Midterm Study Questions Flashcards
Why do we have both Neurological and Psychiatric categories? Why not just one category?
Because the way psychology developed without the focus on the brain.
Also we can’t yet trace all the psychiatric disorders to brain yet. The two do potentially could be combined in the future but it would require convincing people who were not taught to think of them as the same.
What is NeuroSky?
A tool that measures brain waves from outside the head. It can be used to play games or as a tool for psychological health.
What types of backgrounds do individuals come from that work in the field of biopsychology? What is the advantage of this variety?
Biological psychology is a field that includes many players who come from quite different backgrounds: psychologists, biologists, physiologists, engineers, neurologists, psychiatrists, and many others.
What are the five viewpoints for the exploration of the biology of behaviour? Be prepared to give an example of how these can be applied to the study of a behavioural question.
In our pursuit to understand the biological bases of behavior, we use several different perspectives. Because each one yields information that complements the others, the combination of perspectives is especially powerful. The five major perspectives are:
- Describe behaviour
- Evolution of behaviour
- Development of behaviour over the lifespan
- Biological mechanisms of behaviour
- Neurological and Psychiatric Disorders
Be familiar with the concepts in Box 1.1
We Are All Alike, and We Are All Different
We Are All Alike, and We Are All Different
Each person has some characteristics shared by…
- All animals use DNA to store genetic information.
- All vertebrates have a backbone and spinal cord
- All mammals suckle their young.
- All primates have a hand with an opposable thumb and a relatively large, complex brain.
- All humans use symbolic language to communicate with each other.
- Some people like to eat beets (no one knows why).
- No two people, even identical twins, are alike in each and every way, as individual experiences leave their unique stamp on every brain.
What is ontogeny? Why is it important to study the nervous systems control of behaviour over the lifespan? Do you think it would be appropriate to study diseases of aging in a child/young animal? Why or why not?
The process by which an individual changes in the course of its lifetime—that is, grows up and grows old.
Observing the way in which a particular behavior changes during ontogeny may give us clues to its functions and mechanisms. For example, we know that learning ability in monkeys increases over several years of development. Therefore, we can speculate that prolonged maturation of brain circuits is required for complex learning tasks.
In some case it would be appropriate to study diseases of aging in a child/young animal if there are similar functions that could be observed that would give insight in to the location or nature of the human disorder. It would not give any concrete answers but point researchers a direction to continue studies in.
How can the research that Biopsychologist do in non-human animals apply to the study of human problems?
Most study in animals are not directly transpherable to human problems but the similar structures and elements can be studied to give clues on how they might work in humans and point researchers a direction to continue research in.
Please come up with an example of each of the three main approaches to the study of the neuroscience of behaviour (not the ones in the textbook)
- Manipulating the body to effect behavior.
Somatic intervention – administer a drug
Behavior affected – working memory - Experience affects the body and brain.
Behavior intervention – expose to threat of harm
Somatic effects - measure levels of neurotransmitters - Body and behavioral measures covary
Somatic variables – activation in brain when looking at art
Behavior variables – art training and ability
What is neuroplasticity? How does the environment affect our nervous systems?
The ability of the nervous system to change in response to experience or the environment.
Experience can affect the number or size of neurons, or the number or size of connections between neurons.
How are social psychology and biopsychology related?
Cooke et al. (2000) took young rats, just weaned from their mother, and either raised each male in a cage alone or raised them with other males to play with. Examination of these animals as adults found only one brain difference between the groups: a region of the brain known to process odors was smaller in the isolated males than in the males raised with playmates (FIGURE 1.4). Was it the lack of play (N. S. Gordon et al., 2003), the lack of odors to investigate, or the stress of isolation that made the region smaller? Whatever the mechanism, social experience affects this brain structure.
Here’s an example of how social influences can affect the human brain. When people were asked to put a hand into moderately hot water (47°C), part of the brain became active, presumably because of the discomfort involved (Rainville et al., 1997). But subjects who were led to believe the water would be very hot had a more activated brain than did subjects led to believe the discomfort would be minimal (FIGURE 1.5), even though the water was the same temperature for all subjects. The socially induced psychological expectation affected the magnitude of the brain response, even though the physical stimulus was exactly the same.
In most cases, biological and social factors continually interact and affect each other in an ongoing series of events as behavior unfolds.
What are some of the common levels of analysis that are used to study nervous system function?
The scope of experimental approaches. A scientist may try to understand behavior by monitoring molecules, nerve cells, brain regions, or social environments, or some combination of these levels of analysis.
Levels • Social level • Organ level • Neural system level • Brain region level • Circuit level • Cellular level • Synaptic level • Molecular level
If I was to design a new drug what types of information could I gain by studying behaviour at the various levels of analysis that are listed in the textbook (1.5)?
New Depression Medication
Social level – effect on mood, attention, motivation
Organ level – side effects in the digestive system
Neural system level – the changes in the overall activation patterns in the brain
Brain region level – the changes in the brain regions associated with depression
Circuit level – changes in the circuits in the areas of the brain that are most affected by the drug
Cellular level – transmission speed changes in a single neuron
Synaptic level – the changes in the levels of neurotransmitters released or reabsorbed
Molecular level – changes in sodium levels
What is consciousness – what do we know about the brains control of it? Will we ever understand how the brain generates it?
experience.
• Consciousness matters; it permits us to do certain important things, like planning and mentally “simulating” what might happen in the future.
• Consciousness is bound up somehow with the activity of the brain.
• We are not aware of all of our brain’s activities. Some brain activity, and therefore some of our behavior, is unconscious.
• The deepest parts of our brain are important for arousal.
• The topmost parts of the brain are responsible for whatever we experience from moment to moment.
Be able to label the parts of a neuron on a diagram. Also make sure you can define what each part does.
The basic unit of the nervous system, each composed of a cell body, receptive extension(s) (dendrites), and a transmitting extension (axon).
Dendrite - One of the extensions of the cell body that are the receptive surfaces of the neuron.
Cell body or soma - The region of a neuron that is defined by the presence of the cell nucleus. Also contains mitochondrion and ribosomes.
Axon hillock A cone-shaped area from which the axon originates out of the cell body. Functionally, the integration zone of the neuron.
Axon- A single extension from the nerve cell that carries nerve impulses from the cell body to other neurons.
The axon has two quite different functions: rapid transmission of electrical signals along the outside of the axon, and the much slower transportation of substances inside the axon, to and from the axon terminals.
Axon terminal - Also called synaptic bouton. The end of an axon or axon collateral, which forms a synapse on a neuron or other target cell.
What is the input, integration, conduction and output zone of a neuron?
Input zone
- The part of a neuron that receives information, from other neurons or from specialized sensory structures. Usually corresponds to the cell’s dendrites.
Integration zone
- The part of the neuron that initiates nerve electrical activity. Usually corresponds to the neuron’s axon hillock.
Conduction zone
- The part of the neuron over which the nerve’s electrical signal may be actively propagated. Usually corresponds to the cell’s axon.
Output zone
- The part of a neuron, usually corresponding to the axon terminals, at which the cell sends information to another cell.
How long can neurons be?
In a griaf – 15 feet
In a whale - 30 feet
In a human – several feet
What are glia cells?
Glial cells support neuronal activity
There are 4 types that we need to know for the class.
Glial cells respond to injury by edema, or swelling, and are also susceptible to tumors.
What does glia mean?
Glue
Why would neurons come in different shapes and sizes?
Neurons are remarkably diverse in shape, their forms reflecting their highly specialized functions.
What is/are the difference(s) between a multipolar, bipolar and unipolar neuron? What does there morphology suggest about their function?
Multipolar neuron - A nerve cell that has many dendrites and a single axon. They are the most common type of neuron.
Bipolar neuron - A nerve cell that has a single dendrite at one end and a single axon at the other end. This type of neuron is especially common in sensory systems, such as vision.
Unipolar neuron -Also called monopolar neuron. A nerve cell with a single branch that leaves the cell body and then extends in two directions; one end is the receptive pole, the other end the output zone. Such cells transmit touch infor-mation from the body into the spinal cord.
What is the difference between a motor, sensory and interneuron?
Motoneuron Also called motor neuron. A nerve cell that transmits motor messages, stimulating a muscle or gland.
Sensory neuron A neuron that is directly affected by changes in the environment, such as light, odor, or touch.
Interneuron A neuron that is neither a sensory neuron nor a motoneuron; it receives input from and sends output to other neurons. Shortest of the three.
What is the difference between an oligodendrocyte and Schwann cell?
Oligodendrocyte - A type of glial cell that forms myelin in the central nervous system.
Schwann cell- The glial cell that forms myelin in the peripheral nervous system.
Are all axons myelinated?
