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Chapter 4

Psychology 2220A/B Chapter Notes - Chapter 4: Axon Hillock, Substantia Nigra, Saltatory Conduction


Department
Psychology
Course Code
PSYCH 2220A/B
Professor
Scott Mac Dougall- Shackleton
Chapter
4

Page:
of 4
A small group of nerves called the substantia nigra were dying - these neurons make dopamine which they deliver to the striatum
As the substantia nigra is dying, the amount of dopamine delivered to the striatum decreases
The striatum helps control movement, but it needs dopamine for that
The lizard, a case of parkinson's disease - what was happening in his brain?
-
L-dopa - the chemical precursor of dopamine - penetrates the BBB and is converted into dopamine once inside the brain -> effective
treatment
Dopamine isn't an effective treatment for PD b/c it doesn't readily penetrate the blood-brain barrier
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RESTING MEMBRANE POTENTIAL
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RECORDING THE MEMBRANE POTENTIAL
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Requires the tip of one electrode inside (intracellular requires microelectrodes) and one outside the neuron
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RESTING MEMBRANE POTENTIAL
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Both tips in the extracellular fluid (outside the neuron), voltage diff = 0
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Indicates that the potential inside the resting neuron is about 70 mV less than that outside the neuron
When tip of intracellular electrode is inserted into a neuron, a steady potential of about -70mV is recorded
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Thus, neuron's resting potential = -70mV (polarized membrane)
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IONIC BASIS OF THE RESTING POTENTIAL
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Random motion = high to low concentration gradient
Electrostatic pressure
The unequal distribution of charge in the resting membrane can be understood in terms of the interaction of four factors:
-
Sodium ions (Na+) - higher [] OUTSIDE a resting neuron
Potassium ions (K+) - higher [] INSIDE a resting neuron
Chloride ions (Cl-) - higher [] OUTSIDE a resting neuron
Various negatively charged protein ions - stay inside the neuron
Four ions contribute to the resting potential:
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When neurons are at rest, the unequal distribution of cl- ions across the neural membrane is maintained in equilibrium by the balance bw the
tendency for cl- ions to move down their concentration gradient into the neuron and the 70mV driving them out
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90mV of electrostatic pressure would be required to keep intracellular K+ ions from moving down their concentration gradient and leaving the
neuron
-
120mV of pressure is acting to force Na+ ions into resting neurons
The concentration of Na+ ions that exists outside of a resting neuron is such that 50mV of outward pressure would be required to keep Na+ ions
from moving down their concentration gradient into the neuron, which is added to the 70mV of electrostatic pressure acting to move them in the
same direction
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K+ ions are continuously being driven out of resting neurons by 20mV of pressure and that, despite the high resistance of the cell membrane
to the passage of Na+ ions, those ions are continuously being driven in by the 120mV of pressure
Confirmation of Hodgkin and Huxley's calculations:
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Passive factors: continously drive k+ ions out of the resting neuron and na+ ions in
Sodium-potassium pumps
Active factors: k+ ions must be actively pumped in and na+ ions must be actively pumped out to maintain the resting equilibri um
Fig 4.2 - the passive and active factors that influence the distribution of na+, k+, and cl- ions across the neural membrane:
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Point of equilibrium of cl- ions inside and outside the cell = at -70mV
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GENERATION AND CONDUCTION OF POSTSYNAPTIVE POTENTIALS
May depolarize the receptive membrane (decrease the membrane potential, from -70 to -67 for ex)
May hyperpolarize the receptive membrane (increase the membrane potential, -70 to -72)
When neurotransmitters bind to postsynaptic receptors, they typically have one of two effects:
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Excitatory postsynaptic potentials (EPSPs) - postsynaptic depolarizations - increase the chance that a neuron will fire
Inhibitory post synaptic potentials (IPSPs) - postsynaptic hyperpolarizations - decrease the chance that a neuron will fire
Graded responses - their amplitudes are proportional to the intensity of the signals that elicit them
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Rapid - assumed to be instantaneous
1.
Some neurons have a mechanism for amplifying dendritic signals that originate far form their cell bodies
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Decremental - decrease in amplitude as they travel through the neuron (but they never travel very far along an axon)
2.
The transmission of postsynaptic potentials has two important characteristics:
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INTEGRATION OF POSTSYNAPTIC POTENTIALS AND GENERATIO OF ACTION POTENTIALS
But, AP's are actually generated in the adjacent section of the axon
Axon hillock - until recently, it was believed that AP's started here (the conical structure at the junction between the cell body and the a xon)
Whether or not a neuron fires depends on the balance between the excitatory and inhibitory signals reaching its axon - if the sum reaches the
threshold of excitation (usually -65mV), an AP is generated near the axon hillock
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It is an all-or-none response
Not a graded response - their magnitude is not related to the intensity of the stimuli that elicit them
AP lasts for 1 ms - reversal of the membrane potential from about -70 to +50 mV
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Two simultaneous EPSPs sum to produce a greater EPSP
i.
