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What roles do circular connection structures play in the brain?

What roles do circular connection structures play in the brain?


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Most neural network simulations are strictly linear, one reason being they don't want to deal with circular connections (and infinite feedback loops if you dont have the right mechanisms). You can deal with them at the cost of some efficiency, but I'm curious about whether in the real brain, circular connections play an important role, or are they really not necessary?

To be clear, I mean any structure where you have a Neuron A, Neuron B, and Neuron C (or a thousand more) and the structure is similar toA > B > C > Aor generally at some point Neuron A ends up having a path where its own output can lead back to itself.

What roles do circular connections play in the brain? Or more simply: Are they useful and what are a few reasons why?


'Circular connections', as you refer to them, are super common in the nervous system. This motif usually referred to as feedback connections, and serves a variety of roles.

Connectivity studies can be broadly grouped in to those that look at brain areas, and those that look at individual neurons (usually within a single brain area).

My background is more the latter, so that's what I'll focus on.

Firstly, your question misses an important distinction: inhibitory neurons. So if neuron C was inhibitory, we would have a negative feedback loop, a classical circuit that can be used to produce a homeostatic like signal, keeping a system within certain bounds; a delayed feedback loop can also act as a 'signal terminator', allowing an action to be stopped once it reaches a certain threshold. Lastly, under some circumstance, feedback loops can produce oscillations, which are applicable to a number of tasks.

But more generally, recurrent connectivity is hugely important in the cortex. The majority of inputs to neurons come from neighbouring excitatory neurons (see https://www.ncbi.nlm.nih.gov/pubmed/7638624), and if A connects to B then B is more likely to connect to A than by chance (see http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1054880&tool=pmcentrez&rendertype=abstract for a really nice study on this).

So why? For a variety of reasons. Networks with feedback mechanisms can do more, is the basic answer; from negative feedback for homeostasis, to persistent network states. My personal feeling is that too much of computational neuroscience models a network as an operator - it takes an image, say, and outputs what it thinks the image is. And whilst that is important, it's not what the brain is. We need to maintain a constant internal model of the world around us, rather than going 'that thing is a cat. That thing is a burger'. Perhaps recurrent activity maintains the cortex in a certain state - knowing that the cat is there - and inputs serve to move the state so that we can update our internal models when the sensory environment changes.


Hypothalamus Activity and Hormone Production

About the size of a pearl, the hypothalamus directs a multitude of important functions in the body. Located in the diencephalon region of the forebrain, the hypothalamus is the control center for many autonomic functions of the peripheral nervous system. Connections with structures of the endocrine and nervous systems enable the hypothalamus to play a vital role in maintaining homeostasis. Homeostasis is the process of maintaining bodily equilibrium by monitoring and adjusting physiological processes.

Blood vessel connections between the hypothalamus and pituitary gland allow hypothalamic hormones to control pituitary hormone secretion. Some of the physiological processes regulated by the hypothalamus include blood pressure, body temperature, cardiovascular system functions, fluid balance, and electrolyte balance. As a limbic system structure, the hypothalamus also influences various emotional responses. The hypothalamus regulates emotional responses through its influence on the pituitary gland, skeletal muscular system, and autonomic nervous system.


Roles of Connective Tissue

Connective tissue in the human body, is the biological duct tape holding the whole system together. Connective tissue gives shape to organs, stores/transports minerals and nutrients, provides protection and increases flexibility. These are just some of the roles of this tissue–the role of connective tissue varies depending on the nature of nearby structures.

Roles of Connective Tissue In Brief:

  • Storage, Absorption and Waste Disposal Related to Metabolic function (blood, adipocytes/fat, lymphatic tissue)
  • Transportation of vitamins, minerals, energy, proteins, water, oxygen and other substances (blood)
  • Protection against harmful contaminants, impact and friction (cartilage, scar tissue)
  • Immunity and Defense (white blood cells, skin, scar tissue)
  • Structural Support (tendons, ligaments, bone, cartilage)
  • Thermal Insulation (adipocytes/fat)
  • Blood Production (bone marrow, lymphatic tissue)

Let’s take a look at some of these roles in more depth.


The Biological Basis of Aggression

One need only pick up the daily newspaper to see how serious a problem violence is in today’s society. Although the incidence of violent behavior in the US has fallen significantly in the past few years, there is still about an 80% chance that a person will be the victim of a violent crime during his or her lifetime. Even more troubling is the trend of increasing violence among the very young. After each school shooting, there is a media blitz of experts searching to explain how and why troubled teens sometimes turn to violence. Much of what they say is the result of research on the psychobiology of aggression, a field that has recently experienced many breakthroughs in identifying correlates of violent behavior. Some researchers claim that we are coming closer to predicting from a brain scan or a blood test whether a person is at risk for committing an act of violence. Ethical complications aside, a closer look at the neurobiology of aggression shows why we are unlikely to find a conclusive test for potential violent behavior. While there are many biological factors associated with aggression, their predictive value remains still quite low.

