Neural conduction and synaptic transmission
It is hard to cure Parkinson’s disease, because dopamine does not easily travel across the blood-
brain barrier, however treatments are in progress to treat the dopamine deficiency. L-Dopa is a
treatment that is prescribed for Parkinson’s. This medicine can be transmitted through the blood-
brain barrier, restoring the deprived dopamine receptors.
Resting membrane potential
Difference in potential inside and outside the cell
Rest potential is -70mV. This means the inside potential is lower inside the cell than outside the cell.
Ionic basis of the resting potential
Potassium ions inside a resting cell, sodium ions outside a cell. There are two different types of
pressure on the cell. Electrostatic due to the sodium ions outside the cell being attracted to the
negative -70mV charge inside the cell. The second pressure is due to random motion pressure when
sodium channels travel down the ion channel.
Generation, conduction, and integration of postsynaptic potentials
Neurotransmitters release from the axon terminals and bind to the postsynaptic neuron. This causes
depolarisation or hyperpolarisation. So, the resting potential increases or decreases after this neuron
fires and triggers neurotransmitter binding. Excitatory postsynaptic potentials depolarise the neuron,
increasing firing likelihood, whilst inhibitory postsynaptic potentials are a result of hyperpolarisation.
These potentials are proportionate to the intensity of the signals that elicit them, so weak signals
cause small postsynaptic potentials.
Transmission is instantaneous.
Integration of postsynaptic potentials and generation of action potentials
Action potentials are generated in the axon initial segment.
Spatial summation: Excitatory postsynaptic potentials are produced simultaneously, and this sum
then doubles the EPSP value. Like adding amplitudes of two constructive interference wave graphs.
An IPSP and an EPSP cancel each other out and sum to zero. So, many presynaptic neurons release
enough neurotransmitters at once, all having an individually low potential, but when you sum each
one, it can fire an action potential due to exceeding the rest potential.
Temporal summation: Synapses sum to form a greater signal if the postsynaptic potentials are
produced in rapid succession. The second stimulus will be superimposed by the second stimulus. So,
one presynaptic neuron releases many neurotransmitters over time, which then all sums together
over time, adding to the possibility of firing an action potential. Involved in pain responses.
Usually, for the muscle movement to occur, ACh must be present at the postsynaptic neuron, as this
would allow the sodium channels to open and close, guiding ions down the excitatory sarcolemma
membrane, which then reaches the sarcoplasmic reticulum, stimulating calcium ion release for the
appropriate spasm. The SR usually stores these ions for release after stimulation via the action
, potential shoot. One action potential will cause one slight twitch, but many at once, the result of
constant stimulation, causing a full contraction.
Conduction of Action potentials
They travel through voltage-activated ion channels – these open or close depending on the
membrane potential of the cell.
Na ions that make it through the high pressures are pumped straight out. Electrostatic pressure may
cause some to push through the membrane, but they are easily filtered out due to no access through
the rest of the channel. Random motion means that sodium ions do not travel appropriately if they
do enter the cell when they should not be there.
Depolarisation occurs when the EPSP is exciting the membrane. This causes ion channels to open,
rising the rest potential of -70mV to +50mV. Potassium ions are pushed out of the cell after sodium
ions take over, whilst the remaining unattended potassium ions are repelled out of the cell due to
inner positive charge. If there is only one action potential acting on the membrane, then
repolarisation occurs quickly, where the low excitation levels allow more potassium ions to exit the
cell and later close, allowing hyperpolarisation to occur, inhibiting the response at the membrane,
which is done so by an IPSP.
Refractory periods – 1 to 2 milliseconds after the inhibition of an action potential, it is impossible to
elicit another one. This is absolute, but only after a few more seconds, does the membrane reach the
relative refractory period, where upon significant stimulation, another action potential can be fired.
After this period, the threshold returns to normal.