Two simultaneous IPSPs sum to produce a greater IPSP
ii.
A simultaneous IPSP and EPSP cancel each other out
iii.
Spatial summation - three possible combinations:
1.
Two EPSPs elicited in rapid succession sum to produce a larger EPSP
i.
Temporal summation - two possible combinations:
2.
Neurons integrate in 2 ways: over space and over time
Integration - adding/combining a number of individual signals into one overall signal
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Neural Conduction and Synaptic Transmission
January-12-12
12:00 PM
Chapter 4 Page 1
Two IPSPs elicited in rapid succession sum to produce a larger IPSP
ii.
CONDUCTION OF ACTION POTENTIALS
IONIC BASIS OF ACTION POTENTIALS
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Voltage-activated ion channels - ion channels that open or close in response to changes in the level of the membrane potential
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K+ ions near the membrane are driven out of the cell (b/c of high internal concentration and later b/c of the positive intern al charge
Na+ channels close after 1ms - marks the end of the rising phase; beginning of repolarization (falling phase) by the continued efflux of K+
ions
Once repolarization has been achieved, the K+ channels gradually close
When the membrane potential of the axon is reduced to the threshold of excitation, the voltage-activated sodium channels open wide, and na+
ions rush in - this drives the membrane from -70 to +50
-
A single AP has little effect on the relative concentrations of various ions inside/outside the neuron
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Draw figure 4.6
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REFRACTORY PERIODS
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Absolute refractory period - a brief period of about 1-2 ms after the initiation of an action potential which it is impossible to elicit a second one
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Relative refractory period - follows the absolute ref period - the period during which it is possible to fire the neuron again, but only by applying
higher-than-normal levels of stimulation
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It is responsible for the fact that AP's normally travel along axons in only one direction - an AP cannot reverse direction since the portions of
an axon over which an AP has just travelled are left momentarily refractory
1.
Responsible for the fact that the rate of neural firing is related to the intensity of stimulation (must be intense in order to surpass the
relative refractory)
2.
The refractory period is responsible for two important characteristics of neural activity:
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AXONAL CONDUCTION OF ACTION POTENTIALS
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The conduction of AP's along an axon is nondecremental - AP's don't grow weaker as they travel along the axonal membrane
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AP's are conducted more slowly than postsynaptic potentials
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Reason for these differences is that the conduction of EPSPs and IPSPs is passive; whereas the axonal conduction of action potentials is largely
active
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Antidromic conduction - if electrical stimulation of sufficient intensity is applied to the terminal end of an axon, an AP will be generated and will
travel along the axon back to the cell body
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Orthodromic conduction - axonal conduction in the natural direction - from cell body to terminal buttons
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CONDUCTION IN MYELINATED AXONS
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Axonal sodium channels are concentrated at the nodes of ranvier
In myelinated axons, ions can pass through the axonal membrane only at the nodes of ranvier - the gaps between adjacent myelin segments
The axons of many neurons are insulated from the extracellular fluid by segments of fatty tissue called myelin
-
When an AP is generated in a myelinated axon, the signal is conducted passively (instantaneously and decrementally) along the first segment of
myelin to the next node of ranvier - unmyelinated = not passive
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Myelination increases the speed of axonal conduction
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Saltatory conduction - the transmission of action potentials in myelinated axons
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THE VELOCITY OF AXONAL CONDUCTION
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Ex. Mammalian motor neurons - max velocity in humans is ~60m/sec; in cats, 100m/sec
Conduction is faster in large-diameter axons and myelinated axons
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CONDUCTION IN NEURONS WITHOUT AXONS
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Do not normally display AP's
Conduction in interneurons is usually passive and decremental
Interneurons - neurons that either lack axons, or have very short axons
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THE HODGKIN-HUXLEY MODEL IN PERSPECTIVE
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The Hodgkin-Huxley model was based on the study of squid motor neurons - b/c they are large
-
The simplicity, size, and accessibility of squid motor neurons was both the pro and con to this research - made it difficult to apply to the human
brain b/c so complex
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Many cerebral neurons fire continually even when they receive no input
The axons of some cerebral neurons can actively conduct both graded signals and action potentials
Action potentials of all motor neurons are the same, but AP's of diff classes of cerebral neurons vary
Many cerebral neurons have no axons and do not display AP's
The dendrites of some cerebral neurons can actively conduct AP's
The H-H model must thus be applied to cerebral neurons with caution - some properties of cerebral neurons not shared by motor neurons
Many neurons arent motor neurons in the human brain..