The first hurdle in researching aggression is how to define it. It is an easier task with animals, who tend to display stereotyped patterns of violence such as killing to gain food or territory. With humans and non-human primates, classifying aggression becomes more difficult because there is complication of intent. Punishment, for example, represents an especially gray area. Should spanking be considered an aggressive act? What about capital punishment? Indeed, almost all acts we consider aggressive have been socially sanctioned by some cultures over the years. To simplify matters, many psychologists and ethologists find it useful to classify aggressive behavior into one of three main categories: (1) predatory aggression, which refers to stalking and killing of other species, (2) social aggression, which is unprovoked aggression that is directed an members of the same species for purposes of establishing dominance, and (3) defensive aggression, which refers to attacks delivered when an animal is cornered by a threatening aggressor. There is evidence from animal studies that suggests the different types of aggression are controlled by different subsets of brain structures within the limbic system, including the amygdala, the septum, and the hypothalamus (figure 1). For example, in the rat, lesions of the lateral septum decrease social aggression but increase predatory aggression, suggesting that neural substrates for offensive and defense aggression are intertwined but separate.

Is it in the Genes?
One of the earliest attempts to link genetics and violent behavior occurred during the 1960s, when researchers thought they had discovered a propensity for violence in men born with an extra Y chromosome. Although the studies attracted a lot of attention at the time, further examination of XYY males revealed that they did not display any particularly violent tendencies. Furthermore, XYY males are extremely rare, and thus the syndrome could not possibly explain the frequency and prevalence of violent behavior around the globe. Scientists agree that there is probably a genetic component to aggression because violent behavior tends to run in families. However, with a complex behavior like aggression, it is especially difficult to separate genetic and environmental contributions. Most likely it is possible to inherit a predisposition to violence, but psychologists also stress that modeling aggressive behavior in the home is the surest method for propagating violence.

A large body of research implicates the amygdala as a key brain structure for mediating violence. One of the first indications that the amygdala might be important for fear and aggression came from Kluver and Bucy’s 1939 descriptions of monkeys who had their temporal lobes removed. They noted that the animals were remarkably tame and showed little fear. Later research indicated that docile behavior associated with Kluver-Bucy syndrome is likely mediated by the amygdala, as selective removal of that structure produced similar effects on fear and aggression. It is also possible to increase aggression through modulation of the amygdala. In animals, electrical stimulation of the amgydala augments all types of aggressive behavior, and there is evidence for a similar reaction in humans. Sniper Charles Whitman, who killed several people from the University Tower at Texas, left a note behind that begged people to examine his brain for possible dysfunction. His autopsy revealed he had a tumor pressing into his amygdala.

“Sniper Charles Whitman, who killed several people from the University Tower at Texas, left a note behind that begged people to examine his brain for possible dysfunction. His autopsy revealed he had a tumor pressing into his amygdala.”

Hormones and Serotonin
Testosterone is another attractive candidate for mediating aggression because males in of all ages, races and cultures are more physically aggressive than their female counterparts. In animals, testosterone is linked to social aggression. Reducing testosterone in the alpha male by castrating him eliminates his dominant social status, and restoring testosterone through injection causes him to regain his social status. However, administering testosterone to males with less social status does not usually allow them to take over the alpha male position, indicating that there is not a direct relationship between testosterone and position in the dominance hierarchy. There is some evidence in humans that high testosterone males are more likely to be socially aggressive, but no evidence that they are necessarily more violent. Often they are successful in professions that thrive on competition, such as successful leading of a company, running for president, or pursuing a sports career. Also, a few psychologists have suggested that females are not necessarily less aggressive than males rather, they display a different kind of aggression. Females are more likely to show non-violent types of aggression such as ostracizing their peers or spreading false rumors with the intent to cause pain. Thus, while there does seem to be a connection between testosterone and physical aggression, a person’s testosterone level will not necessarily be a good predictor of aggressive behavior.