During the absolute refractory period, during depolarisation and repolarisation, it is not possible for
second stimulus to trigger an action potential, no matter how large the magnitude is. The relative
refractory period occurs during hyperpolarisation, and if the stimulus applied is higher than the
It is hard to cure Parkinson’s disease, because dopamine does not easily travel across the blood-
brain barrier, however treatments are in progress to treat the dopamine deficiency. L-Dopa is a
treatment that is prescribed for Parkinson’s. This medicine can be transmitted through the blood-
brain barrier, restoring the deprived dopamine receptors.
Resting membrane potential
Difference in potential inside and outside the cell
Rest potential is -70mV. This means the inside potential is lower inside the cell than outside the cell.
Ionic basis of the resting potential
Potassium ions inside a resting cell, sodium ions outside a cell. There are two different types of
pressure on the cell. Electrostatic due to the sodium ions outside the cell being attracted to the
negative -70mV charge inside the cell. The second pressure is due to random motion pressure when
sodium channels travel down the ion channel.
Generation, conduction, and integration of postsynaptic potentials
Neurotransmitters release from the axon terminals and bind to the postsynaptic neuron. This causes
depolarisation or hyperpolarisation. So, the resting potential increases or decreases after this neuron
fires and triggers neurotransmitter binding. Excitatory postsynaptic potentials depolarise the neuron,
increasing firing likelihood, whilst inhibitory postsynaptic potentials are a result of hyperpolarisation.
These potentials are proportionate to the intensity of the signals that elicit them, so weak signals
cause small postsynaptic potentials.
Transmission is instantaneous.
Integration of postsynaptic potentials and generation of action potentials
Action potentials are generated in the axon initial segment.
Spatial summation: Excitatory postsynaptic potentials are produced simultaneously, and this sum
then doubles the EPSP value. Like adding amplitudes of two constructive interference wave graphs.
An IPSP and an EPSP cancel each other out and sum to zero. So, many presynaptic neurons release
enough neurotransmitters at once, all having an individually low potential, but when you sum each
one, it can fire an action potential due to exceeding the rest potential.
Temporal summation: Synapses sum to form a greater signal if the postsynaptic potentials are
produced in rapid succession. The second stimulus will be superimposed by the second stimulus. So,
one presynaptic neuron releases many neurotransmitters over time, which then all sums together
over time, adding to the possibility of firing an action potential. Involved in pain responses.
Usually, for the muscle movement to occur, ACh must be present at the postsynaptic neuron, as this
would allow the sodium channels to open and close, guiding ions down the excitatory sarcolemma
membrane, which then reaches the sarcoplasmic reticulum, stimulating calcium ion release for the
appropriate spasm. The SR usually stores these ions for release after stimulation via the action
, potential shoot. One action potential will cause one slight twitch, but many at once, the result of
constant stimulation, causing a full contraction.
Conduction of Action potentials
They travel through voltage-activated ion channels – these open or close depending on the
membrane potential of the cell.
Na ions that make it through the high pressures are pumped straight out. Electrostatic pressure may
cause some to push through the membrane, but they are easily filtered out due to no access through
the rest of the channel. Random motion means that sodium ions do not travel appropriately if they
do enter the cell when they should not be there.
Depolarisation occurs when the EPSP is exciting the membrane. This causes ion channels to open,
rising the rest potential of -70mV to +50mV. Potassium ions are pushed out of the cell after sodium
ions take over, whilst the remaining unattended potassium ions are repelled out of the cell due to
inner positive charge. If there is only one action potential acting on the membrane, then
repolarisation occurs quickly, where the low excitation levels allow more potassium ions to exit the
cell and later close, allowing hyperpolarisation to occur, inhibiting the response at the membrane,
which is done so by an IPSP.
Refractory periods – 1 to 2 milliseconds after the inhibition of an action potential, it is impossible to
elicit another one. This is absolute, but only after a few more seconds, does the membrane reach the
relative refractory period, where upon significant stimulation, another action potential can be fired.
After this period, the threshold returns to normal.
During the absolute refractory period, during depolarisation and repolarisation, it is not possible for
second stimulus to trigger an action potential, no matter how large the magnitude is. The relative
refractory period occurs during hyperpolarisation, and if the stimulus applied is higher than the