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SYNAPTIC TRANSMISSION: CHEMICAL TRANSMISSION OF SIGNALS AMONG NEURONS
STRUCTURE OF SYNAPSES
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Dendritic spines - nodules of various shapes that are located on the surfaces of many dendrites
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Axodendritic synapses - synapses of axon terminal buttons on dendrites
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Axosomatic synapses - synapses of axon terminal buttons on somas (cell bodies)
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Dendrodendritic synapses - capable of transmission in either direction
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Axoaxonic synapses - can mediate presynaptic facilitation and inhibition (can selectively influence one particular synapse rather than the entire
presynaptic neuron)
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presynaptic neuron)
Directed synapses - synapses at which the site of NT release and the site of NT reception are in close proximity
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Nondirected synpases - synapses at which the site of release is at some distance from the site of reception (string of beads)
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SYNTHESIS, PACKAGING, AND TRANSPORT OF NEUROTRANSMITTER MOLECULES
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Typically made in the cytoplasm of the terminal button and packaged in synaptic vesicles by the button's golgi complex
Contained in smaller vesicles
Small - several types
Assembled in the cytoplasm of the cell body on ribosomes; they are then packaged in vesicles by the cell body's golgi complex and
transported by microtubules to the terminal buttons at 40cm/day
Contained in larger vesicles
Large - Neuropeptides - short amino acid chains comprising between 3 and 36 amino acids; short proteins
Two types of NTs: small and large
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Many neurons contain 2 NT's - coexistence - usually involve one small NT and one neuropeptide (large NT)
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RELEASE OF NEUROTRANSMITTER MOLECULES
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Exocytosis - the process of NT release
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When stimulated by action potentials, these channels open, Ca2+ ions enter the button and cause synaptic vesicles to fuse wit h the
presynaptic membrane and empty their contents into the synaptic cleft
When a neuron is at rest, synaptic vesicles that contain small molecule NTs tend to congregate near sections of the presynaptic membrane that
are rich in voltage-activated calcium channels
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Small NTs - typically released in a pulse each time an AP triggers a momentary influx of Ca2+ ions through the presynaptic membrane
Neuropeptides - typically released gradually in response to general increases in the level of intracellular ca2+ ions
Differs bw small NTs and neuropeptides:
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ACTIVATION OF RECEPTORS BY NEUROTRANSMITTER MOLECULES
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Receptors - a protein in the postsynaptic membrane that contains binding sites for only particular NTs
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Thus, an NT is a ligand of its receptor
Ligand - any molecule that binds to another
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Advantage: they enable one NT to transmit diff kinds of msgs to diff parts of the brain
Receptor subtypes - the diff types of receptors to which a particular NT can bind
Most NTs can bind to diff types of receptors
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When an NT binds to an ionotropic receptor, the associated ion channel usually opens or closes immediately - inducing an immediate
postsynaptic potential
Ionotropic receptors - those receptors that are associated with ligand-activated ion channels
-
More prevalent than ionotropic receptors
Slow to develop, but last longer
The subunit may move along the inside surface of the membrane and bind to a nearby ion channel - thus inducing an EPSP or IPSP
Or it may trigger the synthesis of a second messenger (NTs = first messenger)
When an NT binds to a metabotropic receptor, a subunit of the associated G protein breaks away - then, depending on the type of G
protein...
The bind to their neuron's own NT
1.
They're located on the presynaptic membrane
2.
Function is to monitor the number of NTs in the synapse, to reduce subsequent release when high levels, and to increase relea se when
low levels
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Autoreceptors - metabotropic receptors that have two unconventional characteristics:
Metabotropic receptors - those receptors that are associated with signal proteins and G proteins
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Function - the transmission of rapid, brief excitatory or inhibitory signals to adjacent cells
Small NT's tend to be released into directed synapses and to activate either ionotropic or metabotropic receptors that act directly on ion
channels
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Function - the transmission of slow, diffuse, long-lasting signals
Neuropeptides tend to be released diffusely and mostly all bind to metabotropic receptors that act through second messengers
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REUPTAKE, ENZYMATIC DEGRADATION, AND RECYCLING
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The majority of NTs, once released, are almost immediately drawn back into the presynaptic buttons by transport mechanisms
-
Reuptake - more common
Other NTs are degraded in the synapse by enzymes
-
Ex. NT acetylcholine is broken down by acetylcholinesterase
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Enzymatic degradation
Two message-terminating mechanisms:
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Recycled
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GLIAL FUNCTION AND SYNAPTIC TRANSMISSION
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Gap junctions
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Electrical synapses
Gap junctions - narrow spaces bw adjacent neurons that are bridged by fine tubular channels (connexions) that contain cytoplasm
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First demonstrated in mammals in the 1970s
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Communication across them is very fast bc it doesn't involve active mechanisms
Permit communication in either direction
Although less selective than synapses, gap junctions have two advantages:
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NEUROTRANSMITTERS
Three classes of conventional small NTs...
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AMINO ACID NTs
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Glutamate - most prevalent excitatory NT in the CNS - common in the proteins we consume
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Aspartate - common in the proteins we consume
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Glycine - common in the proteins we consume
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Synthesized by modifying glutamate
Gamma-aminobutyric acid (GABA) - most prevalent inhibitory NT in the CNS (has excit effects at some synapses though)
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