Several lines of converging evidence indicate that the neurotransmitter serotonin plays a key role in mediating aggressive and violent behavior. Mice with a selective knockout of the serotonin 1B receptor show an increase in aggression. Similarly, depleting serotonin levels in vervet monkeys increases their aggressive behavior, whereas augmenting serotonin levels reduces aggression and increases peaceable interactions like grooming. Serotonin has also been implicated in human aggression. For example, pharmacological interventions that augment serotonergic efficacy have been shown to reduce hostile sentiment and violent outbursts in aggressive psychiatric patients. Also, people with a history of impulsively violent behavior, such as arsonists, violent criminals, and people who die by violent methods of suicide show low levels of the serotonin in their cerebral spinal fluid. These findings represent an interesting correlation, but it is important to remember that the direction of effect is unclear. It may be that aggressive behavior induces low serotonin levels in the cerebral spinal fluid rather than vice versa.

Measures of brain functioning such as the EEG have long suggested that violent criminals have impaired neurological processes, but the recent advancement of neuroimaging techniques has allowed researchers to examine violent offenders’ brains in more detail. Adrian Raine and colleagues have conducted the largest and most thorough study to date, in which they used positron emission tomography (commonly called a PET scan) to compare brain activity in 41 convicted violent offenders to activity in 41 age matched control subjects. They found that the people convicted of murder had reduced activity in the prefrontal cortex and increased activity in subcortical regions such as the thalamus. This finding fits nicely with previous research showing that the damage to the prefrontal cortex impairs decision making and increasing impulsive behavior. Indeed, Raine’s work is perhaps the best evidence yet that impaired brain functioning may underlie some types of violent aggression. However, it is important to remember that his subjects lie at the extreme end of a spectrum and may not be typical of most aggressors. Also, there are plenty of examples of people with prefrontal cortex damage who do not commit violent acts, so PET scans cannot be used to ferret out potential murders.

Reducing Violent Behavior
Researchers have been successful in identifying biological factors associated with aggression but have had less luck figuring out how these factors might contribute to pathological aggression and violence. At this point, there is no neurological marker to identify a person at risk for violent behavior, and it seems unlikely that a definitive test will ever exist. As the example of high testosterone males illustrates, aggression can often be channeled into healthy and beneficial behaviors. Thus it seems the best road to reducing dangerous kinds of aggression is learning more about the factors that shape aggressive behavior. Many people point to the media as a key instigator of violence, citing statistics about the thousands of dramatized murders American children watch on television each year, and there is some evidence to support this idea. However, television cannot possibly be the sole mediator of violent behavior. Toronto receives the same television programming as Chicago but the crime rate in the Canadian city is not even a tenth of the American one. The hard truth about pathological aggression is that it does tend to propagate through families, and once started, the cycle can be very difficult to break. Research on the neurobiology of aggression has already provided some valuable clues about possible targets for biological intervention, but there is no quick fix. The good news is that scientists in the fields of psychology, sociology and biology are increasingly aware of their mutual interest in this topic. Each brings a piece of the puzzle to the table, and their unique combination offers our best hope for understanding the complex behavior of pathological aggression.

References:
Fuller, RW, “The influence of fluoexetine on aggressive behavior.” Neuropsychopharmacology, 14: 77-81, 1996.

Mann, JJ. “Role of the serotonergic system in the pathogenesis of major depression and suicidal behavior,”Neuropsychopharmacology, 21 (2): 99S-105S, 1999.

Raine, A., Buchsbaum, M., LaCasse, L., “Brain abnormalities in murders indicated by positron emission tomography,” Biological Psychiatry, 42: 495-508, 1997.

Virkkunen, M, Rawlings, R., Tokola, R., Poland, RE, Guidotti, A. Nemoff, D. Bisette, G., Kalogeras, K., Karonen, SL, Linnoila, M. “CSF Biochemistries, glucose metabolism, and diurnal activity rhythms in alcoholic, violent offenders, fire setters, and healthy volunteers,” Arch of General Psychiatry, 51: 20-27, 1994.


New Findings Reveal Surprising Role of the Cerebellum in Reward and Social Behaviors

A new study in rodents has shown that the brain’s cerebellum—known to play a role in motor coordination—also helps control the brain’s reward circuitry. Researchers found a direct neural connection from the cerebellum to the ventral tegmental area (VTA) of the brain, which is an area long known to be involved in reward processing and encoding. These findings, published in Science, demonstrate for the first time that the brain’s cerebellum plays a role in controlling reward and social preference behavior, and sheds new light on the brain circuits critical to the affective and social dysfunction seen across multiple psychiatric disorders. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health.

“This type of research is fundamental to deepening our understanding of how brain circuit activity relates to mental illnesses,” said Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Findings like the ones described in this paper help us learn more about how the brain works, a key first step on the path towards developing new treatments.”

