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Summary study book Biopsychology [RENTAL EDITION] of John P. J. Pinel, Steven Barnes - ISBN: 9780135863688 (Chapter 4-7)
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Psych Chapter 4: Neural SignalingParkinson’s Disease
→ typically the first and most symptoms include shaking hands (tremors) where the
hands may shake worse when they are at rest (tremor-at-rest).
- The other symptoms of Parkinson’s disease (lizard like-changes). These
include rigid muscles, a marked poverty of spontaneous movements, difficulty
in starting to move, and slowness in executing voluntary movements once
they have been initiated.
- Reptilian stare is often used to describe the characteristic lack of blinking and
the widely opened eyes gazing out of a motionless face.
→ This occurs when a group of neurons called the substantia nigra (black
substance) which produce dopamine begin dying. *Typically delivers dopamine to
the striatum which helps to control movement
- Dopamine is not an effective treatment because it does not readily penetrate
the blood−brain barrier. However, knowledge of dopaminergic transmission
has led to the development of an effective treatment: L-dopa, the chemical
precursor of dopamine, which readily penetrates the blood−brain barrier and
is converted to dopamine once inside the brain.
Action Potentials and Resting Potential
Resting Membrane Potential: The difference in electrical charge between the inside
and the outside of a cell
→ To record a neuron’s membrane potential, you must position the tip of one
electrode inside the neuron where the tip of the intracellular electrode must be fine
enough to pierce the neural membrane without damaging it and the tip of another
electrode outside the neuron in the extracellular fluid
- The intracellular electrodes are called microelectrodes and their tips are less
than one-thousandth of a millimeter in diameter
- When both electrode tips are in the extracellular fluid, the voltage difference
between them is zero.
- When the tip of the intracellular electrode is inserted into a neuron that is at
rest (not receiving signals from other cells), a steady potential of about −70
millivolts (mV) is recorded **neuron’s resting potential which is considered to
be polarized (it has a membrane potential that is not zero).
Movement of Ions through an Action Potential
→ The salts in neural tissue separate into positively and negatively charged particles
called ions: sodium ions and potassium ions in the body where each ion carries a
single positive charge.
→ In resting state neurons have more Na+ ions outside the cell than inside and more
K+ ions inside than outside. This unequal distribution is maintained through ion
,channels where each type of ion channel is specialized for the passage of particular
ions (Na+ or K+).
→ Na+ ions face pressure to enter the cell at resting state due to
- The electrostatic pressure from the resting membrane
potential: Because opposite charges attract, the
positively charged Na+ ions are attracted to the -70
mV charge inside resting neurons.
- The pressure for Na+ ions to move down their
concentration gradient to become evenly distributed.
**More likely to move from areas of high concentration
to areas of low concentration
→ The sodium ion channels in resting neurons are closed,
thus greatly reducing the flow of Na+ ions into the neuron.
- Where the potassium ion channels are open in resting
neurons, but only a few K+ ions exit because the
electrostatic pressure that results from the negative
resting membrane potential largely holds them inside.
- Although some Na+ ions do manage to enter resting
neurons despite the closed sodium channels and
some K+ ions do exit which creates an equilibrium.
This is known as the sodium–potassium pumps where
3 Na+ ions inside the neuron for two K+ ions outside.
- Transporters (mechanisms in the membrane of a cell
that actively transport ions or molecules across the
membrane)
Generation, conduction, and Integration of Postsynaptic
Potentials
→ Disturbances of the membrane resting potential occur as a
result of input from cells that synapse on a neuron.
→ Disturbances of the resting membrane potential are termed
postsynaptic potentials (PSPs). All of these, both EPSPs and
IPSPs, are graded potentials. This means that the amplitudes of
PSPs are proportional to the intensity of the signals they
generate
→ When neurons fire, they release neurotransmitters from their
terminal buttons which diffuse across the synaptic clefts and
interact with specialized receptor molecules on the receptor
membranes of the next neuron.
