Term
| Describe the different types of neurons: |
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Definition
Sensory (afferent) conduct impulses from sensory recptors into the CNS Motor (efferent) conducts impulses out of CNS; 2 types, somatic and autonomic Interneurons (association) are only found in the CNS and serve integrative functions of the nervous system. |
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Term
| Describe the different types of supporting cells in the PNS: |
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Definition
Schwann cells, which form myelin sheaths around peripheral axons Satellite cells, which support neuron cell bodies in the PNS |
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Term
| Describe the different types of supporting cells (known as neuroglia) in the CNS: |
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Definition
Oligodendrocytes- form myelin sheths around CNS axons Microglia- phagocytose foreign and degraded material in the CNS Astrocytes- help regulate external environment of neurons in the CNS Ependymal cells- line ventricle of brain and central canal of spinal cord |
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Term
| Identify the myelin sheath, and describe how it is formed in the PNS: |
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Definition
| A Schwann cell wraps around the axon, forming several layers, squeezing the cytoplasm to the outside. The outer part is known as the neurilemma, or sheath of Schwann. The many layers of myelin underneath the neurilemma is the myelin sheath. This provides insulation around the axon, exposing the noses of Ranvier. |
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Term
| Identify the myelin sheath, and describe how it is formed in the CNS: |
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Definition
| Oligodendrocytes have tentacles which branch to many axons, forming myelin sheaths around them. This is unlike a Schwann cell, which wraps around only one axon. This forms the white matter of the CNS. |
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Term
| Describe the nature and significance of the blood-brain barrier: |
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Definition
| Capillaries in the brain do not have pores between adjacent endothelial cells (they are joined by tight junctions). This means that molecules can only pass through by diffusion, active transport and exocytosis and endocytosis. This is a very selective process, only certain nonpolar molecules (ex. O2) and organic molecules (ex. alcohol) can pass through the plasma membranes of capillaries. Everything else requires ion channels and carrier proteins. |
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Term
| Draw a neuron, label its parts and describe the function of its parts: |
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Definition
Dendrite- receptive area that transmits electrical impulses to the cell body Cell body- enlarged portion that contains nucleus Myelin sheath- insulating covering of axon, essential for saltatory conduction of impulses Axon- conducts impulses away from cell bidy Synaptic terminals- release neurotransmitters to stimulate dendrite to produce or inhibit action potentials |
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Term
| Describe sensory neurons in terms of structure, location and function: |
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Definition
| Conducts afferent impulses to CNS. They are pseudounipolar- one of the branched processes receives sensory stimuli, and produces nerve impulses, the other delivers nerve impulses to synapses within the brain or spinal cord. |
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Term
| Describe motor neurons in terms of structure, location and function: |
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Definition
| Efferent, conducts impulses away from the CNS. They are multipolar, with several dendrites and one axon extending from its cell body. There are 2 types- somatic and autonomic. Somatic are responsible for reflex and voluntary control of skeletal muscles. Autonomic are responsible for innervation of smooth muscle, cardiac muscle and glands. |
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Term
| Describe interneurons in terms of structure, location and function: |
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Definition
| Bipolar, with a dendrite extending from a process on one side of cell body, and an axon extending from a process on the other side. These are responsible for the integrative functions of the nervous system and are only found in the CNS. |
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Term
| How does the neurilemma promote nerve regeneration? |
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Definition
| After injury, Schwann cells in the PNS form a regeneration tube, which is believed to secrete chemicals that attract the growing axon tip, and the tube helps guide the regenerating axon to its proper destination. In the CNS, some neurons die as a result of injury, and then other neurons and oligodendrocytes die because they produce "death receptors". Inhibitory proteins in the myelin sheths and glial scarring blocks and prevents axon regeneration in the CNS. In the PNS, these inhibitory proteins are also produced, but then the Schwann cells stop producing them, allowing for axon regeneration. |
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Term
| Describe the clinical significance of the blood-brain barrier: |