The cerebellum plays a well-recognized role in the coordination and regulation of motor activity. However, research has also suggested that this brain area contributes to a host of non-motor functions. For example, abnormalities in the cerebellum have been linked to autism, schizophrenia, and substance use disorders, and brain activation in the cerebellum has been linked to motivation, social and emotional behaviors, and reward learning, each of which can be disrupted in psychiatric disorders.

These earlier findings led Kamran Khodakhah, Ph.D. , of the Albert Einstein College of Medicine, New York, and colleagues to wonder if there was a direct connection between the cerebellum and the VTA—a brain structure involved in controlling reward and motivational behaviors. To examine this, the researchers used a technique called optogenetics, in which the neurons of animals are genetically modified, so they can be controlled using pulses of light. The researchers used this technique in mice, activating neurons in the cerebellum which connected to the VTA. The researchers found that activating the cerebellar neurons led to increased activation in the VTA of mice, indicating a working connection between these two brain structures.

Once the neural connection between these two brain structures was confirmed, the researchers investigated whether inputs from the cerebellum to the VTA influenced reward-related and social preference behavior. The researchers placed mice in a square-shaped open chamber and used pulses of light to activate cerebellar neurons linked to the VTA whenever mice entered a specific part of the chamber, called the “reward quadrant.” Mice showed a strong preference for spending time in the reward quadrant, freely choosing to spend more than 70 percent of their time in this area. In addition, the researchers found that mice were willing to work for activation in this brain area and to spend time in conditions they would usually not prefer (light vs. darker areas) to receive this activation. Together, the findings suggest that activation of the cerebellar projections to the VTA is rewarding for mice and that the cerebellum plays a role in reward-related behaviors.

To examine whether the inputs from the cerebellum into the VTA impacted social behaviors, the researchers tested mice using a three-chamber social task in which the mice could choose to spend time in a chamber with another mouse (the social chamber), in an empty central chamber, or in a chamber containing a non-social object. At baseline, mice preferred to be in the social chamber, but after researchers inactivated the cerebellar projections into the VTA, the mice no longer showed this preference. In addition, continuous silencing of the cerebellar-VTA pathway was found to completely prevent the expression of social preference behavior in the mice, findings which indicate that inputs from the cerebellum into the VTA are necessary for social preference behavior in mice.

Heatmaps showing the amount of time a mouse spent in locations of the open field chamber at baseline (left) and during optogenetic stimulation of the cerebellar input to the VTA (right). The “reward quadrant” is located in the upper right section of the field. Credit: Albert Einstein College of Medicine

The results of this study suggest a potentially major—and previously unrecognized—role for the cerebellum in the creation and control of reward and social preference behaviors. Although there is much left to explore, the identification of this direct neural pathway may help explain the role of this circuit in disorders that involve reward-related and social-processing systems, such as addiction, autism, and schizophrenia, and may point to future targets for intervention and symptom management.

“The role of cerebellar circuitry in mental-health relevant behaviors is an understudied area, one in which we have just begun to see increased interest, said Janine Simmons, M.D., Ph.D., chief of the NIMH Social and Affective Neuroscience Program. “We are always excited to see innovation of this type in the behavioral neurosciences, and these results demonstrate how much remains to be learned.”

In future studies, the researchers plan to test whether the cerebellum-VTA pathway can be manipulated, using drugs or optogenetics, to treat addiction and prevent relapse after treatment.

“Cerebellar abnormalities are also linked to a number of other mental disorders such as schizophrenia,” said Dr. Khodakhah. “We want to find out whether this pathway also plays a role in those disorders.”


New Findings Reveal Surprising Role of the Cerebellum in Reward and Social Behaviors

NIH-funded study sheds new light on brain circuits related to affective and social dysfunction.

Heatmaps showing the amount of time a mouse spent in locations of the open field chamber at baseline (left) and during optogenetic stimulation of the cerebellar input to the VTA (right). The “reward quadrant” is located in the upper right section of the field. Albert Einstein College of Medicine

A new study in rodents has shown that the brain’s cerebellum—known to play a role in motor coordination—also helps control the brain’s reward circuitry. Researchers found a direct neural connection from the cerebellum to the ventral tegmental area (VTA) of the brain, which is an area long known to been involved in reward processing and encoding. These findings, published in Science, demonstrate for the first time that the brain’s cerebellum plays a role in controlling reward and social preference behavior, and sheds new light on the brain circuits critical to the affective and social dysfunction seen across multiple psychiatric disorders. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health.

