ALL cells have a potential difference across their membranes [with potentials ranging from -20 mV to -100 mV, negative on the inside of the cell]. Key point: all potentials are determined by two factors; first, the presence of open ion channels (ion conductance, g) that are selective for different ion species and second the unequal distribution of inorganic ions between the cell interior and the cell exterior [the ions are K⁺ and Na⁺] that are maintained by active transport [Na⁺/K⁺_ATPase pump].

a)The Role of Ion gradients and ion channels [pg 131]. The resting membrane potential is a K⁺ potential because the is 100 times more permeable to K⁺ than it is to Na⁺ - [ this is 'Keynes' observation].

b)The role of active transport. The magnitude of the membrane potential is dependent on the ion concentration difference across the membrane. A great deal of cellular energy goes into maintaining these ion concentration differences [make sure to review the ion concentration differences as given in the last lecture - see table from previous lecture]. The Na⁺/K⁺ pump actually contributes to membrane potentials in two ways. The vast majority is directly from the concentration differences. But recall that the pump moves 2 K⁺ in for each 3 Na⁺ moved out. This unequal movement of ions is called electrogenic and will contribute a small amount to the membrane potential [typically less than 5%].

2.Quantifying the membrane potential. [page 129-131, equation 5-4]. You should be able to write this equation, label the abbreviations and explain how this demonstrates the basis of membrane potentials [later we will add action potentials to this as well]. You can omit Cl^- in your considerations. Typical exam questions will ask you what happens to E when specific ion concentrations are varied, and when permeability/conductance values are varied.

3.Demonstrating the basis of the resting membrane potential. Fig 5-14 shows a simple experiment that demonstrates the importance of K⁺ to membrane potentials (recall that in the resting cell [K⁺]_o = 2.5 mEq and [K⁺]_i = 140 mEq). If we experimentally increase [K⁺]_o to 140 mEq (so [K⁺]_o = [K⁺]_i then the ratio = 1. The log of 1 = 0, meaning that membrane potential should go to zero. Fig. 5-14 shows that this indeed happens and is predicted quite nicely by the Goldman equation (obviously you should be able to draw/label this figure and explain what is shown). In lecture I mentioned one use of this information; iv injections are used to kill animals, including humans, by rendering their cells electrically neutral.

September 22, 2006 -- Action Potentials.

1.Neurons: While membrane potentials are found in all living cells action potentials are typically found in only a few cell types. One type of cell that may [not all of them do] develop action potentials is the neuron. So we begin this lecture with an introduction to neurons. [Pages 113-115, Figs 5-1 and 5-2 - be able to draw/label/describe a neuron as shown in Fig 5-2]. The neurons that are shown in these figures are cells specialized for developing action potentials. And the action potentials are important for carrying signal-information from one end of the cell to the other.

2.Action potentials: [pages 132-150]. Action potentials are a rapid, all-or-nothing reversal of the membrane potential [see Fig. 5-16]. The physiological mechanisms that produce action potentials are the same as those responsible for membrane potentials. So review items #1 and #2 from the last lecture, especially the Goldman equation. This equation was used to describe the resting membrane potential. It also describes the action potential. In most simple terms: a)when the membrane is a potassium potential it is in the range of -70 mV inside. b)when the membrane is a sodium potential it is in the range of +60 mV inside. Going from -70 mV to + 60 mV and back to -70 mV very rapidly (about 3 milliseconds) is a rapid reversal of membrane potential (an action potential). How can this be produced. Exam the Goldman equation. Now imagine rapid changes in Na⁺ and K⁺ permeabilities (conductances, g). These rapid changes in g are the basis of the action potential and are shown in Fig. 5-20 (see also handout figure which better illustrates the relationship of changes in g and membrane potential. You will be expected to draw this figure and with the Goldman equation describe an action potential.

3.Steps in the action potential [see figs 5-16 & 5-20]:

a)A stimulus raises membrane potential from its baseline towards zero [this is called depolarization].

b)If the depolarization reaches threshold it becomes regenerative, self sustaining. The mechanism for this is described on pg 143 [fig 5-24] and is called the Hodgkin cycle. In brief, at threshold depolarization sodium channels open [this increases sodium conductance, g_Na] which further depolarizes the membrane which further increases g_Na. Note that this is a rare example of a positive feedback loop. This happens very rapidly [about 0.5 milliseconds]. The rapid rise in g_Na does the following: The increase raises membrane Na⁺ g to about 100-fold greater than K⁺ g so for a brief time the membrane potential is a Na⁺ potential.

c)After the rapid rise in membrane potential it rapidly recovers [called repolarization - see figs 5-16, 5-20]. Two changes account for repolarization. First, there is a rapid drop in g_Na and second there is a slower rise in g_K [handout figure and fig 5-20]. [[hint-make sure you can explain what should happen to membrane potential when g_Na and/or g_K is/are increased/decreased].

d)Notice in the handout fig and fig 5-20 that g_Na recovers very rapidly and g_K recovers more slowly. So for a brief period g_Na is back to baseline and g_K is still elevated. This produces a membrane potential that is even more negative than baseline, a condition called hyperpolarization. Hyperpolarization versus depolarization are key to understanding how sensory systems and the nervous system work!

e)Instructors pet! If you have heard about action potentials you undoubtedly have heard about sodium ions 'rushing' across the membrane during depolarization. This is decidedly NOT the case. Read the brief description of Intracellular ions and … on page 146. Notice that the ion diffusion during an action potential is on the order of 10^-12 moles [0.000000000001 moles] or picomoles, not measurable by anyone's standards. This is why we use g and not permeability. It is the charge reversal that is important, not ion diffusion.