No
Many thin, short axons lack myelin but still are surrounded by oligodendrocytes or Schwann cells, which segregate the unmyelinated axons
What is the node of Ranvier? Why is it important?
Node of Ranvier - A gap between successive segments of the myelin sheath where the axon membrane is exposed.
It is important because it serves to facilitate the rapid conduction of nerve impulses
What are the roles of astrocytes and microglia?
Glial Cells
Astrocyte - A star-shaped glial cell with numerous processes (extensions) that run in all directions.
Microglial cells Also called microglia. Extremely small glial cells that remove cellular debris from injured or dead cells.
What is a dendritic spine/synapse??
Synapse - The tiny gap between neurons where information is passed from one to the other.
Studding the dendrites of many neurons are outgrowths called dendritic spines that, by effectively increasing the surface area of the dendrites, allow for extra synaptic contacts. Both the number and structure of dendritic spines may be rapidly altered by experience, such as training or exposure to sensory stimuli
How does information go from one neuron to another via the synapse
Information is transmitted from the axon terminal of the presynaptic neuron to the receptive surface of the postsynaptic neuron through the synaptic cleft. The synaptic cleft is the gap of about 20–40 nanometers (nm) that separates the presynaptic and postsynaptic membranes.
Presynaptic axon terminals contain numerous tiny spheres, called synaptic vesicles, each 30–140 nm in diameter. Each vesicle contains a specialized chemical substance, a neurotransmitter, which the neuron uses to communicate with postsynaptic neurons. In response to electrical activity in the axon, these vesicles fuse with the presynaptic membrane, releasing molecules of neurotransmitter into the cleft. After crossing the cleft, the released neurotransmitter interacts with postsynaptic receptors: specialized protein molecules that capture and react to molecules of the neurotransmitter.
What is/are the difference(s) between the central and peripheral nervous systems?
a natural subdivision into a peripheral nervous system (all nervous system parts that are outside the bony skull and spinal column) and a central nervous system (CNS), consisting of the brain and spinal cord
What is/are the general functions of the cranial nerves? be familiar with what they are – for example if I asked you for five areas of the face that the cranial nerves process neural information for you should be able to answer this
Cranial nerves serve the sensory and motor systems of the head and neck.
Three cranial nerves are exclusively sensory pathways to the brain: the olfactory, the optic and the nerve is concerned with hearing and balance.
Five nerves are exclusively motor pathways from the brain: three nerve pathways innervate muscles to move the eye; one pathway controls neck muscles; and one controls the tongue.
The remaining cranial nerves have both sensory and motor functions. One serves facial sensation and it controls chewing movements through other axons. Another set of nerves control facial muscles and receive taste sensation, there are nerves that receive sensation from the throat and control the muscles there. And the vagus (X) nerve extends far from the head, running to the heart, liver, and intestines
What is the somatic part of the peripheral nervous system?
Spinal nerves–also called somatic nerves, connected to the spinal cord
Each spinal nerve is the fusion of two distinct branches, or roots:
- Dorsal (back) root–carries sensory information from the body to the spinal cord
- Ventral (front) root–carries motor information from the spinal cord to the muscles
What is the main difference between the ventral and dorsal roots of the spinal cord?
Each spinal nerve is the fusion of two distinct branches, or roots:
- Dorsal (back) root–carries sensory information from the body to the spinal cord
- Ventral (front) root–carries motor information from the spinal cord to the muscles
What is the sympathetic and parasympathetic nervous system? What are they a part of? Where do they originate in the spinal cord?
The autonomic nervous system has three major divisions:
- Sympathetic nervous system
- Parasympathetic nervous system
- Enteric nervous system
Sympathetic nervous system - A component of the autonomic nervous system that arises from the thoracic and lumbar spinal cord. In general, sympathetic activation prepares the body for action: blood pressure increases, the pupils of the eyes widen, and the heart quickens. This set of reactions is sometimes called simply the “fight or flight” response.
Parasympathetic nervous system - A component of the autonomic nervous system that arises from both the cranial nerves and the sacral spinal cord. Generally helps the body to relax, recuperate, and prepare for future action, sometimes called the “rest and digest” response.
How does development relate to the way the structures of the brain are categorized as part of the telencephalon, diencephalon, mesencephalon, metencephalon and myelencephalon?
Neural tube - An embryonic structure with subdivisions that correspond to the future forebrain, midbrain, and hindbrain.
The walls of this neural tube are made of cells, and the interior is filled with fluid. A few weeks after conception, the human neural tube begins to show three separate swellings at the head end: the forebrain (or prosencephalon), the midbrain (or mesencephalon), and the hindbrain (or rhombencephalon).
About 50 days after conception, the forebrain and hindbrain have already developed clear subdivisions. At the very front of the developing brain is the telencephalon, diencephalon, mesencephalon, metencephalon, and myelencephalon.
What are the meninges, why are they important?
Meninges are the three protective sheets of tissue—dura mater, pia mater, and arachnoid—that surround the brain and spinal cord.
Dura mater -The outermost of the three meninges that surround the brain and spinal cord.
Pia mater - the innermost of the three meninges that surround the brain and spinal cord
Arachnoid - The thin covering (one of the three meninges) of the brain that lies between the dura mater and pia mater.
What is meningitis?
An acute inflammation of the meninges, usually caused by a viral or bacterial infection.
Potentially lethal medical emergency characterized in early stages by headache, fever, and stiff neck as the inflamed meninges press on the brain.
What is CSF – where is it made, where does it flow, where is it re-absorbed. Do we make what we need on a daily basis?
What is CSF? Cerebrospinal fluid (CSF) - The fluid that fills the cerebral ventricles.
where is it made? Choroid plexus - A highly vascular portion of the lining of the ventricles that secretes cerebrospinal fluid. Specialized membrane the lines the lateral ventricles produces CSF by filtering blood.
where does it flow? Ventricular system - A system of (CSF) fluid-filled cavities inside the brain. The middle layer of Meninges call Arachnoid - suspends the brain in a bath of cerebrospinal fluid (CSF).
where is it re-absorbed? CSF is absorbed back into the circulatory system through: large veins beneath the top of the skull.
Do we make what we need on a daily basis? First, it acts mechanically as a shock absorber for the brain: floating in CSF, the brain is protected from sudden movements of the head that would smash it against the inside of the skull.
Second, CSF provides a medium for the exchange of
materials, including nutrients, between
What do the ventricles do?
ventricular system - A system of fluid-filled cavities inside the brain.
The CSF circulating through the ventricular system has at least two
main functions. First, it acts mechanically as a shock absorber for the brain: floating in CSF, the brain is protected from sudden movements of the head that would smash it against the inside of the skull. Second, CSF provides a medium for the exchange of materials, including nutrients, between blood vessels and brain tissue.
lateral ventricle - A complexly shaped lateral portion of the ventricular system within each hemisphere of the brain.
third ventricle - The midline ventricle that conducts cerebrospinal fluid from the lateral ventricles to the fourth ventricle.
fourth ventricle - The passageway within the pons that receives cerebrospinal fluid from the third ventricle and releases it to surround the brain and spinal cord.
It has three small openings allow CSF to exit the ventricular system and circulate over the outer surface of the brain and spinal cord.
What behaviours are the four lobes of the brain involved in?
Frontal lobe - The most anterior portion of the cerebral cortex.
important for movement and high-level cognition
Parietal lobe - Large regions of cortex lying between the frontal and occipital lobes of each cerebral hemisphere. It receives sensory information from the body and participate in spatial cognition.
Temporal lobes - Large lateral cortical regions of each cerebral hemisphere, continuous with the parietal lobes posteriorly, and separated from the frontal lobe by the Sylvian fissure. Auditory information damage here can impair hearing the temporal lobes are also particularly associated with the sense of smell, and with aspects of learning and memory.
Occipital lobes - Large regions of cortex covering much of the posterior part of each cerebral hemisphere. Receive and process information from the eyes, giving rise to the sense of vision.
What is the difference between white and grey matter?
White matter - A shiny layer underneath the cortex that consists largely of axons with white myelin sheaths. Which consists mostly of fiber tracts. It gains its appearance from the whitish fatty myelin that ensheathes and insulates the axons of many neurons. White matter mostly transmits information.
Gray matter - Areas of the brain that are dominated by cell bodies and are devoid of myelin. On the exterior is dominated more by nerve cell bodies and dendrites, which are devoid of myelin. A simple view is that gray matter primarily processes information,
What is the difference between fissures, gyri and sulci?
The lumpy convolutions of the paired cerebral hemispheres are the result of elaborate folding together of a thick sheet of brain tissue called the cerebral cortex which is made up mostly of neurons and their fibers. The resulting ridges of tissue, called gyri, are separated from each other by furrows called sulci.