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Definition
| Because of the tight junctions of the endothelium of brain capillaries, it produces difficulties in the chemotherapy of brain diseases. Drugs that could enter other organs may not be able to enter the brain, because of the ion channels and carrier proteins needed for molecules to enter the brain. Many types of antibiotics and chemicals can't enter, and there is also a metabolic component- including many enzymes that can inactivate toxic molecules. |
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Term
| Step by step, describe how an action potential is produced: |
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Definition
| 1) stimulus causes depolarization to occur, allowing Na+ to enter the cell's Na+ channels (because if depolarization level reaches -70mV to -55mV Na+ gates open) 2) this causes the inside of the cell to become more positive, because Na+ rushes down its electrochemical gradient, because its concentration was lower inside the cell 3) This promotes a positive feedback loop, because further depolarization causes more Na+ gates to open, ect, ect.. because Na+ gates are voltage-regulated. This causes the rate of Na+ entry and depolarization to accelerate explosively 4) This rapidly reverses the membrane potential from -70mV to +30mV, which inactivates Na+ channels, causing a rapid decrease in Na+ permeability. 5) The depolarization stimulus causes voltage-gated K+ channels to open, and K+ rapidly diffuses out of the cell. 6) Since K+ is positive, the diffusion of K+ out causes the insisde of the cell to become more negative, restoring the cells original resting membrane potential back to -70mV. this is repolarization, and competes the negative feedback loop. |
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Term
| Describe the all or none law of action potentials: |
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Definition
| Depolarization has to reach a certain threshold or the voltage-regulated gates remain closed. When it reaches that threshold the gates open, and this produces a maximum potential change. Since the channels are only open for a fixed period of time and are soon inactivated (lasting until the membrane has repolarized) all action potentials have about the same duration. Since the concentration gradient for Na+ is relatively constant, the amplitudes of the action potentials are about equal in all axons at all times (from -70mV to +30mV, or about 100 mV in total amplitude). |
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Term
| Describe the effect of increased stimulus strength on action potential production: |
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Definition
| The code for stimulus stength is not amplitude modulated (AM), because action potentials are all-or-none events. So, when a greater stimulus strength is applied, identical action potentials are produced more frequently (more produce per sec.). Therefore, the code for stimulus strength is frequency modulated (FM). When an entire collection of axons (in a nerve) are stimulated, different axons will be stimulated at different intensities. A weak stimulus will activate axons with low thresholds, stronger stimuli will activate axons with higher thresholds. As stimulus intensity increases, more and more axons will be stimulated. |
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Term
| How do absolute refractory periods affect the frequency of action potential production? |
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Definition
As stimulus strength is increased, the frequency of action potentials will increase accordingly. As the action potentials are produced with increasing frequency, the time between successive action potentials will decrease- but only up to a minimum time interval. The interval between successive action potentials will never become so short as to allow a new action potential to be produced before the preceeding one has finished. This is because when a voltage-regulated channel is opened for depolarization for a set time, it enters an inactve state, and can't be opened by depolarization. |
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Term
| How do relative refractory periods effect the frequency of action potential production? |
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Definition
| During the time when Na+ channels are still in the process of recovering from their inactivated state and K+ channels are still open, it is considered a relative refractory period. Since Na+ channels don't all close at the same time, a very strong depolarization stimulus would be able to depolarize an axon in which enough Na+ channels are closed (but some are inactive). Since the K+ channels are still open and in the process of repolarizing, it would have to be a very strong stimulus to overcome the outward diffusion of K+. |
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Term
| How are action potentials conducted by unmyelinated axons? |
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Definition
| Every patch of membrane that contains Na+ and K+ channels can produce an action potential. The spread of depolarization by the cable properties of an axon is fast compared to the time it takes to produce an action potential. So the more action potentials along a given stretch of axon that have to be produced, the slower the conduction. Since action potentials must be produced at every fraction of a micrometer in an unmyelinated axon, the conduction rate is relatively slow. |
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Term