September 25, 2006 -- Propagation of Action Potentials.

1.Introduction: Read pages 155-157 for an introduction of terms. You should know the terms: receptor potential, passive electrotonic spread, neurotransmitters, postsynaptic/presynaptic.

2.Transmission of information within a single neuron. There are three important points here:

a)Passive spread of electrical signals [pg 157 - 159, fig 6-3]. A depolarization produces a discharge which will spread similar to an electrical current. And the cell is able to conduct the current depending on its cable properties - electrical properties that affect conductoin of a signal over distance. Cable properties are important because they conduct current very very quickly; about 1,000 meters per second! However, there is a downside, resistance. The energy of the current is dissipated very quickly. So if distances are very short (a millimeter or two at most) electrotonic spread is fast and sufficient. For greater distances the discharge must be renewed or it will die out.

b)Propagation of action potentials. [pgs 159 - 164]. As the current passes through the axoplasm of a neuron it can also pass through the cell membrane of the cell. This produces discharge [depolarization]. If the depolarization reaches threshold then another action potential will occur and the discharge will be renewed. This renewed discharge will then spread electrotonically. If the process is repeated every millimeter or so the discharge will crawl along the cell length. The advantage is that the discharge can cover long distances. The disadvantage is that the renewal action potentials take a relatively long time, so axonal propagation reduces the speed of conduction to about 0.1 meter per second. You have some neurons in your leg that are about a meter long. So at this conduction rate it would take about 10 seconds for a signal to travel this neuron. Not sufficient is it!

c)Rapid, saltatory conduction in myelinated axons. [pgs 164-167, figs 6-6, 6-7]. Cell adaptations have increased the speed of conduction to a reasonable level. The upper end appears to be about 100 meters per second. This increase in speed of conduction is achieved via two mechanisms. The first is the diameter of the cell [axon of a nerve]. The larger the diameter of the cell the lower the resistance and so the farther a discharge will travel before dissipating. Unfortunately, this also poses a burden of large cell size [takes up too much room]. Another solution is called saltatory conduction [literally 'jumping' conduction]. This process takes advantage of electrotonic spread and discharge. The key is an insulation sheathing surrounding neurons. This is shown in fig 6-6 where the oligodendrocytes send out cellular extensions that envelope axons of neurons. This sheathing, called myelin, insulates the cell so that discharge cannot leak out, preserving it in the axoplasm where it spreads electrotonically (1,000 m/s). Myelin is discontinuous and in the gap regions [called nodes of Ranvier] discharge is renewed via action potentials. In this way the discharge passes electrotonically from node to node and is renewed at each node via action potentials. Since fewer of the slow discharge renewals are required the speed of conduction is greatly increased [from 0.1 m/s in a naked cell up to 100 m/s in a large myelinated cell]. Since the discharge appears to jump from node to node it is called saltatory conduction.

September 27, 2006 -- Synaptic Transmission - communication between cells.

1.Synapse-The site of information processing between neurons. There are two types of synaptic connection:

a)electrical synapses-[pgs 166-167-also called gap junctions, pg 167] regions of membrane contact with high capacitance. Depolarizations traveling along one cell membrane are transferred to the adjacent membrane directly through the region of high capacitance. This type of synapse provides a very rapid transfer of information, but is nondirectional [information will flow equally well in either direction].

b)Chemical synapses-Most information transfer is via chemical synapses. In these cases there is close proximity between a terminus of one cell [called the axon or axon terminus] and a terminus of an adjacent cell [called a dendrite, although the connection may be directly on a cell body]. In this synapse a neurotransmitter is released from the axon terminus, diffuses across a synaptic cleft [the short distance between the adjacent cells] and links to a receptor site on the dendrite or cell body. On linking the neurotransmitter will alter the characteristics of the receptor to produce a change in post synaptic membrane potential [PSP]. One of the advantages of this type of synapse is modulation and results from three characteristics of this type of synapse: i.Many axon termini synapse with each cell, ii.each synaptic connection can be either excitatory [EPSP] or inhibitory [IPSP]. iii.many excitatory inputs are necessary to depolarize the cell membrane to threshold [to produce an action potential in the second neuron]. Imagine many axon termini with synaptic connections on one cell. Inputs from the sum of these termini will determine output from the downstream neuron. Excitatory neurons will tend to excite the neuron, but that excitation may be countered by input from the inhibitory neurons. Whether output occurs is determined by the sum of all the inputs. This is integration of information!!

c)Advantages/disadvantages to chemical synapses:

i.one advantage is that neurotransmitter is always axon-dendrite so there is one-way information flow. This is important in controlling information exchange.

