Neurophysiology II
>E. Graded potentials
>>1. Typically, one delivery of Nt onto a postsynaptic cell is not enough to
trigger an AP. It will cause some depolarization, but not to threshold.
More than one depolarization events are typically required to reach
threshold and generate an AP. What can bring a cell to threshold?
>>>>Spatial summation- many stimuli (ex. Nt) arrive at once
>>>>Temporal summation- many stimuli arrive in rapid succession
>>2. Excitatory Post-Synaptic Potentials (EPSP) and Inhibitory PostSynaptic Potentials (IPSP)
>>>An EPSP is a change in membrane potential that will make a neuron
more likely to reach threshold. That is, it is a depolarized potential. A
neuron that experiences an EPSP is "excited," or needs less stimulation
to reach threshold. For example, in an EPSP, a few chemically-gated Na+
channels are opened. A partially depolarized neuron is said to be
facilitated (it is more likely to reach threshold).
>>>An IPSP is a change in membrane potential that will make a neuron
less likely to reach threshold. That is, a hyperpolarized potential. A
neuron that experiences an IPSP is "inhibited," or needs more
stimulation to reach threshold. For example, in an IPSP, chemicallygated K+ or Cl- channels are opened.
*Take a minute to draw a neuron with chemically gated Na+, K+, and Clchannels. Draw where these ions are in a resting cell (in or out of the
cell). Now show yourself, with arrows, which direction each would travel
if its channels were open. What effect will the movement of each have on
the voltage (will the interior become more positive or more negative)?
>F. Synapses, where neurons talk: anatomy and events
>>1. Types of synapses
>>>a. Electrical- relatively uncommon; neurons share ions via gap
junctions
>>>b. Chemical- the most common
-the “sending” neuron is called presynaptic; the “receiving” neuron
is called postsynaptic
-presynaptic and postsynaptic neurons are separated by a space
called the synaptic cleft
-neurotransmitters travel from the presynaptic neuron to the
postsynaptic neuron (or other effector cell, like a muscle cell)
across the cleft. The neurotransmitter will bind to a receptor on
the postsynaptic cell, causing it to respond in some way.
-The neurotransmitter will then be disposed of, either by
degradation- the Nt will be broken down by enzymes in the
cleft; then the remnants will be sucked back up by the
presynaptic cell and recycled (ex, acetylcholine), or
reuptake- the Nt will be sucked back up intact by the
presynaptic cell for re-use (ex, serotonin)
>>2. Synaptic delay- transmission across chemical synapses is the ratelimiting step in any neural pathway; that is, it’s the slowest step. It’s still
pretty darn fast, though, at most ~5 ms!
>>3. Synaptic Potentiation- in many cases, when neurons talk to each
other a lot, they get much more efficient at it. This is likely one of the
bases of memory formation; not only conscious memory, but also “reflex
memory” and “muscle memory.” There are many potential mechanisms
for potentiation, none of which are fully understood. Here is a brief
overview of a few:
-presynaptic neurons can grow collaterals to postsynaptic neurons
when they talk a lot.
-presynaptic neurons can build more Ca2+ channels at their
terminals that go to postsynaptics they talk to a lot, increasing the
amount of Nt released per action potential.
-postsynaptic neurons can build more NMDA receptors (N-methyl
D-aspartate): these open in response to depolarization. NMDA
receptors are Ca2+ channels. When the postsynaptic cell is
depolarized, they open and Ca2+ enters the cell. That event will
cause the postsynaptic cell to change its sensitivity to the
presynaptic cell. For example, it may cause the postsynaptic cell
to build more chemically-gated Na+ channels on its dendrites.
That way, the next time the presynaptic cell sends an EPSP, the
postsynaptic cell will experience MORE Na+ influx and will be more
likely to respond with an action potential.
>>3. AxoAxonic synapses- another way AP generation can be affected.
These are synapses between axons of neurons. One neuron can release a
Nt/Nmodulator onto a synaptic terminal of another neuron. This will
affect the PREsynaptic activity of the second neuron. For example, when
serotonin is released onto the axon of a neuron, that neuron's Ca++
channels will remain open longer than usual in response to an AP. So,
the neuron that received the serotonin at its axon will release more Nt
than usual onto a postsynaptic cell. Clear as mud, right?
*Take a minute to draw three neurons: the presynaptic cell and the
postsynaptic cell as usual. Now, draw the third neuron. This third
neuron should have its synaptic terminal synapse with the synaptic
terminal of the presynaptic neuron. Use arrows to indicate serotonin
coming from that 3rd cell onto the presynaptic cell. Now draw Ca++
channels opening on the presynaptic cell, and Nt being released from it
to the postsynaptic cell.
III. Neurotransmitters & Neuromodulators- I will not focus on
differentiating between the two; I will group them together in this info.
>A. Actions- *Keep in mind that the action of a neurotransmitter
(whether it's excitatory or inhibitory, and whether it's direct or indirect)
depends on the receptors of the postsynaptic cell. For instance, skeletal
muscle contains receptors that open Na+ channels (excited) in response
to Ach; while cardiac muscle contains receptors that open K+ or Clchannels (inhibited) in response to Ach.
>>1. Direct- cause Na+, K+, or Cl- channels to open in response to
binding of Nt. These have fast, short-term effects.
>>2. Indirect- cause the postsynaptic cell to change in some way, making
it more or less sensitive to direct Nt (for example, could cause the
postsynaptic cell to build more Na+ channels, so that each EPSP would
be stronger because more sodium would enter with ONE stimulus).
Indirectly acting Nt initiate a cascade of chemical reactions that include
"second-messenger" chemicals: when the Nt binds, chemicals within the
cell "respond" and "send messages" to the nucleus (ex, “we need more
Na+ channels”).
>B. Specific Nt; know structural class, whether it acts directly, indirectly
or both; whether it is excitatory, inhibitory or both; whether it is used by
the CNS, PNS or both; and general function. Keep in mind the
function/s listed are oversimplified and often not the only function/s.
>>1. Ach- direct & indirect, excitatory(E) to skeletal muscle, inhibitory(I)
to cardiac. Used in PNS and CNS.
>>2. Biogenic Amines (amino acid derivatives)
a. NorEpinephrine (NE)- indirect, usually E, PNS & CNS. Among
other functions- emergency response.
b. Serotonin- indirect & direct, I, CNS. Mood regulation.
c. Dopamine- indirect, I or E, CNS & PNS. Mood regulation,
postural muscle control.
>>4. Glutamate- an amino acid. direct, E, CNS. Learning and memory.
Overrelease kills neurons and is associated with stroke.
>>5. Opioids- a peptide. (incl. endorphins)- indirect, I, CNS. Pain
reduction.
>>6. CO (carbon monoxide)-a gas. not well understood, may be involved
with memory and concentration.
*This is a VERY short list, and not all Nt have been discovered.