“This type of research is fundamental to deepening our understanding of how brain circuit activity relates to mental illnesses,” said Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Findings like the ones described in this paper help us learn more about how the brain works, a key first step on the path towards developing new treatments.”

The cerebellum plays a well-recognized role in the coordination and regulation of motor activity. However, research has also suggested that this brain area contributes to a host of non-motor functions. For example, abnormalities in the cerebellum have been linked to autism, schizophrenia, and substance use disorders, and brain activation in the cerebellum has been linked to motivation, social and emotional behaviors, and reward learning, each of which can be disrupted in psychiatric disorders.

These earlier findings led Kamran Khodakhah, Ph.D., of the Albert Einstein College of Medicine, New York, and colleagues to wonder if there was a direct connection between the cerebellum and the VTA—a brain structure involved in controlling reward and motivational behaviors. To examine this, the researchers used a technique called optogenetics, in which the neurons of animals are genetically modified, so they can be controlled using pulses of light. The researchers used this technique in mice, activating neurons in the cerebellum which connected to the VTA. The researchers found that activating the cerebellar neurons led to increased activation in the VTA of mice, indicating a working connection between these two brain structures.

Once the neural connection between these two brain structures was confirmed, the researchers investigated whether inputs from the cerebellum to the VTA influenced reward-related and social preference behavior. The researchers placed mice in a square-shaped open chamber and used pulses of light to activate cerebellar neurons linked to the VTA whenever mice entered a specific part of the chamber, called the “reward quadrant.” Mice showed a strong preference for spending time in the reward quadrant, freely choosing to spend more than 70 percent of their time in this area. In addition, the researchers found that mice were willing to work for activation in this brain area and to spend time in conditions they would usually not prefer (light vs. darker areas) to receive this activation. Together, the findings suggest that activation of the cerebellar projections to the VTA is rewarding for mice and that the cerebellum plays a role in reward-related behaviors.

To examine whether the inputs from the cerebellum into the VTA impacted social behaviors, the researchers tested mice using a three-chamber social task in which the mice could choose to spend time in a chamber with another mouse (the social chamber), in an empty central chamber, or in a chamber containing a non-social object. At baseline, mice preferred to be in the social chamber, but after researchers inactivated the cerebellar projections into the VTA, the mice no longer showed this preference. In addition, continuous silencing of the cerebellar-VTA pathway was found to completely prevent the expression of social preference behavior in the mice, findings which indicate that inputs from the cerebellum into the VTA are necessary for social preference behavior in mice.

The results of this study suggest a potentially major—and previously unrecognized—role for the cerebellum in the creation and control of reward and social preference behaviors. Although there is much left to explore, the identification of this direct neural pathway may help explain the role of this circuit in disorders that involve reward-related and social-processing systems, such as addiction, autism, and schizophrenia, and may point to future targets for intervention and symptom management.

“The role of cerebellar circuitry in mental-health relevant behaviors is an understudied area, one in which we have just begun to see increased interest, said Janine Simmons, M.D., Ph.D., chief of the NIMH Social and Affective Neuroscience Program. “We are always excited to see innovation of this type in the behavioral neurosciences, and these results demonstrate how much remains to be learned.”

In future studies, the researchers plan to test whether the cerebellum-VTA pathway can be manipulated, using drugs or optogenetics, to treat addiction and prevent relapse after treatment.

“Cerebellar abnormalities are also linked to a number of other mental disorders such as schizophrenia,” said Dr. Khodakhah. “We want to find out whether this pathway also plays a role in those disorders.”

This press release describes a basic research finding. Basic research increases our understanding of human behavior and biology, which is foundational to advancing new and better ways to prevent, diagnose, and treat disease. Science is an unpredictable and incremental process— each research advance builds on past discoveries, often in unexpected ways. Most clinical advances would not be possible without the knowledge of fundamental basic research.

About the National Institute of Mental Health (NIMH): The mission of the NIMH is to transform the understanding and treatment of mental illnesses through basic and clinical research, paving the way for prevention, recovery, and cure. For more information, visit the NIMH website.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit www.nih.gov.

NIH&hellipTurning Discovery Into Health ®

Reference

Carta, I., Chen, C. H., Schott, A., Dorizan, S., & Khodakhah, K. (in press). Cerebellar modulation of the reward circuitry and social behavior. Science. Online January 17, 2019.


Information About Carl Wernicke

Carl Wernicke was a German doctor who was born in 1848. He was killed in an accident in 1905, reportedly while riding his bike. Wernicke is often classified as a neuropsychiatrist. He believed that patients with psychiatric problems had problems in a specific region or pathway in their brain rather than in the brain as a whole.