A fissure is a deep sulcus
Be familiar with the three major fissures.
Sylvian fissure Also called lateral sulcus. A deep fissure that demarcates the temporal lobe.
Central sulcus A fissure that divides the frontal lobe from the parietal lobe.
Longitudinal fissure – the fissure that runs from the back to the front
Be familiar with the three major fissures.
Why are the pre- and post-central gyri important?
Postcentral gyrus - The strip of parietal cortex, just behind the central sulcus, that receives somatosensory information from the entire body.
Precentral gyrus - The strip of frontal cortex, just in front of the central sulcus, that is crucial for motor control.
What is the limbic system? What is its primary function? Hippocampus, amygdale, cingulate cortex, mammillary bodies – what do they do?
Limbic system - A loosely defined, wide-spread group of brain nuclei that innervate each other to form a network. Curving through each hemisphere, alongside the basal ganglia. It is critical for emotion and learning. Limbic structures near the base of the brain, especially the hypothalamus, help to govern highly motivated behaviors, like sex and aggression, and regulate the hormonal systems of the body.
Hippocampus - A medial temporal lobe structure that is important for learning and memory.
Amygdala - A group of nuclei in the medial anterior part of the temporal lobe. It has several subdivisions with diverse functions such as emotional regulation and odor perception.
Cingulate gyrus - A cortical portion of the limbic system, found in the frontal and parietal midline. Implicated in many cognitive functions, including the direction of attention.
Mammillary bodies - are important for emotion, learning, and memory.
What is the limbic system? What is its primary function? Hippocampus, amygdale, cingulate cortex, mammillary bodies – what do they do?
What are the basal ganglia? What is its primary function? Striatum, thalamus, amygdale, nucleus accumbens – what do they do?
Basal ganglia - A group of forebrain nuclei, including caudate nucleus, globus pallidus, and putamen, found deep within the cerebral hemispheres. The basal ganglia are very important in motor control.
Striatum The caudate nucleus and putamen together.
Thalamus - The brain regions that surround the third ventricle. Acts as a switchbox, directing almost all incoming sensory information to the appropriate regions of the cortex for further processing, and receiving instructions back from the cortex to control which sensory information is transmitted.
Amygdala - A group of nuclei in the medial anterior part of the temporal lobe. It has several subdivisions with diverse functions such as emotional regulation and odor perception.
Nucleus accumbens - A region of the forebrain that receives dopaminergic innervation from the ventral tegmental area.
What are the functions of the superior and inferior colliculi?
Superior colliculi - Paired gray matter structures of the dorsal midbrain that receive visual information and are involved in direction of visual gaze and visual attention to intended stimuli.
Inferior colliculi - Paired gray matter structures of the dorsal midbrain that receive auditory information.
What are the functions of the substantia nigra, hypothalamus (four behaviours), pituitary?
Hypothalamus - Part of the diencephalon, lying ventral to the thalamus.
It is packed with discrete nuclei involved in many vital functions, such as hunger, thirst, temperature regulation, sex, and many more. Furthermore, because the hypothalamus also controls the pituitary gland, it serves as the brain’s main interface with the hormonal systems of the body.
Substantia nigra - A brainstem structure in humans that innervates the basal ganglia. Contains neurons that release the transmitter dopamine.
Pituitary gland - Also called hypophysis. A small, complex endocrine gland located in a socket at the base of the skull. Includes anterior pituitary and posterior pituitary. Hormone secretion
What is the main function of each of the cerebellum, pons, medulla and reticular formation?
Cerebellum - t is involved in the central regulation of movement. Has long been known to be crucial for motor coordination and control, but we now know it also participates in certain aspects of cognition, including learning.
Pons - part of the brainstem connecting midbrain to medulla. Within the pons are important motor control and sensory nuclei, including several nuclei from which cranial nerves arise.
Reticular formation -An extensive region of the brainstem that is involved in arousal (waking). Variety of behaviors, including sleep and arousal, temperature regulation, and motor control.
What are the three main arteries in the brain proper? Please be able to speculate how damage (stroke) to one of these areas might affect behaviour – what would you ‘see’?
Anterior cerebral arteries - Two large arteries, arising from the carotids, that provide blood to the anterior poles and medial surfaces of the cerebral hemispheres. (stroke here would cause damage in movement and high-level cognition, receiving sensory information from the body and participate in spatial cognition.)
Middle cerebral arteries - Two large arteries, arising from the carotids, that provide blood to most of the lateral surfaces of the cerebral hemispheres. (stroke here would can impair hearing, the sense of smell, and with aspects of learning and memory)
Posterior cerebral arteries - Two large arteries, arising from the basilar artery, that provide blood to posterior aspects of the cerebral hemispheres, cerebellum, and brainstem. (stroke here would cause problems with motor coordination and control, important motor control and sensory nuclei, including several nuclei from which cranial nerves arise and heart problems and death)
What is an MRI, fMRI or a PET scan? Be able to compare and contrast these two forms of imaging the human brain (you need to read these on your own)
magnetic resonance imaging (MRI)
magnetic resonance imaging (MRI)
A noninvasive technique that uses magnetic energy to generate images that reveal some structural details in the living brain.
MRI images are derived from radio frequency energy, the patient’s head is placed in the center of an extremely powerful circular magnet that causes all the protons in the brain’s tissues to line up in parallel, instead of in their usual random orientations. the protons are knocked over by a strong pulse of radio waves. When this pulse is turned off, the protons relax back to their original configuration, emitting radio waves as they go. a powerful computer uses this density-based information to generate a detailed cross-sectional map of the brain
With their higher resolution, MRI images can reveal subtle changes in the brain, such as the loss of myelin that is characteristic of multiple sclerosis
What is an MRI, fMRI or a PET scan? Be able to compare and contrast these two forms of imaging the human brain (you need to read these on your own)
positron emission tomography (PET)
positron emission tomography (PET)
A technique for examining brain function by combining tomography with injections of radioactive substances used by the brain.
the objective is to obtain images of the brain’s activity rather than details of its structure, and it has proven to be very valuable for both experimental and medical purposes.
we can generate metabolic maps of the brain that identify the regions that contribute to specific functions.
What is an MRI, fMRI or a PET scan? Be able to compare and contrast these two forms of imaging the human brain (you need to read these on your own)
functional MRI (fMRI)
functional MRI (fMRI)
Magnetic resonance imaging that detects changes in blood flow and therefore identifies regions of the brain that are particularly active during a given task.
has revolutionized cognitive neuroscience research, producing images with reasonable speed and excellent sharpness
uses high-powered, rapidly oscillating magnetic-field gradients to detect small changes in brain metabolism, particularly the moment-to-moment use of oxygen
scientists can use fMRI data to create computer-generated images that reflect the activity of different parts of the brain while people engage in
various experimental tasks
The detailed activity maps provided by fMRI reveal how networks of brain structures collaborate on complex cognitive processes. The fMRI image generally reflects synaptic inputs and local processing, rather than the production of neural impulses
What is the sodium/potassium pump? Why is it important?
sodium-potassium pump
The energetically expensive mechanism that pushes sodium ions out of a cell, and potassium ions in.
It pumps three sodium ions (Na+) out of the cell for every two K+ ions pumped in.
The sodium-potassium (Na+-K+) pump continually pushes Na+ ions out and pulls K+ ions in. This ion pump requires considerable energy.
How does the sodium-potassium pump causing a net buildup of negative charges inside the cell?
The sodium-potassium pump causes a buildup of K+ ions inside the cell, but recall that at rest the membrane is much more permeable to K+ ions than Na+ ions. That means K+ ions will tend to leave the interior, down their concentration gradient, causing a net buildup of negative charges inside the cell.
What are hyperpolarization and depolarization – how are they different?
They are both passive graded potentials that effect the charge of the cell and impact if threshold is reached and action potential starts.
Hyperpolarization
An increase in membrane potential (the interior of the neuron becomes even more negative, relative to the outside)
So if the neuron already has a resting membrane potential of, say, –60 mV, hyperpolarization makes it even farther from zero, maybe –70 mV
Depolarization
A reduction in membrane potential (the interior of the neuron becomes less negative).
In other words, depolarization of a neuron brings its membrane potential closer to zero.
What is a voltage activated channel? When is the NA+ channel activated and inactivated by voltage?
voltage-gated Na+ channel
A Na+- selective channel that opens or closes in response to changes in the voltage of the local membrane potential; it mediates the action potential.
It is a tubular, membrane-spanning protein, but its central Na+-selective pore is ordinarily closed. When the cell membrane becomes depolarized to threshold levels, the channel’s shape changes, opening the pore to allow Na+ ions through.
the voltage-gated Na+ channel, is really quite a complicated machine. It monitors the axon’s polarity, and at threshold the channel changes its shape to open the pore, shutting down again just a millisecond later. The channel then “remembers” that it was recently open and refuses to open again for a short time. These properties produce and enforce the properties of the action potential.