| How are action potentials conducted by myelinated axons? |
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Definition
| In a myelinated axon, there are basically only Na+ channels concentrated in the nodes of Ranvier. Action potentials only occur at the nodes and metaphorically "leap" from node to node (saltatory conduction). Myelinated axons conduct impulses faster because the voltage-gated channels are only at the nodes, and they have more cablelike spread of depolarization (which is faster) and fewer sites where action potentials are produced (which is slower) than unmyelinated axons. |
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Term
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Definition
| A change in the cell, in which positive charges flow into the cell, due to appropriate stimulation. |
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Term
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Definition
| A return to the resting membrane potential. |
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Term
| Describe the structure and function of electrical synapses: |
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Definition
| They are synapses between two cells that are electrically coupled and joined by gap junctions. They are present in cardiac and some smooth muscle (ex. uterus) where they allow action potentials to spread from cell to cell, so the organ can contract as a unit. |
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Term
| Describe the structure and function of chemical synapses: |
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Definition
| This is how the majority of transmission of impulses across neurons occurs. It is one-way and requires the release of neurotransmitters. The neurotransmitters originate in the terminal boutons, and are released from the presynaptic membrane in synaptic vesicles. They are passed across the synaptic cleft to the post-synaptic membrane (which could be another neuron, or an effector organ) bind to receptor proteins and are taken in to the postsynaptic cell through ligand-regulated gates, which open into ion channels. |
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Term
| Identify the nature of excitatory postsynaptic potentials: |
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Definition
| Since the ligand-regulated channels are opened by a number of different mechanisms, the effects of opening the channels vary. When the neurotransmitter causes the ion channels to open, it is considered excitatory- because it can produce a depolarization, which can produce an action potential. This depends on the summation of ESPS, because if it doesn't produce a high enough depolarization it can't reach threshold and won't cause action potentials to fire. |
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Term
| Identify the nature of inhibitory postsynaptic potentials: |
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Definition
| Sometimes ligand-regulated channels produce a hyperpolarization, where the inside of the postsynaptic membrane becomes more negative, This inhibits the production of action potentials. |
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Term
| Describe the relationship between axon activity and the amount of neurotransmitters released: |
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Definition
| When there is a greater frequency of action potentials at the axon terminal, there is a greater entry of Ca2+, and thus a greater number of synaptic vesicles undergoing exocytosis and releasing neurotransmitter molecules. As a result, a greater frequency of action potentials by the presynaptic axon will result in greater stimulation of the postsynaptic axon. |
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Term
| Describe the sequence of events by which action potentials stimulate the release of neurotransmitters from presynaptic axons: |
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Definition
1) Action potential conducted by axon reaches axon terminal 2) Voltage-gated Ca2+ channels open 3) Ca2+ binds to sensor protein in cytoplasm 4) Ca2+-protein complex stimulates fusion and exocytosis of neurotransmitter |
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Term
| Distinguish between voltage-regulated and ligand-regulated ion channles: |
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Definition
Voltage-regulated channels are found primarily in the axons and open in response to depolarization Ligand-regulated channels are found in the post-synaptic membrane and open in response to the binding of postsynaptic receptor proteins to their neurotransmitter ligands. |
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Term
| Explain how ligand-gated channels produce synaptic potentials, using the nicotinic ACh receptors as an example: |
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Definition
| Two of the five polypeptide units of nicotinic ACh receptors conatin ACh binding sites, and the channel opens when both sites bind to ACh. The opening of this channel permits the simultaneous diffusion of Na+ and K+ out of the postsynaptic cell. The flow of Na+ predominates because of the steeper electrochemical gradient. This produces the depolarization of an EPSP. |
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Term
| Explain how G-protein-coupled channels produce synaptic potentials, using the muscarinic ACh as an example: |
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Definition