Wernicke discovered the region now named in his honour and found that damage in the area produced aphasia. He was only 26 years old when he published the results of his discovery. He referred to the disorder resulting from the damage as sensory aphasia. The name was later changed to honour his work.

Aphasia is often caused by strokes, especially in older people. Strokes occur in younger people as well, however. Aphasia may also develop due to tumours, head trauma, and infections.


Pathogen Transmission

An infection starts with exposure to a pathogen. The natural site or home for a pathogen is known as a reservoir and can either be animate (human or animal) or inanimate (water, soil, food). A pathogen can be picked up from its reservoir and then spread from one infected host to another. Carriers play an important role in the spread of disease, since they carry the pathogen but show no obvious symptoms of disease. A disease that primarily occurs within animal populations but can be spread to humans is called a zoonosis, while a hospital-acquired infection is known as a nosocomial infection.

The mechanism by which a pathogen is picked up by a host is referred to as mode of transmission, with the main mechanisms listed below:

Direct contact

Direct contact includes host-to-host contact, such as through kissing or sexual intercourse, where one person might come in contact with another person&rsquos skin or body fluids. An expectant mother may transmit a pathogen to her infant by vertical contact while pregnant, or during the act of giving birth.

Droplet transmission

Droplet transmission is often considered to be a form of direct contact as well. It involves transmission by respiratory droplets, where an infected host expels the pathogen in tiny droplets by coughing or sneezing, which are then inhaled by a host nearby. These droplets are not transmitted through the air over long distances, nor do they remain infectious for very long.

Indirect contact

Indirect contact involves the transfer of the infectious agent through some type of intermediary, such as a contaminated object or person. The pathogen might be deposited on an inanimate object, called a fomite, which is then used by another person. This could include a shared toy or commonly-touched surface, like a doorknob or computer keyboard. Alternatively, a healthcare worked might transmit a pathogen from one patient to another, if they did not change their gloves between patients.

Airborne transmission

Airborne transmission occurs due to pathogens that are in small particles or droplets in the environment, which can remain infectious over time and distance. An example might be fungal spores that are inhaled during a dust storm.

Fecal-oral transmission

Fecal-oral transmission occurs when an infected host is shedding the pathogen in their feces which contaminate food or water that is consumed by the next host.

Vectorborne transmission

Vectorborne transmission occurs when an arthropod vector, such as mosquitoes, flies, ticks, are involves in the transmission. Sometimes the vector just picks up the infectious agents on their external body parts and carries it to another host, but typically the vector picks up the infectious agent when biting an infected host. The agent is picked up in the blood, and then spread to the next host when the vector moves on to bite someone else.


Frog Dissection: External and Internal

  • Contributed by Shannan Muskopf
  • High School Biology Instructor at Granite City School District
  • Sourced from Biology Corner

External Anatomy

1. Observe the dorsal and ventral sides of the frog. Dorsal side color ___________ Ventral side color ____________

2. Examine the hind legs. How many toes are present on each foot? ______ Are they webbed? _____

3. Examine the forelegs. How many toes are present? ________Are the toes webbed? _______

4. Use a ruler to measure your from the tip of the head to the end of the frog's backbone. Compare the length of your frog to other frogs

5. Locate the frog's eyes, the nictitating membrane is a clear membrane that attached to the bottom of the eye. Use tweezers to carefully remove the nictitating membrane. You may also remove the eyeball.

What color is the nictitating membrane? _____________ What color is the eyeball? _________________

6. Just behind the eyes on the frog's head is a circular structure called the tympanic membrane. The tympanic membrane is used for hearing. Measure the diameter (distance across the circle) of the tympanic membrane. Diameter of tympanic membrane = ___________cm

7. Feel the frog's skin. Is it scaly or is it slimy? ____________

Anatomy of the Frog's Mouth

Pry the frog's mouth open and use scissors to cut the angles of the frog's jaws open. Cut deeply so that the frog's mouth opens wide enough to view the structures inside.

1. Locate the tongue. Play with the tongue. Does it attach to the front or the back of the mouth? __________ (You may remove the tongue). Draw a sketch of the tongue, paying attention to its shape.

2. In the center of the mouth, toward the back is a single round opening, the esophagus. This tube leads to the stomach. Use a probe to poke into the esophagus.

3. Close to the angles of the jaw are two openings, one on each side. These are the Eustachian tubes. They are used to equalize pressure in the inner ear while the frog is swimming. Insert a probe into the Eustachian tube.