What is the difference in how an AP is conducted down an unmyelinated or myelinated fiber?
nodes of Ranvier
A gap between successive segments of the myelin sheath where the axon membrane is exposed.
small gaps spaced about every millimeter along the axon
saltatory conduction
The form of conduction that is characteristic of myelinated axons, in which the action potential jumps from one node of Ranvier to the next.
because the myelin insulation offers considerable resistance to the flow of ionic currents across the membrane, the action potential jumps from node to node.
The evolution of rapid saltatory conduction in vertebrates has given them a major behavioral advantage over invertebrates, in which axons are unmyelinated and mostly small in diameter, and thus slower in conduction.
What are tetrodotoxin, saxitoxin and batratoxin? How do they affect NA+ voltage sensitive channels?
tetrodotoxin (TTX) and saxitoxin
(STX) selectively block voltage-gated sodium channels, thereby preventing the production of action potentials; paralysis and death rapidly follow.
Tetrodotoxin
A toxin from puffer fish ovaries that blocks the voltage-gated sodium channel, preventing action potential conduction.
batrachotoxin,
A toxin, secreted by poison arrow frogs, that selectively interferes with Na+ channels it forces Na+ channels to stay open, with lethal results.
What are endogenous and exogenous ligands?
A substance that binds to receptor
molecules, such as those at the surface of
the cell. Ligands fit receptors exactly and activate or block them:
endogenous ligand
Any substance, produced within the body, that selectively binds to the type of receptor that is under study.
Endogenous ligands–neurotransmitters and hormones
exogenous ligand
Any substance, originating from outside the body, that selectively binds to the type of receptor that is under study.
Exogenous ligands–drugs and toxins from outside the body
What are postsynaptic potentials?
postsynaptic potential
A local potential that is initiated by stimulation at a synapse, can vary in amplitude, and spreads passively across the cell membrane, decreasing in strength with time and distance.
given neuron, receiving synapses from hundreds of other cells, is subject to hundreds or thousands of postsynaptic potentials. When integrated, this massive array of local potentials determines whether the neuron will reach threshold and therefore generate an action potential of its own.
Synapses Cause Graded, Local changes in the Postsynaptic Membrane Potential
What are EPSP’s and IPSP’s?
Transmitters bind to postsynaptic receptors and cause an EPSP or IPSP.
EPSPs or IPSPs spread toward the postsynaptic axon hillock
The IPSPs and EPSPs in the postsynaptic cell spread throughout its interior. If the integration of all the EPSPs and IPSPs depolarizes the axon hillock enough, the postsynaptic neuron will fire an action potential of its own.
excitatory postsynaptic potential (EPSP)
A depolarizing potential in the postsynaptic neuron that is caused by excitatory connections. EPSPs increase the probability that the postsynaptic neuron will fire an action potential.
inhibitory postsynaptic potential (IPSP)
A hyperpolarizing potential in the postsynaptic neuron that is caused by inhibitory connections. IPSPs decrease the probability that the postsynaptic neuron will fire an action potential.
When the inhibitory neuron is stimulated, the postsynaptic effect is an increase of the resting membrane potential. This hyperpolarization moves the cell membrane potential away from threshold—decreasing the probability that the neuron will fire an action potential
the differences between AP’s and PSP’s
postsynaptic potential
A local potential that is initiated by stimulation at a synapse, can vary in amplitude, and spreads passively across the cell membrane, decreasing in strength with time and distance.
A given neuron, receiving synapses from hundreds of other cells, is subject to hundreds or thousands of postsynaptic potentials. When integrated, this massive array of local potentials determines whether the neuron will reach threshold and therefore generate an action potential of its own.
Generally, the combined effect of many excitatory synapses is needed to elicit an action potential in a postsynaptic neuron.
the membrane response is passive
a graded response - The greater the stimulus, the greater the response
action potential
The propagated electrical message of a neuron that travels along the axon to the presynaptic axon terminals.
Stimulation of an excitatory presynaptic neuron causes it to produces an all-or-none action potential that spreads to the end of the axon, releasing transmitter.
How is the action potential unlike the passive graded potentials
the action potential is actively propagated (or regenerated) down the axon, through ionic mechanisms
What are electrical synapses? How do they differ from chemical synapses?
Also called gap junction. The region between neurons where the presynaptic and postsynaptic membranes are so close that the action potential can jump to the postsynaptic membrane with-out first being translated into a chemical message.
the presynaptic membrane comes even closer to the postsynaptic membrane than it does at chemical synapses.
At electrical synapses, the facing membranes of the two cells have relatively large channels arranged to allow ions to flow from one neuron directly into the other.
As a consequence, the electrical current that is associated with neural activity in one neuron can flow directly across the gap junction to affect the other neuron.
Transmission at these synapses closely resembles action potential conduction along the axon.
Electrical synapses therefore work with practically no time delay, in contrast to chemical synapses, where the delay is on the order of a millisecond—slow in terms of neurons.
Because of the speed of their transmission, electrical synapses are frequently found in neural circuits that mediate escape behaviors in invertebrates.
They are also found where many fibers must be activated
What is synaptic transmission? What is the sequence of events that are required for synaptic transmission to occur?
- Action potential travels down the axon to the axon terminal.
- Voltage-gated calcium channels open and calcium ions (Ca2+) enter.
- Synaptic vesicles fuse with membrane and release transmitter into the cleft.
- Transmitters bind to postsynaptic receptors and cause an EPSP or IPSP.
- EPSPs or IPSPs spread toward the postsynaptic axon hillock.
- Transmitter is inactivated or removed–action is brief.
- Transmitter may activate presynaptic autoreceptors, decreasing release
What is an agonist vs. an antagonist?
Agonist
A molecule, usually a drug, that binds a receptor molecule and initiates a response like that of another molecule, usually a neurotransmitter.
Examples
carine and nicotine
antagonist
A molecule, usually a drug, that interferes with or prevents the action of a transmitter.
How do curare, bungarotoxin and nicotine work?
They are all exogenous ligands. Exogenous ligands–drugs and toxins from outside the body.
curare
An alkaloid neurotoxin that causes paralysis by blocking acetylcholine receptors in muscle. molecules that interfere with or prevent the action of a transmitter—in the manner that curare
or bungarotoxin blocks the action of ACh—are called antagonists.
bungarotoxin
A neurotoxin, isolated from the venom of the banded krait, that selectively blocks acetylcholine receptors.
Antagonist
A Nicotinic Acetylcholine (ACh)
The two ligand-binding sites normally bind ACh molecules, but they also bind exogenous ligands like nicotine and other nicotinic drugs.
Molecules such as nicotine that act like a transmitter at a receptor are called agonists of that transmitter.
What are ionotropic and metabotropic receptors?
The recognition of transmitter molecules by receptor molecules controls the opening of ion channels in two different ways.
Ionotropic receptors
Metabotropic receptors
Ionotropic receptors open when bound by a transmitter (also called a ligand-gated ion channel).
A receptor protein that includes an ion channel that is opened when the receptor is bound by an agonist.
A directly control an ion channel. When bound by the transmitter, the ion channel opens and ions flow across the membrane.
Metabotropic receptors
A receptor protein that does not contain an ion channel but may, when activated, use a G protein system to alter the functioning of the postsynaptic cell.
Recognize the synaptic transmitter, but they do not directly control ion channels. Instead, they activate molecules known as G proteins.
G proteins
A class of proteins that reside next to the intracellular portion of a receptor and that are activated when the receptor binds an appropriate ligand on the extracellular surface. Are proteins that bind the compounds guanosine diphosphate (GDP), guanosine triphosphate (GTP), and other guanine nucleotides. Sometimes the G protein itself acts to open ion channels, but in other cases the G protein activates another, internal chemical signal to affect ion channels..
What happens to neurotransmitter after it is released into the synaptic cleft?
When a chemical transmitter such as ACh is released into the synaptic cleft, its postsynaptic action is not only prompt but usually very brief as well. This brevity ensures that the message is repeated faithfully.
The prompt cessation of transmitter effects is achieved in one of two ways:
Degradation. Transmitter can be rapidly broken down and thus inactivated by a special enzyme—a process known as degradation
Reuptake. Alternatively, transmitter molecules may be rapidly cleared from the synaptic cleft by being taken up into the presynaptic terminal—a process known as reuptake.
Know the steps of neurotransmitter action listed in Fig. 3.12.
- Action potential travels down the axon to the axon terminal.
- Depolarization of the presynaptic terminal leads to influx of Ca2+.