,→ When neurotransmitter molecules bind to postsynaptic receptors, they typically
have one of two effects, depending on the receptor, and type of postsynaptic
neuron.
- They may slightly depolarize the receptive membrane (decrease the resting
membrane potential). Postsynaptic depolarizations are called excitatory
postsynaptic potentials (EPSPs) as they increase the likelihood that the neuron
will fire.
- They may hyperpolarize it (increase the resting membrane potential).
Postsynaptic hyperpolarizations are called inhibitory postsynaptic potentials
(IPSPs) because they decrease the likelihood that the neuron will fire.
→ EPSPs and IPSPs both travel passively from their sites of generation at synapses,
usually on the dendrites or cell body.
- Transmission is so rapid that it can be assumed to be instantaneous. *Although
the duration of PSPs varies considerably,
- The transmission of PSPs is decremental meaning they decrease in amplitude
as they travel through the neuron where most PSPs do not travel more than a
couple of millimeters from their site of generation before they fade out
completely.
→ The PSPs created at a single synapse typically have little effect on the firing of the
postsynaptic neuron but whether a neuron fires is determined by the net effect of
their activity.
- Whether a neuron fires depends on the balance between the excitatory and
inhibitory signals reaching its axon.
- It was once believed that action potentials were generated at the axon hillock
(the conical structure at the junction between the cell body and the axon), but
they are actually generated in the adjacent section of the
axon, called the axon initial segment
→. If the sum (summation over space and over time) of the
depolarizations and hyperpolarizations (graded EPSPs and IPSPs)
reaching the axon initial segment is sufficient to depolarize the
membrane at its threshold of excitation (about -65 mV) an action
potential is generated (lasting for 1 millisecond).
→ Action potentials occur when the neuron becomes depolarized
to -65mV where it will then rise to about +50 mV in an all-or-none
response. **This is not a graded responses
Their magnitude is not related in any way to the intensity of the
stimuli that elicit them. Some neurons display APs that have a
longer duration, have a lower amplitude, or involve multiple
spikes.
, → As a neuron is stimulated, it becomes less polarized until the
threshold of excitation is reached and firing occurs. Stimulating
a neuron more intensely does not increase the speed or
amplitude of the resulting action potential.
**combinations of spatial summation to create an action
potential
- Local EPSPs that are produced simultaneously on
different parts of the receptive membrane sum to form a
greater EPSP
- Simultaneous IPSPs sum to form a greater IPSP,
- EPSPs and IPSPs sum to cancel each other out.
- Temporal summation occurs when PSPs produced in
rapid succession at the same synapse sum to form a
greater signal. This is because, if a particular synapse is
activated and then activated again before the original
PSP has completely dissipated, the effect of the second stimulation will be
superimposed on the lingering PSP produced by the first.
- Accordingly, it is possible for a brief subthreshold excitatory stimulus to fire a
neuron if it is administered twice in rapid succession.
- In the same way, an inhibitory synapse activated twice in rapid succession can
produce a greater IPSP than that produced by a single stimulation.
→ Because PSPs are transmitted decrementally, synapses near the axon had been
assumed to have the most influence on the firing of the neuron. However, it has been
demonstrated that some neurons have a mechanism for amplifying dendritic signals
that originate far from their axon
Conduction of Action Potentials
→ Action potentials are generated through the action of voltage-gated ion channels
that open or close in response to changes in membrane potential
→ When the membrane potential is depolarized to the threshold of excitation by a
sufficiently large EPSP. The voltage-gated sodium channels in the axon membrane
open wide, and Na+ ions rush in, suddenly raising the membrane potential −70 to
about +50 mV.
→ The rapid change in the membrane potential due to the influx of Na+ ions then
triggers the opening of voltage-gated potassium channels where K+ ions near the
membrane are driven out of the cell through these channels.
- This occurs until the action potential is at its peak where the sodium channels
then close which marks the end (about 1mms) of the rising phase of the AP
and the beginning of the repolarization phase, due to the continued efflux of
K+ ions.
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