| These are opened by the binding of a neurotransmitter to its receptor protein, but the receptor and ion channel are different, seperate membrane proteins. So the binding of the neurotransmitter opens the channel indirectly. The muscarinic ACh receptors are formed from a single subunit, and binds to one ACh molecule. When ACh binds to the receptor it activates G-proteins in the cell membrane (composed of alpha, beta and gamma subunits). Alpha subunit dissociates from the other two subunits (which stick together and form a beta-gamma complex). Depending on the specific case, either the alpha of the beta-gamma complex then diffuses down the membrane until it binds to an ion channel, causing it to open or close. This indirectly affects the permeability of K+ channels, causing either a depolarization or hyperpolarization. |
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Term
| Describe the action and significance of acetylcholinesterase (AChE): |
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Definition
| It is an enzyme present on the post-synaptic membrane, or immediately outside the membrane with its active site facing the synaptic cleft. AChE hydrolyzes ACh into acetate and choline, inactivating ACh, and stopping the activity in the postsynaptic cell. Acetate and choline can reenter the presynaptic axon terminals and then be resynthesized into ACh. |
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Term
| State a location at which ACh has stimulatory effects: |
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Definition
| In the smooth muscle cells of the stomach the binding of ACh to its muscarinic receptors can cause a G-protein alpha subunit to dissociate, and bind to K+ channels. This causes the K+ channels to close and results in the outward diffusion of K+ to reduce below resting levels. The reduction of the outward flow of K+ produces a depolarization, producing an EPSP, resulting in contractions of the stomach. |
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Term
| State a location in which ACh has inhibitory effects: |
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Definition
| In the heart muscle cells, the binding of the ACh to its muscarinic receptors can cause the G-protein beta-gamma subunits to dissociate and bind to gated K+ channels. This causes K+ channels to open, causing outward diffusion of K+ out of the cell. This results in hyperpolarization of the cell, producing an IPSP, slowing the heart rate. |
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Term
| Compare the properties of EPSPs and action potentials and state where these events occur in a postsynaptic neuron: |
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Definition
| Action potentials occur in the axons where voltage-regulated channels are located, whereas EPSPs occur in the dendrites and cell body. Action potentials have a threshold, EPSPs have no threshold, because the ACh released from a single synaptic vesicle produces a tiny depolarization of the postsynaptic membrane. When more vesicles are stimulated to release ACh, the depolarization is correspondingly greater (meaning it is graded in magnitude). This is not the case with all-or-none action potentials. Since EPSPs can be graded and have no refractory period, they are capable of summation. Action potentials are incapable of summating due to their all-or-none nature and refractory periods. |
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Term
| Explain how EPSPs produce action potentials in the postsynaptic neuron: |
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Definition
| The dendrites and cell body are the receptive area of the neuron, and where the receptor proteins for neurotransmitters are located. If enough neurotransmitter is received (since they summate) and the depolarization is at or above threshold when it reaches the initial segment of the neuron (right around the axon hillock) the EPSP will stimulate the production of an action potential. Gradations in the strength of the EPSP determines the frequency with which action potentials will be produced at the axon hillock, and the action potentials at this point serve as the depolarization stimuli for the next region, and so on. |
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Term
| Explain how the monoamine neurotransmitters are inactivated at the synapse: |
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Definition
| The stimulatory effects of the monoamines, like those of ACh, must be quickly inhibited as to maintain proper neural control. It is stopped by 1) reuptake of the neurotransmitter molecules from the synaptic cleft into the presynaptic axon terminal, then 2) degradation of the monoamine by an enzyme within the axon terminal called monoamine oxidase (MAO). |
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Term
| Identify the significance of the nigrostriatal dopamine system: |
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Definition
| The cell bodies of the nigrostriatal dopamine system is in part of the midbrain called substantia nigra, which sends fibers to the group of nuclei known as the corpus striatum. Thses regions are part of the basal nuclei, which is in the cerebrum, which is responsible for initiation of skeletal movements. Parkinson's disease is caused by degradation of domaminergic neurons in the substantia nigra and is treated by L-dopa and MAO inhibitors. |
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Term
| Identify the significance of the mesolimbic dopamine system: |
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Definition
