Download The action potential and the synapses

The action potential and the
synapses
Lesson nr. 16 - Psychobiology
Phases of the action potential
The action potential consists in a sudden and transient modification
of the neuronal membrane potential that can be divided into 3
distinct phases:
rising phase (strong depolarization)
descent phase (strong hyperpolarization)
recovery phase (mild depolarization)
The action potential is triggered because in the membrane, is
reached the threshold value (-55 mV) that allows the opening of
voltage-gated Na + channels
+ 56 mV
- 89 mV
Duration and amplitude of the action potential
In addition to the 3 phases described above,
The potential is also characterized by two important
parameters:
Duration. In most cases, it corresponds to about 4-6
msec and depends by the kinetics of opening and
subsequent obliteration of the voltage dependent Na
+ and K + channels, and thus by the specific channel
subtypes (isoforms) expressed on neuronal
membranes.
Amplitude. It corresponds to the potential variation
between the maximum and the minimum peak. It
does not depend directly from the channels, but by
the concentration of free ions present in the intraand extra-cellular space.
The consequence of this is that all the potential
generated in the same neurons have always an
amplitude similar, and that for the neuron, the only
possible alternative is the emission or non-emission
of an action potential (all-or-none phenomenon).
Self-regeneration of the action potential
The action potential takes place in a specific region of the membrane
region, very small in size, and therefore represents a local
phenomenon.
However, the action potential also strongly influences the distribution
of electrical charges in its immediate vicinity generating a
depolarization gradient that will bring the voltage-gated channels in
the immediate surroundings to reach their threshold, allowing the
propagation of potential.
Modulation of the nerve information
As said, the action potential is defined as an
all-or-none phenomenon, therefore, is not
possible to modulate its intensity as is the
case for example with the volume of our
voice.
It arises at this point the problem of how
neurons can modulate the intensity of
nervous stimuli.
The solution adopted is the variation of the
frequency of emission (of potential trains)
Modulation of the nerve information
The synapse
The chemical synaptic junctions have the task of
transforming the electric information into chemical
information and are composed of:
Pre-synaptic junction
Synaptic cleft
Post-synaptic junction
Neurotransmitters
They are molecules that mediate the unidirectional transmission of
the nerve stimulus in the chemical synapses.
Are conventionally divided into:
The low molecular weight neurotransmitters are synthesized in the
cytosol of the presynaptic termination and, subsequently, by means of
active transport, are absorbed inside of the numerous vesicles in the
synaptic terminal. When a signal reaches the synaptic terminal, a few
vesicles at a time, release their neurotransmitter into the synaptic cleft.
This process generally takes place over a period of one millisecond.
classical neurotransmitters (small, electric or rapid metabolic
reactions)
Neuropeptides (large, more complex functions, slow dynamic and
continuous)
The neuropeptides, instead, are synthesized as part of large protein
molecules by ribosomes of the neuronal soma. These proteins are
immediately transported into the endoplasmic reticulum and then
inside of the Golgi apparatus, where two changes occur. At first, the
protein from which the neuropeptide is cleaved enzymatically will be
divided into smaller fragments, some of which constitute the
neuropeptide as such or a precursor thereof; later, the Golgi apparatus
Bundling neuropeptide in small vesicles that bud from it. Thanks to the
axonal flow vesicles are transported to the ends of the nerve endings,
ready to be released into the nerve terminal with the arrival of an
action potential. Typically the neuropeptides are released in much
smaller quantities than the classic neurotransmitters, but this is offset
by the fact that neuropeptides are much more powerful.
The pre-synaptic terminal
Choline-acetyl-transferase (ChAT)
Acetylcholine inserted in the
vesicles and ready to be released
in a quantum way in intersynaptic space, after the arrival of
the Ca2 +
Acetylcholine = Choline + acetate
Group (acetilCoA)
Vesicular Acetylcholine Transporter
(VAChT) + vesicular proton pump
The post-synaptic terminal
The post-synaptic terminal is
characterized by the absence of
the vesicles, and for the presence
of post-synaptic membrane, on
which are placed the ionotropic or
metabotropic receptors sensitive
to the neurotransmitter that will
transform the chemical impulse
again into an electrical pulse.
The space below the post-synaptic
membrane is the post-synaptic
density, an aggregate of proteins,
enzymes, etc ...
When the ligand opens the
channels on the post-synaptic side
it generates the so-called
excitatory or inhibitory postsynaptic potential
The spatial or temporal summation of post-synaptic potential
The elimination of the neurotransmitter from the inter-synaptic space
The correct operation of a chemical synapses, is based on the constant
relationship between incoming action potentials and amount of
neurotransmitter released in the synaptic cleft. This presupposes the
existence of disposal mechanisms of neurotransmitter in the inter-synaptic
space. These mechanisms need to be very accurate because it is clear that
excessive or insufficient removal of the latter would cause a hypo- or hyperactivation of the synapses.
These removal mechanisms are of three types:
•
Enzymatic degradation (NT is degraded by enzymes placed on the outer
face of the postsynaptic membrane, i.e. acetylcholinesterase, COMT,
sulfotransferase; then reported in the pre-synaptic membrane by specific
transporters)
•
Retrograde uptake (re-uptake by a specific retrograde transporter, i.e.
DAT, NET, SERT. Once reported in the pre-synaptic button can be
reinserted in the vesicles, or degraded by another enzyme called
monoamine oxidase - MAO)
•
Extrasynaptic diffusion (mechanism used for GABA and for the glutamate,
consist in the spreading of the NT outside the synaptic cleft, and
subsequent uptake is dependent by retrograde transporters of astrocytes)
Electric synapse
Also called gap junctions, allowing fast and bidirectional
transfer of nerve information, connecting two cells as if they
were a single cell, called metabolic syncytium.