To what structure does the Eustachian tube attach? _____________________

4. Just behind the tongue, and before you reach the esophagus is a slit like opening. (You may need to use your probe to get it to open up). This slit is the glottis, and it is the opening to the lungs. The frog breathes and vocalizes with the glottis. Use your probe to open the glottis and compare that opening to the esophagus.

5. The frog has two sets of teeth. The vomerine teeth are found on the roof of the mouth. The maxillary teeth are found around the edge of the mouth. Both are used for holding prey, frogs swallow their meals whole and do NOT chew. Run you finger over both sets of teeth and note the differences between them.

6. On the roof of the mouth, you will find the two tiny openings of the nostrils, if you put your probe into those openings, you will find they exit on the outside of the frog.

7. Label each of the structures underlined above.

Frog Dissection: Internal Anatomy

Dissection Instructions

  1. Place the frog in the dissecting pan ventral side up.
  2. Use scissors to lift the abdominal muscles away from the body cavity. Cut along the midline of the body to the forelimbs.
  3. Make transverse (horizontal) cuts near the arms and legs.
  4. Life the flaps of the body wall and pin back.

*If your specimen is a female, the body may be filled with eggs. You may need to remove these eggs to view the organs.

Locate each of the organs below. Check the box to indicate that you found the organs.

  1. Fat Bodies --Spaghetti shaped structures that have a bright orange or yellow color, if you have a particularly fat frog, these fat bodies may need to be removed to see the other structures. Usually they are located just on the inside of the abdominal wall.
  2. Peritoneum ­ A spider-web like membrane that covers many of the organs you may carefully pick it off to get a clear view
  3. Liver--The largest structure of the the body cavity. This brown colored organ is composed of three lobes. The right lobe, the left anterior lobe, and the left posterior lobe. The liver is not primarily an organ of digestion, it does secrete a digestive juice called bile. Bile is needed for the proper digestion of fats.
  4. Heart - at the top of the liver, the heart is a triangular structure. The left and right atrium can be found at the top of the heart. A single ventricle located at the bottom of the heart. The large vessel extending out from the heart is the conus arteriosus.
  5. Lungs - Locate the lungs by looking underneath and behind the heart and liver. They are two spongy organs.
  6. Gall Bladder --Lift the lobes of the liver, there will be a small green sac under the liver. This is the gallbladder, which stores bile. (hint: it kind of looks like a booger)
  7. Stomach--Curving from underneath the liver is the stomach. The stomach is the first major site of chemical digestion. Frogs swallow their meals whole. Follow the stomach to where it turns into the small intestine. The pyloric sphincter valve regulates the exit of digested food from the stomach to the small intestine.
  8. Small Intestine--Leading from the stomach. The first straight portion of the small intestine is called the duodenum, the curled portion is the ileum. The ileum is held together by a membrane called the mesentery. Note the blood vessels running through the mesentery, they will carry absorbed nutrients away from the intestine. Absorption of digested nutrients occurs in the small intestine.
  9. Large Intestine--As you follow the small intestine down, it will widen into the large intestine. The large intestine leads to the cloaca, which is the last stop before solid wastes, sperm, eggs, and urine exit the frog's body. (The word "cloaca" means sewer)
  10. Spleen--Return to the folds of the mesentery, this dark red spherical object serves as a holding area for blood.
  11. Esophagus--Return to the stomach and follow it upward, where it gets smaller is the beginning of the esophagus. The esophagus is the tube that leads from the frogs mouth to the stomach. Open the frogs mouth and find the esophagus, poke your probe into it and see where it leads.

If you have not located each of the organs above, do not continue on to the next sections!

Removal of the Stomach:

Cut the stomach out of the frog and open it up. You may find what remains of the frog's last meal in there. Look at the texture of the stomach on the inside.

What did you find in the stomach?

Measuring the Small intestine: Remove the small intestine from the body cavity and carefully separate the mesentery from it. Stretch the small intestine out and measure it. Now measure your frog. Record the measurements below in centimeters. Frog length: _______ cm Intestine length ________ cm

Urogenital System

The frog's reproductive and excretory system is combined into one system called the urogenital system. You will need to know the structures for both the male and female frog

Kidneys - flattened bean shaped organs located at the lower back of the frog, near the spine. They are often a dark color. The kidneys filter wastes from the blood. Often the top of the kidneys have yellowish stringy fat bodies attached.

Testes - in male frogs, these organs are located at the top of the kidneys, they are pale colored and round.

Oviducts - females do not have testes, though you may see a curly structure around the outside of the kidney, these are the oviducts. Oviducts are where eggs are produced. Males can have structures that look similar, but serve no actual purpose. In males, they are called vestigial oviducts.