| The neurons of the mesolimbic dopamine system originate in the midbrain and send axons to structures in the forebrain that are part of the limbic system. The dopamine released by the these neurons may be involved in behavior and reward. many addicitive drugs are known to activate dopaminergic pathways which arise in the midbrain and terminate in the nucleus accumbens in the forebrain. When these drugs bind to the reuptake transporters of dopamine, they block the reuptake into the presynaptic axon endings. This causes overstimulation of the neural pathways that use dopamine as a neurotransmitter, increasing the rewarding feelings. |
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Term
| List the monoamines, and indicate their chemical relationships: |
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Definition
| Epinephrine, norepinephrine, dopamine and seratonin. Seratonin is derived from the amino acid tryptophan. Epinephrine, norepinephrine and dopamine are derived from the amino acid tyrosine and form a subfamily of monoamines called catecholamines. Epinephrine (AKA adrenaline) is a hormone secreted by the adrenal gland, not a major neurotransmitter, while norepinephrine functions as both a hormone and a neurotransmitter (a neurohormone). |
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Term
| How can the inactivation of monoamines at the synapse be clinically manipulated? |
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Definition
| By MAO inhibitors. These block monoamine oxidase, and enzyme primarily responsible for degrading monoamine neurotransmitters. The blocking of MAOs causes an increase of the amount of neurotransmitters in the synaptic cleft, promoting, rather than inhibiting their effect. |
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Term
| Describe the relationship between dopaminergic neurons, Parkinson's disease and schizophrenia: |
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Definition
| Drugs used to treat schizophrenia act against the D2 subtype of dopaminergic receptor, which can cause side effects resembling Parkinson's disease. This suggests that overactivity of the mesolimbic dopamine pathways contributes to schizophrenia, which also helps explain why people suffering from Parkinson's disease could develop schizophrenia if they are treated with too much L-dopa (which increases dopaminergic transmission). |
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Term
How does cocaine produce its effects in the brain? |
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Definition
| Cocaine binds to the reuptake transporters for dopamine, norepinephrine and seratonin and blocks their reuptake into the presynaptic axon endings. This results in overstimulation of those neural pathways that use dopamine as a neurotransmitter, producing feelings of euphoria. |
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Term
| What are the dangers of cocaine abuse? |
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Definition
| It causes social withdrawal, depression, dependence upon even higher doses, and serious cardiovascular and renal disease, which can cause heart disease and kidney failure. |
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Term
| Explain the action and significance of GABA and glycine as inhibitory neurotransmitters: |
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Definition
GABA and glycine hyperpolarize the postsynaptic membrane, producing an IPSP. The binding of glycine and GABA to its receptor proteins causes chloride channels (Cl-) to open in the postsynaptic membrane, causing Cl- to diffuse in, making the the membrane potential even more negative than it is at rest, and therefore farther from the threshold depolarization required to stimulate action potentials. With glycine, this is important in motor control, because when flexor muscles are stimulated, the antagonistic muscles are inhibited, and vice versa. With GABA, purkinje cells mediate the motor functions of the cerebellum by producing IPSPs in their postsynaptic neurons. |
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Term
| Describe some of the other categories of neurotransmitters in the CNS: |
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Definition
Amines, catecholamines, Choline derivative, amino acids, polypeptides, lipids, gases, purines |
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Term
| Describe CCK (a polypeptide found in the CNS): |
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Definition
Some polypeptides (AKA neuropeptides) function as hormones in other organs (such as in the small intestine) are also produced in the brain and may function as neurotransmitters. CCK is secreted as a hormone from the small intestine but when secreted as a neurotransmitter it may produce feelings of satiety in the brain afterwards. |
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Term
| Describe endocannabinoids (a lipid that functions as a neurotransmitter in the CNS): |
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Definition
| They function as retrograde neurotransmitters. They are released from the postsynaptic neuron and diffuse backward to the axons of presynaptic neurons. Once they are back in the presynaptic neuron, they bind to their receptors and inhibit the release of neurotransmitter from the axon. This can reduce the release of either inhibitory GABA or excitatory glutamate. They modify the actions of many neurotransmitters in the brain. |
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Term