ii.another advantage is that modulation enables integration of information.

iii.the main disadvantage is that chemical transmission is very slow compared to gap junctions.

iv.another disadvantage is that these synapses can fatigue [neurotransmitter production cannot keep pace with output need].

d)Sequence of steps in synaptic activity [see pg 167-172, fig 6-10]:

i.Action potential reaches axon terminus. The depolarization activates voltage-gated Ca⁺⁺ channels.

ii.Ca⁺⁺ diffused into presynaptic terminus and fuses with synaptic vesicles holding neurotransmitter.

iii.Ca⁺⁺ links vesicles with membrane of axon terminus. With fusion the vesicles open releasing neurotransmitter into synaptic cleft [this is a fluid filled space, but of very very small dimensions].

iv.Neurotransmitter diffuses across synaptic cleft where some will link to receptor site. Linking of neurotransmitter to receptor activates ion channels coupled to the receptor. Synapses vary in their activity, some are excitatory some are inhibitory. The neurotransmitter and the receptor can be the same. What differs is the ion channel connected to the receptor molecule. As described on pages 178-180, fig 6-19, if the ion channel is a Na⁺ channel the membrane is depolarized somewhat [this is an EPSP]. If the ion channel is a K⁺ channel the membrane is hyperpolarized somewhat [this is an IPSP].

v.Very important-as neurotransmitter encounters postsynaptic membrane it also encounters a neurotransmitter inactivator which disables the neurotransmitter. The neurotransmitter rapidly disappears which stops the synaptic activity [you have already learned about one inactivator. Remember acetylcholine which is a very common somatic neurotransmitter. It is deactivated (actually split into acetyl- and choline) by an enzyme acetylcholinesterase. The acetyl and choline are recycled into the axon terminus where they are reconstituted into acetylcholine].

e)Strange, but with all the activity described in the last section I hope you realized that nothing was said about actually producing an action potential in the post-synaptic cell. This event is describe on pages 198-202, fig 6-41, 6-42, 6-43, 6-44. There are two points here. First, information integration occurs. Neurons often have thousands of axon termini forming synapses with them. Some are excitatory, some inhibitory. Whether there is an action potential depends on how much input comes from the excitatory neurons and how much comes from the inhibitory neurons. Second, since even excitatory activity produces only small depolarizations many excitatory inputs are required for the post-synaptic cell to reach threshold. There are two ways of summation of inputs that can produce this. The first is called temporal summation. Here one nerve may fire many times in rapid succession producing multiple depolarizations. These may sum and if the depolarization reaches threshold then an action potential will occur. The second is called spatial summation. Here several excitatory nerves may fire at one time, all activating the post-synaptic membrane at one time. If this summed depolarization reaches threshold then an action potential will occur.

f)Almost done: There is one more important point. Imagine a series of axon termini with synaptic connections to the same nerve. Now imagine all being excitatory and all firing rapidly. Each will produce an EPSP in some region of the post-synaptic cell. These potentials will spread electrotonically [very fast - 1,000 m/s] through the cell axoplasm. The potential could dissipate through the membrane but most regions have a low capacitance. When the potential reaches the Axon Hillock however it encounters a region of very high capacitance. Here the potential readily passes through the membrane depolarizing it to threshold producing an action potential [hence Axon Hillocks are know as spike (action potential) initiating zones]. The current from these action potentials then pass into the axon of the neuron.

September 29, 2006 -- Sensory Mechanisms - I. All sensory receptors do essentially the same thing, they respond to some change in environment [internal or external] by initiating or modifying the firing rate [action potentials] of sensory neurons. So they are transducers. There are many types of sensory cells: chemical [pages 230-238], mechanoreception [pages 238 - 252], electrical and thermal [pages 250-251], photo/vision [pages 252-272]. Interestingly while the receptors themselves are quite unique the processes by which the cue is converted into action potentials in sensory neurons is pretty common. Further, these mechanisms are very similar to what we just covered in synaptic transmission [see pages 216 -223 and figs 7-3]. Another important feature is input-output relations [pages 223-224]. Changes in environmental features can be tremendous [sunlight is 10⁹ times more intense than moonlight and audible sound intensity varies over 10¹²-fold]. This would not be a problem except that sensory neuron action potential frequency is maximal at about 1,000 cycles/second; that is 10³ range. So how can 10⁹-10¹² range be coded for by neurons with a capacity of 10³? The answer is multi-fold, but a major feature is that sensory systems encode changes in environment as log units [see fig. 7-8b].

An in-depth look at one sensory receptor, the mechanoreceptor that is called the vertebrate hair cell [pages 238-249, figs 7-24, 7-25, 7-27, 7-29, 7-30] - you should cover these pages and figures in great detail]! The sequence will be as follows:

1.How does the hair cell work as a transducer [see fig 7-24, be able to draw it and describe the events]?

2.How does the hair cell enable amphibians and fish to detect the presence of and position of predators, etc? [see fig 7-25 and text].

3.How does the hair cell account for equilibrium, static and dynamic [see fig 7-27 and text on pages 242-244].

October 2, 2006 -- Exam II - in STAD 140.