Bladder - An empty sac located at the lowest part of the body cavity. The bladder stores urine.

Cloaca - mentioned again as part of the urogenital system - urine, sperm and eggs exit here.

Label the parts of the urogenital system.

Post Lab Questions

1. The membrane holds the coils of the small intestine together: _________________________

2.This organ is found under the liver, it stores bile: ___________________________

3. Name the 3 lobes of the liver: _____________________, ____________________, ___________________

4. The organ that is the first major site of chemical digestion: _______________________

5. Eggs, sperm, urine and wastes all empty into this structure: __________________________

6. The small intestine leads to the: _______________________________

7. The esophagus leads to the: ______________________________

8. Yellowish structures that serve as an energy reserve: _________________________

9. The first part of the small intestine(straight part): ____________________________

10. After food passes through the stomach it enters the: _________________________

11. A web-like membrane that covers the organs: ___________________________

12. Regulates the exit of partially digested food from the stomach: _____________________

13. The large intestine leads to the _______________________

14. Organ found within the mesentery that stores blood: __________________________


Conclusions

Cruciform structures are fundamentally important for a wide range of biological processes, including DNA transcription, replication, recombination, control of gene expression and genome organization. The putative mechanistic roles of cruciform binding proteins in transcription, DNA replication, and DNA repair are shown in Figure 5. Alternative DNA structures, including cruciforms, are often formed at sites of negatively supercoiled DNA by perfect or imperfect inverted repeats of 6 or more nucleotides. Longer DNA palindromes present a threat to genomic stability as they are recognized by junction-resolving enzymes. Shorter palindromic sequences are essential for basic processes like DNA replication and transcription. The presence of cruciform structures may also play an important role in epigenetics, such that cruciform structures are protected from DNA methylation. For example, the Dam methylase is not able to modify its GATC target site when it occurs in a cruciform or hairpin conformation. The center of a long perfect palindrome located in bacteriophage lambda has also been shown to be methylation-resistant in vivo[40]. Moreover, the centers of long palindromes are hypo-methylated as compared to identical sequences in non-palindromic conformations [40]. To this end, transient cruciforms can directly influence DNA methylation and therefore provide another layer for regulation of the DNA code. Proteins that bind to cruciforms can be divided into several categories. In addition to a well defined group of junction-resolving enzymes, we have classified cruciform binding proteins into groups involved in transcription and DNA repair (PARP, BRCA1, p53, 14-3-3), chromatin-associated proteins (DEK, BRCA1, HMG protein family, topoisomerases), and proteins involved in replication (MLL, WRN, 14-3-3, helicases) (see Table 1). Within these groups are proteins indispensable for cell viability, as well as tumor suppressors, proto-oncogenes and DNA remodeling proteins. Similarly, triplet repeat expansion, a phenomenon important in several genetic diseases, including Friedreich's ataxia, cardiomyopathy, myotonic dystrophy type I and other neurological disorders, can change the spectrum of cruciform binding proteins. Lastly, single nucleotide polymorphisms and/or insertion/deletion mutations at inverted repeats located in promoter sites can also influence cruciform formation, which might be manifested through altered gene regulation. A deeper understanding of the processes related to the formation and function of alternative DNA structures will be an important component to consider in the post-genomic era.

Scheme of the putative mechanistic roles of cruciform binding proteins in transcription, DNA replication, and DNA repair. A) A model for the structure-specific binding of transcription factors to a cognate palindrome-type cruciform implicated in transcription. The equilibrium between classic B-DNA and the higher order cruciform favors duplex DNA, but, when cruciform binding proteins are present, they either preferentially bind to and stabilize the cruciform or bind to the classic form and convert it to the cruciform. This interaction results in both an initial melting of the DNA region covered by transcription factor and an extension of the melt region in both directions. The melting region continues to extend in response to the needs of the active transcription machinery. B) A model for the initiation of replication enhanced by extrusion to a cruciform structure. Dimeric cruciform binding proteins interact with and stabilize the cruciform structure. The replisome is assembled concomitantly and is assumed to include polymerases, single-strand binding proteins and helicases. C) Model for the influence of cruciform binding proteins on DNA structure in DNA damage regulation. Naked cruciforms are sensitive to DNA damage and are covered by proteins in order to protect these sequences from being cleaved. In these cases, a deficiency in cruciform binding proteins can lead to DNA breaks. Here, cruciform-DNA complexes can also serve as scaffolds to recruit the DNA damage machinery.