- Ca2+ promotes exocytosis, the fusion of vesicles with the presynaptic membrane, which releases transmitter into the cleft.
- The binding of transmitter to receptor molecules in the postsynaptic membrane opens channels, permitting ion flow and initiating an excitatory orinhibitory postsynaptic potential.
- Excitatory or inhibitory postsynaptic potentials spread passively over dendrites and the cell body to the axon hillock. (EPSP or IPSP)
- A. Enzyme present in the extracellular space breaks down excess transmitter.
B. Reuptake of transmitter slows synaptic action and recycles transmitter for subsequent transmission. - Transmitter binds to autoreceptors in the presynaptic membrane.
What is a reflex circuit?
neural chain
A simple kind of neural circuit in which neurons are attached linearly, end-to-end.
Circuits of Neurons: two kinds of processes
- analog-like signals that vary in strength (such as graded potentials at synapses)
- and digital-like, all-or-none signals (such as action potentials) that vary in frequency.
Two other features that are common to many kinds of neural circuits: convergence and divergence
divergence The phenomenon of neural connections in which one cell sends signals to many other cells.
convergence The phenomenon of neural connections in which many cells send signals to a single cell.
What are the criteria a substance must meet to be considered a classical neurotransmitter?
- The substance exists in presynaptic axon terminals.
- The presynaptic cell contains appropriate enzymes for synthesizing the substance.
- The substance is released in significant quantities when action potentials reach the terminals.
- Specific receptors that recognize the released substance exist on the postsynaptic membrane.
- Experimental application of the substance produces changes in postsynaptic cells.
- Blocking release of the substance prevents presynaptic activity from affecting the postsynaptic cell.
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class.
Gamma-aminobutyric acid (GABA) (-Ve) (Na+)
Gamma-aminobutyric acid (GABA) (-Ve) (Na+)
CATEGORY OF NEUROTRANSMITTER: amino acid
RECEPTOR CATEGORY: ionotropic and metabotropic
RECEPTOR SUBTYPES: GABAA (ionotropic) GABAB (metabotropic), GABAC (ionotropic)
FUNCTION: GABAA receptors are inhibitory in many brain regions,
reducing excitability and preventing seizure activity. GABAB receptors are also inhibitory, by a different mechanism. GABAC receptors produce sustained inhibition, and are found especially in the retina
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class.
Glutamate (+Ve) (Na+)
Glutamate (+Ve) (Na+)
CATEGORY OF NEUROTRANSMITTER: amino acid
RECEPTOR CATEGORY: ionotropic and metabotropic glutamate receptors
RECEPTOR SUBTYPES: AMPA, kainate, and NMDA receptors
(ionotropic), mGluR’s (metabotropic glutamate receptors)
FUNCTION: Glutamate is the most abundant of all neurotransmitters, and the most important excitatory transmitter. Glutamate receptors are crucial for excitatory signals, and NMDA receptors are especially implicated in learning and memory.
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class
. Acetylcholine (Ach) (+Ve) (Na+)
Acetylcholine (Ach) (+Ve) (Na+)
CATEGORY OF NEUROTRANSMITTER: amine neurotransmitter, subtype: quaternary amines
RECEPTOR CATEGORY: ionotropic and metabotropic
RECEPTOR SUBTYPES: Muscarinic receptors (metabotropic), Nicotinic receptors (ionotropic)
FUNCTION: Both are involved in cholinergic transmission in the cortex.
OTHER FUNCTION: A neurotransmitter produced and released by parasympathetic system which uses acetylcholine, which to slow down activity and recover. Generally opposite effects then norepinephrine. Nicotinic receptors are crucial for muscle contraction.
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class
Norepinephrine (NE)
Norepinephrine (NE)
CATEGORY OF NEUROTRANSMITTER: amine neurotransmitter, subtype: monoamine
RECEPTOR CATEGORY: metabotropic
RECEPTOR SUBTYPES: α1, α2, β1, and β2 adrenoceptors (all metabotropic)
FUNCTION: In the brain, NE transmission provides an alerting and
arousing function.
OTHER FUNCTION: Multiple effects in visceral organs; important part of sympathetic nervous system and “fight or flight” responses
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class
Serotonin
Serotonin
CATEGORY OF NEUROTRANSMITTER: amine neurotransmitter, subtype: monoamine subsubtype: Indoleamines
RECEPTOR CATEGORY: metabotropic
RECEPTOR SUBTYPES: 5-HT1 receptor family (5 members), 5-HT2 receptor family (3 members), 5-HT3 through 5-HT7 receptors, All but one subtype (5-HT3) metabotropic
FUNCTION: May be involved in mood, sleep, and higher cognition. 5-HT3 receptors are particularly involved in nausea.
Make sure to know at least one function in the nervous system of each of the neurotransmitters that I listed in class
Dopamine (DA)
Dopamine (DA)
CATEGORY OF NEUROTRANSMITTER: amine neurotransmitter, subtype: monoamine subsubtype: Catecholamine
RECEPTOR CATEGORY: metabotropic
RECEPTOR SUBTYPES: D1 through D5 receptors (all metabotropic), D6 and D7 probable
FUNCTION: Found throughout the forebrain. Involved in complex behaviors, including motor function, reward, higher cognition.
How can neurotransmitters be versatile in their function within the nervous system?
neurotransmitters affect their targets by interacting with receptors,
The transmitter molecule binds to the receptor, changing its shape to open an ion channel (as with fast, ionotropic receptors) or altering chemical reactions within the target cell (as with slow, metabotropic receptors)
Receptors add an important layer of complexity in neural signaling, because any given transmitter may affect various kinds of receptors that differ from one another in structure
What is the difference between an agonist and antagonist?
agonist
A molecule, usually a drug, that binds a receptor molecule and initiates a response like that of another molecule, usually a neurotransmitter.
antagonist
A molecule, usually a drug, that interferes with or prevents the action of a transmitter.
What is the difference between an ionotropic and metabotropic receptor?
ionotropic receptor
A receptor protein that includes an ion channel that is opened when the receptor is bound by an agonist.
metabotropic receptor
A receptor protein that does not contain an ion channel but may, when activated, use a G protein system to open a nearby ion channel.
Can peptides (what are these?) function as neurotransmitters?
peptide neurotransmitter (neuropeptide) A neurotransmitter consisting of a short chain of amino acids. - Functions: reward sensation, control of feeding, sexual behaviors, and social functions. - Examples: Opiates, Endorphins, Oxytocin
How do drugs work within the CNS?
Drug molecules don’t seek out particular receptor molecules.
A drug molecule that has more than one kind of action in the body exhibits this flexibility because it affects more than one kind of receptor molecule.
binding affinity
Also called simply affinity. The propensity of molecules of a drug (or other ligand) to bind to receptors.
The degree of chemical attraction between a ligand and a receptor
efficacy
Also called intrinsic activity. The extent to which a drug activates a response when it binds to a receptor.
After binding, the propensity of a ligand to activate the receptor to which it is bound is termed its efficacy (or intrinsic activity): agonists have high efficacy and antagonists have low efficacy. Partial agonists are drugs that produce a middling response regardless of dose.
So, it is a combination of affinity and efficacy that determines the overall action of a drug that determine where it binds and what it does
What is the difference between a low-affinity and high-affinity drug?
A drug with high affinity for a particular type of receptor will selectively bind to that type of receptor even at low doses, and it will stay bound for a relatively long time. Lower-affinity drugs will bind fewer receptor molecules.
If a particular drug has a low affinity for a receptor, then it will quickly uncouple from the receptor. If a drug has a high affinity for a receptor then the two will stay together for a longer time, and a lower concentration of drug will be sufficient to bind half the receptors.
Why is it important to study dose response curves when initially testing a drug for efficacy?
study dose response curves
A formal plot of a drug’s effects (on the y-axis) versus the dose given (on the x-axis).
When plotted as a graph, the relationship between drug doses and observed effects is called a dose-response curve (DRC). Careful analysis of DRCs reveals many aspects of drugs’ activity and is one of the main tools for understanding pharmacodynamics.
DRCs reveal the effective dose range of a drug and allow comparison of the potencies and efficacies of different drugs
What is the difference between down regulation and up regulation of receptors? How might agonistic and antagonistic drugs influence this process?
down-regulation
A compensatory reduction in receptor availability at the synapses of a neuron.
The effects of an agonist drug augment the effects of the endogenous ligand, enhancing the effect on the postsynaptic cell. The postsynaptic cell may respond by down-regulating (decreasing) the number of receptors it places into the synapse, in order to become less sensitive and more like the pre-drug state.
up-regulation
A compensatory increase in receptor availability at the synapses of a neuron.
a competitive antagonist instead blocks an endogenous substance from having its usual effect, to which the postsynaptic cell may respond by up-regulating (increasing) the number of its receptors in order to become more sensitive and compensate for the lessened effect of the endogenous ligand.