| Describe nitric oxide and carbon monoxide (gases that act as neurotransmitters): |
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Definition
| NO functions by diffusing out of the lipid portion of the presynaptic axon and into neighboring cells. Once in the target cells it stimulates the production of cGMP, which acts as a second messenger. In the PNS, it can cause smooth muscle relaxation in their target organs. CO has also been shown to stimulate the production of cGMP within neurons. It is also believed to promote odor adaptability in olfactory neurons. |
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Term
Explain the significance of glutamate in the brain: |
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Definition
| They function as the major excitatory as neurotransmitters in the CNS. They produce EPSPs and research has revealed that each of the the glutamate receptors encloses an ion channel, similar to the nicotinic ACh receptors. There are 3 subtypes of glutamate receptors, named after the molecules (other than glutamate) that they bind: 1) NMDA receptors 2) AMPA receptors 3) kainate receptors |
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Term
| Explain the significance of NMDA receptors: |
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Definition
| The ion channel will not open, simply by the binding of glutamate to its receptor. Two other conditions must be met at the same time: 1) NMDA receptor must also bind to glycine 2) The membrane must be partially depolarized at this time by a different neurotransmitter molecule that binds to a different receptor. Once open, the NMDA receptor channels permit the entry of Ca2+ and Na+ (and exit of K+) into the dendrites of the postsynaptic axon. |
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Term
| How is nitric oxide produced in the body? |
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Definition
| By nitric oxide synthetase, in the cells of many organs, from the amino acid L-argenine. |
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Term
| Explain the nature of spatial summation at the synapse: |
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Definition
| Results from the convergence (a number of axons synapsing onto one) of presynaptic axon terminals on the dendrites and cell body of a postsynaptic neuron. Since synaptic potentials are graded and lack refractory periods (unlike action potentials) this allows them to summate as they are conducted by the postsynaptic neuron. |
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Term
| Explain the nature of temporal summation: |
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Definition
| The successive activity of a presynaptic axon terminal causes successive waves of transmitter release, resulting in summation of EPSPs in the postsynaptic neuron. This summation helps to determine if the depolarization that reaches the axon hillock will be a sufficient magnitude to generate a new action potential. |
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Term
| Describe long-term potentiation (LTP) and the cause of it: |
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Definition
| When a presynaptic neuron is experimentally stimulated, the excitability is enhanced-or, potentiated- when this neuron pathway is subsequently stimulated. The improved efficacy of synaptic transmission may last hours, or even weeks. It is caused when the presynaptic neuron releases its neurotransmitter 5-15 milliseconds before the postsynaptic neuron fires its action potential. Both LTP and LTD require the diffusion of Ca2+ into the postsynaptic neuron, but with LTP the influx of Ca2+ is large and rapid compared to LTD. |
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Term
| Describe long-term depression (LTD) and the cause of it: |
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Definition
| A brief stimulation of a synapse can cause depression of the same synapse lasting many minutes. The inhibition in LTD is presynaptic. It is produced when the presynaptic neuron releases its neurotransmitter 5-15 milliseconds after the postsynaptic neuron fires its action potential. Both LTP and LTD require the diffusion of Ca2+ into the postsynaptic neuron, but with LTD the influx of Ca2+ is smaller and more prolonged than with LTP. |
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Term
| Explain the nature of postsynaptic inhibition: |
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Definition
| In the brain it is produced by GABA, in the spinal cord it is produced by glycine. EPSPs and IPSPs to a postsynaptic neuron, can summate in an algebraic fashion. The effects of IPSPs reduce or eliminate the ability of EPSPs to generate action potentials in the postsynaptic cell. |
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Term
| Explain the nature of presynaptic inhibition: |
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Definition
| The amount of an excitatory neurotransmitter released at the end of an axon is decreased by the effects of a second neuron, whose axon makes a synapse with the axon of the first neuron (axoaxonic synapse). The neurotransmitter exerting this presynaptic inhibition may be GABA, or excitatory neurotransmitters such as ACh and glutamate. Excitatory neurotransmitters can cause presynaptic inhibition by producing depolarization of the axon terminals, leading to inactivation of Ca2+ channels, decreasing the inflow of Ca2+ into the axon terminals and thus inhibiting the release of neurotransmitter. |
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