What are withdrawal effects?
Once established, drug tolerance is believed to be a major cause of withdrawal symptoms, the unpleasant sensations that occur when one stops using a drug.
withdrawal symptoms
uncomfortable symptoms that arises when a person stops taking a drug that he or she has used frequently, especially at high doses.
Example cocaine withdrawal symptoms: initial agitation and powerful drug cravings, followed by depression and an inability to enjoy anything else in life. Cerebral glucose metabolism is decreased for months after cocaine use is discontinued and may contribute to that depression.
What are the four types of routes of administration listed in Table 4.2? Please be able to compare and contrast the pros and cons of these different routes of administration.
INGESTION
INGESTION Tablets and capsules Syrups Infusions and teas Suppositories EXAMPLES AND MECHANISMS Many sorts of drugs and remedies; depends on absorption by the gut, which is somewhat slower than most other routes TYPICAL SPEED OF EFFECTS Slow to moderate
What are the four types of routes of administration listed in Table 4.2? Please be able to compare and contrast the pros and cons of these different routes of administration.
INHALATION
INHALATION Smoking Nasal absorption Inhaled powders and sprays EXAMPLES AND MECHANISMS Nicotine, cocaine, organic solvents such as airplane glue and gasoline, also used for a variety of prescription drugs and hormone treatments. Inhalation methods take advantage of the rich vascularization of the nose and lungs to convey drugs directly into the bloodstream. TYPICAL SPEED OF EFFECTS Moderate to fast
What are the four types of routes of administration listed in Table 4.2? Please be able to compare and contrast the pros and cons of these different routes of administration.
PERIPHERAL INJECTION
PERIPHERAL INJECTION Subcutaneous Intramuscular Intraperitoneal (abdominal) Intravenous EXAMPLES AND MECHANISMS Nicotine, cocaine, organic solvents such as airplane glue and gasoline, also used for a variety of prescription drugs and hormone treatments. Inhalation methods take advantage of the rich vascularization of the nose and lungs to convey drugs directly into the bloodstream. TYPICAL SPEED OF EFFECTS Moderate to fast
What are the four types of routes of administration listed in Table 4.2? Please be able to compare and contrast the pros and cons of these different routes of administration.
CENTRAL INJECTION
CENTRAL INJECTION
Intracerebroventricular (into ventricular system)
Intrathecal (into spinwal CSF)
Intrathecal (into spinwal CSF)
Intracerebral (directly into a brain region)
EXAMPLES AND MECHANISMS
Central methods involve injection directly into the CNS; used in order to circumvent the blood-brain barrier, to rule out peripheral effects, or to directly affect a discrete brain location.
TYPICAL SPEED OF EFFECTS
Fast to very fast
What factors will influence whether a drug can act on receptors in the brain – be able to describe at least three.
pharmacokinetics
Collective name for all the factors that affect the movement of a drug into, through, and out of the body.
bioavailable
Referring to a substance, usually a drug, that is present in the body in a form that is able to interact with physiological mechanisms. (free to act on the target tissue and therefore not bound to other proteins or in the process of being metabolized or excreted).
The duration of a drug effect is largely determined by the manner in which the drug is metabolized and excreted from the body—via the kidneys, liver, lungs, and other routes. In some cases, the metabolites of drugs are themselves active; this biotransformation of drugs can be a source of unwanted side effects.
biotransformation
The process in which enzymes convert a drug into a metabolite that is itself active, possibly in ways that are substantially different from the actions of the original substance.
Internal Drug depots Some drugs may be stored in depots (collecting in fat or bone, for example), only to reemerge and have physiological effects after long periods of time.
blood-brain barrier
The mechanisms that make the movement of substances from blood vessels into brain cells more difficult than exchanges in other body organs, thus affording the brain greater protection from exposure to some substances found in the blood.
What are the 8 different ways that drugs can influence presynaptic events to alter the signaling properties of the presynaptic neuron?
Illustrates presynaptic processes that are targeted by CNS drugs, with examples of each kind of drug. The most common presynaptic drug effects can be grouped into three main categories:
effects on transmitter production,
(1) Inhibition of transmitter synthesis
(2) Blockade of axonal transport
(3) Interference with the storage of transmitters
effects on transmitter release
(4) Prevention of synaptic transmission
(5) Alteration of synaptic transmitter release
(6) Alteration of transmitter release through modulation of presynaptic activity
effects on transmitter clearance.
(7) Inactivation of transmitter reuptake
(8) Blockade of transmitter degradation
What are the 5 ways that drugs can influence postsynaptic mechanisms?
Another powerful way for drugs to affect synaptic transmission is to modify the ability of postsynaptic neurons to respond to neurotransmitters.
Effects on Transmitter Receptors
(1) Blockade of receptors
(2) Activation of receptors
Effects on Cellular Processes
(3) Regulation of the number of postsynaptic receptors
(4) Modulation of intracellular signals
What are autoreceptors? What are transporters?
autoreceptor
A receptor for a synaptic transmitter that is located in the presynaptic membrane, telling the axon terminal how much transmitter has been released. They monitor how much transmitter they have released; it’s a kind of feedback system. Drugs that alter autoreceptor signals provide a false feedback signal, prompting the presynaptic cell to release more or less transmitter.
transporters
Specialized receptors in the presynaptic membrane that recognize neurotransmitter molecules and return to the presynaptic neuron for reuse.
Drugs can be divided into several classes – what are these and what types of CNS disorders do they treat?
Antipsychotic - A class of drugs that alleviate schizophrenia.
Antidepressants - A class of drugs that relieve the symptoms of depression.
Anxiolytics - A class of substances that are used to combat anxiety.
Benzodiazepine agonists - A class of antianxiety drugs that bind to sites on GABAA receptors. Nowadays, the safest and most specific anxiolytics are the benzodiazepine agonists.
Endogenous opiates - peptides produced in the body that bind to opioid receptors and relieve pain–are also addictive. There are 3 types.
Alcohol - The frontal lobes are the most affected by chronic alcohol use, yet some effects are reversible.Periodic overconsumption, or bingeing, may cause brain damage and reduces neurogenesis.
Tetrahydrocannabinol (THC) - the beneficial effects of marijuana: relieving pain, lowering blood pressure, combating nausea, lowering eye pressure in glaucoma, and so on.
Nicotine - Increases heart rate, blood pressure, hydrochloric acid secretion, and bowel activity. A compound found in plants, including tobacco, that acts as an agonist on a large class of cholinergic receptors.
Cocaine - A drug of abuse, derived from the coca plant, that acts by potentiating catecholamine stimulation.
Amphetamine - A molecule that resembles the structure of the catecholamine transmitters and enhances their activity. Over the short term, amphetamine causes increased vigor and stamina, wakefulness, decreased appetite, and feelings of euphoria.
Hallucinogens - A class of drugs that alter sensory perception and produce peculiar experiences.
Anxiolytics - A class of substances that are used to combat anxiety.
Depressants - drugs that depress or reduce nervous system activity.
Stimulants- Stimulants are excitatory. They therefore have an alerting, activating effect.
What is the main difference between typical and atypical neuroleptics?
antipsychotics - neuroleptics
- typical neuroleptics
- atypical neuroleptics
Neuroleptics are a class of antipsychotic drugs, traditionally dopamine receptor blockers.
Typical neuroleptics are selective dopamine D2 antagonists.
Atypical neuroleptics block serotonin receptors and may reduce negative symptoms of schizophrenia.receptors
Be able to describe/contrast how MAOs, SSRIs and Trycyclics work to treat depression.
They are all antidepressants, which is a class of drugs that relieve the symptoms of depression.Increasing synaptic monoamine availability appears to be a key activity of all antidepressants.
monoamine oxidase (MAO) MAOs break down monoamine neurotransmitters at axon terminals, thereby reducing transmitter activity. By blocking this process, MAO inhibitors allow monoamine neurotransmitters to accumulate at synapses, with an associated improvement in mood.
tricyclic antidepressants
tricyclics block the reuptake of neurotransmitters into presynaptic axon terminals.
selective serotonin reuptake inhibitor (SSRI)
A drug that blocks the reuptake of transmitter at serotonergic synapses. these drugs alleviate depression by selectively allowing serotonin to accumulate in synapses.
Where do anxiolytics work in the CNS (what receptor type).
anxiolytics A class of substances that are used to combat anxiety. Sometimes also called tranquilizers, anxiolytics belong to the general category of depressants: A class of drugs that act to reduce neural activity.
Barbiturate (“downers”)
A powerful sedative anxiolytic derived from barbituric acid, with dangerous addiction and overdose potential.
were originally developed to reduce anxiety, promote sleep, and prevent epileptic seizures. They are still used for those purposes but are also addictive and easily overdosed, often fatally.
benzodiazepine agonists
A class of antianxiety drugs that bind to specific sites on GABAA receptors and enhance the activity of GABA. Because GABAA receptors are inhibitory, benzodiazepines help GABA to produce larger inhibitory postsynaptic potentials than would be caused by GABA alone. This has the end result of reducing the excitability of neurons. Benzodiazepine agonists act on GABAA receptors and enhance the inhibitory effects of GABA.
Nowadays, the safest and most specific anxiolytics are the benzodiazepine agonists, and they are among the most heavily prescribed drugs.
Be able to comment on how benzodiazepines, barbiturates and alcohol may combine to have synergistic effects on GABAa receptors.
GABAA receptors have several different binding sites—some that
facilitate and some that inhibit the effect of GABA
therefore, many different drugs can interact with this receptor complex. For example, benzodiazepines bind to a unique modulatory site on the receptor complex that is distant from where GABA itself binds. The benzodiazepine-binding site is thus an orphan receptor—a receptor for which an endogenous ligand has not been conclusively identified—and the hunt for its endogenous ligand has been intense. Allopregnanolone, a steroid derived from the hormone progesterone, acts on yet another site on the GABAA receptor. Allopregnanolone is elevated during stress and has a calming effect. Alcohol ingestion also increases brain concentrations of allopregnanolone, so this steroid may mediate some of the calming influence of alcohol. Several other progesterone-like neurosteroids (steroids produced in the brain) may act on GABAA receptors to produce anxiolytic, analgesic, and anticonvulsant effects.
Be able to describe at least three ways that alcohol can affect CNS function. What is FAS?
Alcohol up-regulates (increases) the number of receptors for GABA.
depressants: drugs that depress or reduce nervous system activity
The psychoactive effect of alcohol in the nervous system is biphasic: an initial stimulant phase is followed by a more prolonged depressant phase.
Alcohol activates the GABAA receptor–coupled chloride channel, thereby increasing postsynaptic inhibition. This action contributes to social disinhibition, as well as the impairment of motor coordination that occurs after a few drinks.
Alcohol also affects other transmitters. For example, low doses of alcohol stimulate dopamine pathways, and the resulting increase in dopamine may be related to the slightly euphoric feelings that many people experience when having a drink.
Chronic abuse of alcohol damages neurons. Cells of the superior frontal cortex, Purkinje cells of the cerebellum, and hippocampal pyramidal cells show particularly prominent pathological changes. \
The frontal lobes—especially the superior frontal association cortex—are the brain areas that are most affected by chronic alcohol use.
Fetal Alcohol Spectrum Disorder - A disorder, including intellectual disability and characteristic facial anomalies, that affects children exposed to too much alcohol (through maternal ingestion) during fetal development.
bingeing—may cause brain damage. After only 4 days of bingeing on alcohol, rats exhibit neural degeneration in several areas of the brain. Damage is especially evident in the olfactory bulbs and in limbic structures connected with the hippocampus, and it is associated with impairments of cognitive ability.
Alcohol bingeing also significantly reduces the rate of neurogenesis—the formation of new neurons—in the adult hippocampus.
What do opiates do? Where in the brain do you find the highest concentration of opioid receptors (four areas)? Are opiates addictive?
WHAT DO OPIATES DO? Opiates are anxiolytics. Anxiolytics are a class of substances that are used to combat anxiety. Anxiolytics belong to the general category of depressants: drugs that depress or reduce nervous system activity.
Opiates anxiety-fighting properties come at the cost of intoxication, addiction potential, and neuropsychological impairment with long-term abuse, so they are not suitable for therapeutic use.
HOW AND WHERE TO THEY WORK
The opiates morphine, heroin, and codeine bind to specific receptors—opioid receptors.
Opioid receptors are found in the limbic and hypothalamic areas of the brain, and they are particularly rich in the locus coeruleus and in the periaqueductal gray—the gray matter that surrounds the aqueduct in the brainstem.
Endogenous opiates–peptides produced in the body that bind to opioid receptors and relieve pain–are also addictive. The three kinds are enkephalins, endorphins, and dynorphins.
EXAMPLES OF OPIATES
- Morphine
- Heroin
- Codeine
- endogenous opioids
- enkephalins
- endorphins
- dynorphins
What is the active ingredient in marijuana? Where does this compound work in the brain?
What is the active ingredient in marijuana?
Marijuana is derived from Cannabis sativa–its active ingredient is
Δ9-tetrahydrocannabinol (THC)
Where does this compound work in the brain?
As was the case with opiates and benzodiazepines, researchers found that the brain contains cannabinoid receptors that mediate the effects of compounds like THC.
Cannabinoid receptors are concentrated in the substantia nigra, the hippocampus, the cerebellar cortex, and the cerebral cortex; other regions, such as the brainstem, show few of these receptors.
marijuana: How does it influence behaviour?
How does it influence behavior?
The subjective experience of marijuana use is quite variable among individuals: relaxation and mood alteration are the most frequent effects, but stimulation, hallucination, and paranoia also occur in some cases.
Sustained use of marijuana can cause addiction and accelerated cognitive decline, and frequent smoking of marijuana, as with tobacco, can contribute to respiratory diseases.
Adolescents who use marijuana are more likely to develop psychosis in adulthood
- Altered memory formation
- Appetite stimulation
- Reduced pain sensitivity
- Protection from excitotoxic brain damage
marijuana: What neurotransmitter has been identified as endogenous neurotransmitter for cannabinoid receptors?
What neurotransmitter has been identified as endogenous neurotransmitter for cannabinoid receptors?
endocannabinoid
An endogenous ligand of cannabinoid receptors; thus, an analog of marijuana that is produced by the brain.
The most studied endocannabinoid is anandamide, which has diverse functional effects, including alterations of memory formation, appetite stimulation, reduced sensitivity to pain, and protection from excitotoxic brain damage.
Anandamide - An endogenous substance that binds the cannabinoid receptor molecule.
Be able to describe the effects (behaviourally) of nicotine, cocaine and amphetamine. How do they influence neurotransmission in the brain?
Nicotine
Stimulants are excitatory.
They therefore have an alerting, activating effect. Many naturally occurring and artificial stimulants are widely used.
Nicotine
BEHAVIOR EFFECTS
Nicotine in-creases heart rate, blood pressure, secretion of hydrochloric acid in the stomach, and intestinal activity. In the short run, these effects make tobacco use pleasurable. Smoking and nicotine exposure in adolescence has a lasting impact on attention and cognitive development,
NEUROTRANSMISSION
Acts as an agonist on a large class of cholinergic receptors.
Acts as an agonist on nicotinic ACh receptors in the ventral
tegmental area
Be able to describe the effects (behaviourally) of nicotine, cocaine and amphetamine. How do they influence neurotransmission in the brain?
Cocaine
Stimulants are excitatory.
They therefore have an alerting, activating effect. Many naturally occurring and artificial stimulants are widely used.
Cocaine
BEHAVIOR EFFECTS
either chewed or brewed as a tea—to increase endurance, alleviate hunger, and promote a sense of well-being. This use of coca leaves does not seem to cause problems.
Heavy cocaine use raises the risk of serious side effects like stroke, psychosis, loss of gray matter, and severe mood disturbances. chronic cocaine use can provoke symptoms similar to psychosis.
NEUROTRANSMISSION
Like other psychostimulants, cocaine acts by blocking monoamine transporters, especially those for dopamine, slowing reuptake of the transmitters and therefore boosting their effects.
Increases catecholamine stimulation blocks monoamine transporters
Be able to describe the effects (behaviourally) of nicotine, cocaine and amphetamine. How do they influence neurotransmission in the brain?
Amphetamine and the even more potent methamphetamine (“meth” or “speed”)
Stimulants are excitatory.
They therefore have an alerting, activating effect. Many naturally occurring and artificial stimulants are widely used.
Amphetamine and the even more potent methamphetamine (“meth” or “speed”)
BEHAVIOR EFFECTS
Over the short term, amphetamine causes increased vigor and stamina, wakefulness, decreased appetite, and feelings of euphoria.
Addiction and tolerance to amphetamine and methamphetamine develops rapidly, requiring ever larger doses leading to sleeplessness, severe weight loss, and general deterioration of mental and physical condition.
Prolonged use of amphetamine may lead to symptoms that closely resemble those of paranoid schizophrenia: compulsive, agitated behavior and irrational suspicious-ness.
NEUROTRANSMISSION
cause the release of these transmitters from presynaptic terminals even in the absence of action potentials, and when action potentials do reach the axon terminals, amphetamine also potentiates the subsequent release of transmitter.
Once transmitter has been released, amphetamine further enhances activity in two ways:
(1) by blocking the reuptake of catecholamines into the presynaptic terminal and
(2) by providing an alternative target for the enzyme (monoamine oxidase) that normally inactivates them.
What are hallucinogens?
hallucinogens A class of drugs that alter sensory perception and produce peculiar experiences.
BEHAVIOR EFFECTS
alter or distort existing perceptions
The effects are predominantly visual. Users often see fantastic images with intense colors, and they are often aware that these strangely altered perceptions are not real events.
NEUROTRANSMISSION
Hallucinogenic agents are diverse in their neural actions. But many act as serotonin receptor agonists or partial agonists.
Be familiar with the behavioural effects of MDMA and LSD. What neurotransmitter systems do they affect in the brain?
LSD lysergic acid diethylamide (acid)
LSD lysergic acid diethylamide (acid)
BEHAVIOR EFFECTS
. they alter or distort existing perceptions
The effects are predominantly visual. Users often see fantastic images with intense colors, and they are often aware that these strangely altered perceptions are not real events.
Flash Backs
NEUROTRANSMISSION
Act as serotonin receptor agonists or partial agonists. act on serotonin receptors, probably evoking visual phenomena by activating 5HT2A receptors in visual cortex.
Be familiar with the behavioural effects of MDMA and LSD. What neurotransmitter systems do they affect in the brain?
MDMA Also called Ecstasy
MDMA Also called Ecstasy
BEHAVIOR EFFECTS
positive emotions, empathy, euphoria, a sense of wellbeing, and colorful visual phenomena
NEUROTRANSMISSION
Major actions of MDMA in the brain include an increase in the release of serotonin, stimulation of 5HT2A receptors, and changes in the levels of dopamine and certain hormones, such as prolactin.
Several possible psychiatric and cognitive consequences of chronic MDMA use have been described, including memory disturbances
and depression. However, shorter-term MDMA treatment is also being studied in clinical settings, as a possible therapy for treatment-resistant posttraumatic stress disorder.
What are the four models of drug abuse described in the textbook? Be able to critique them (in class notes).
THE PHYSICAL DEPENDENCE MODEL
THE PHYSICAL DEPENDENCE MODEL
sometimes called the withdrawal avoidance model, argues that people keep taking drugs in order to avoid unpleasant withdrawal symptoms. The specific withdrawal symptoms depend on the drug, but they are often the opposite of the effects produced by the drug itself.
The model does a good job of explaining why addicts will go to great lengths to obtain their addicted drug, but it has an important shortcoming: it can’t explain how the addiction gets established in the first place. Why do some people, but not all, start to abuse a drug before physical dependence (tolerance) has ever developed? And how is it that some people can become addicted to some drugs even in the absence of clear physical withdrawal symptoms
What are the four models of drug abuse described in the textbook? Be able to critique them (in class notes).
THE POSITIVE REWARD MODEL
THE POSITIVE REWARD MODEL
people get started with drug abuse, and become addicted, because the abused drug provides powerful reinforcement.
Many addictive drugs cause the release of dopamine in the nucleus accumbens, just like more-conventional rewards such as food, sex, or winning money. dopamine released from axons originating from the ventral tegmental area (VTA), part of the mesolimbocortical dopaminergic pathway, has been widely implicated in the perception of reward. Then the addictive power of drugs may come from their artificial stimulation of this pathway. When the drug hijacks this system, providing unnaturally powerful reinforcement, the user learns to associate the drug-taking behavior with that pleasure and begins seeking out drugs more and more until life’s other pleasures fade into the background.
What are the four models of drug abuse described in the textbook? Be able to critique them (in class notes).
THE MORAL MODEL
THE MORAL MODEL
simply blame the substance abuser for a failure of moral character or a lack of self-control.
However, the “Just Say No” campaign championed by former U.S. First Lady Nancy Reagan in the 1980s did not appear to significantly reduce drug abuse.
What are the four models of drug abuse described in the textbook? Be able to critique them (in class notes).
THE DISEASE MODEL
THE DISEASE MODEL
According to the disease model, the person who abuses drugs requires medical treatment rather than moral exhortation or punishment.
However, the term disease is usually reserved for a state in which we can identify an abnormal physical or biochemical condition that initiates the problem. No abnormal physical or biochemical condition has been found in the case of drug addiction, and the disease model is mute with respect to initial development of addiction, although mounting evidence suggests that some people are genetically more susceptible to addiction than others. Nevertheless, this model continues to appeal to many, and an intensive effort is under way to identify the physiological “switch” that establishes addiction after exposure to a drug.
What are the neural pathways that are involved in drug abuse?
Many addictive drugs cause the release of dopamine in the nucleus accumbens, just like more-conventional rewards such as food, sex, or winning money. interestingly, dopamine release is also linked to
pathological gambling. As we mentioned previously, dopamine released from axons originating from the ventral tegmental area
(VTA), part of the mesolimbocortical dopaminergic pathway, has been widely implicated in the perception of reward. Then the addictive power of drugs may come from their artificial stimulation of this pathway. When the drug hijacks this system, providing unnaturally powerful reinforcement, the user learns to associate the drug-taking behavior with that pleasure and begins seeking out drugs more and more until life’s other pleasures fade into the background.
These higher-order cognitive aspects of addiction depend on glutamatergic inputs from the prefrontal cortex, integrating aspects of memory, attention, and self-control to regulate the functioning of the dopamine reward system.
Cocaine produces long-lasting changes in dopaminergic circuitry, as well as other neurotransmitter systems in the nucleus accumbens, which seems to further augment the pleasure associated with drugs while decreasing the pleasure experienced from other behaviors. The drug’s “pathological” reinforcement of associated behaviors leads to exclusive, compulsive drug seeking. If natural activities like conversation, eating, and even sex no longer provide appreciable pleasure, addicts may seek drugs as the only source of pleasure available to them.
What are four factors that can influence an individual’s susceptibility to substance abuse and ultimately dependence?
The individual and environmental factors that account for this differential susceptibility are the subject of active investigation; they fall into several general categories:
- Biological factors - Sex is a significant variable; males are more likely to abuse drugs than are females. There is also evidence for genetic predisposition.
- Family situation - Family breakup, a poor relationship with parents, or the presence of an antisocial sibling are associated with drug abuse.
- Personal characteristics - Certain traits, such as aggressiveness and poor emotional control, are especially associated with drug abuse. Strong educational goals and maturity are associated with lower likelihood of drug abuse.
Environmental factors - A high prevalence of drug use in the community, and especially in the peer group, predisposes an individual toward drug abuse.
What is stress?
Any circumstance that upsets homeostatic balance. Examples include exposure to extreme cold or heat or an array of threatening psychological states.
Natural response to threat. Can be positive or negative, short term or chronic.
What is the impact of stress?
Less receptive binding to dopamine when stressed which limit happiness potential, Stress can unravel chromosomes, block artery’s, cause ulcers, decrece immune system functioning, cause weight gain (particularly in the abdomen, shorten telomeres, shrink the hippocampus, decrece memory, limit branching of neurons and kill brain cells.
What hormones are at work in the stress system?
Hormones that are the back bones of stress response: adrenalin (epinaphernan), gucalcorticoides.
Why do we have stress (its evolutionary history)?
Survival necessity. It increases functioning of things we might need in an emergency.
How does a person’s rank in their work world affect stress hormone levels and physiology (the Whitehall study)
Stress in the hierarchy in baboons: higher in the hierarchy the lower the stress, and it impacts the health of the low rankers.
British government study.
How is the brain affected by stress?
shrink the hippocampus, decreesed memory, limit branching of neurons and kill brain cells.
What is pleasure in the brain? How is this affected by stress?
Less receptive binding to dopamine when stressed which limit happiness potential
What were the findings of the Dutch Famine Study? How does this relate to stress and its effects?
The babies born during the time have a higher staticall average of health problems, reaction to stress, and psychological problems
In the troop of baboons where many of the alpha males died, due to tuberculosis, what happened to the stress levels of the remaining baboons?
The ones who died where the most aggressive. The lack of aggression in the troop lowered the amount of socially stressful situations and thus the groups stress as a hole went down, and stayed down as they now have a culture that is relatively peaceful and so new conform.
The Effects of Hyperpolarizing Stimuli on a Neuron
applying a hyperpolarizing stimulus to the membrane produces an immediate response that passively follows the stimulus pulse (FIGURE 3.5B; the distortions at the beginning and end of the neuron’s response are caused by the membrane’s ability to store electricity, known as capacitance). The greater the stimulus, the greater the response; so the neuron’s change in potential is called a graded response.
