Neurosciences 5
HC 5
Communication between neurons is enabled by synapses, which are the functional contacts
between two neurons. Synaptic transmission depends on the type of synapse, the type of
neurotransmitter, the release mechanism of neurotransmitters, the type of receptor and the
summation to a new action potential or not. Essentially, there are two types of synapses,
which differ based on their transmission signals from the presynaptic to the postsynaptic
element. The two are:
- Electrical: permit the direct, passive flow of electrical current from one neuron to the
other, via the exchange of ions and small molecules through gap junctions. Current,
in the form of ions, may flow through these intercellular specializations at the
membranous interface between two communicating neurons. Gap junctions contain
connexons, which are transmembrane ion channels that create the pathway for the
flow of current. This type of exchange is really fast, bidirectional, and one-to-one
transmission, being used to synchronize cells in a network of fast responses.
- Chemical: features indirect transmission of an electrical signal through chemical
transduction, in the form of neurotransmitters, which in the end induce an electrical
in the postsynaptic neuron. The space between the pre- and postsynaptic
membrane, the synaptic cleft, is substantially bigger for chemical synapses. Here,
synaptic vesicles of the presynaptic element, may release their content;
neurotransmitters. The chemical agents are messengers between communicating
neurons. The exchange rate is relatively slow, one directional, but most importantly,
the transmission can be regulated.
Signaling transmission at electrical synapses works via the so-called gap junctions, which
contains connexons, which are composed of ion-channel proteins called connexins – the
subunits of connexons. The various types of connexins yield different connexons with
diverse physiological properties; six connexins come together to form one hemi-channel or
connexon. Two hemi-channels are aligned to form a pore that connects the two membranes
and permits the current to flow through. As indicated, transmission if extremely fast,
whereby communication occurs without delay. Also, transmission is bidirectional, as can
small molecules like second messengers pass through connexons; two properties which
permit electrical synapses to synchronize their activity.
Signal transmission at chemical synapses uses synaptic vesicles and neurotransmitters as
primary means of communication. In the presynaptic terminal, the so-called active zone is
where synaptic vesicles release their content, whereas in the postsynaptic terminal contains
the postsynaptic density, where many receptors reside and other structures to induce
excitation of the receiving neuron. Transmission actually has a distinct sequence of events;
synaptic vesicles are formed filled with neurotransmitters action potential invades the
presynaptic terminal voltage-gated calcium channels open calcium influx allows
synaptic vesicle to fuse with the presynaptic membrane exocytosis neurotransmitters
diffuse across the synaptic cleft bind to specific receptors on the postsynaptic membrane
binding changes the ion channel permeability neurotransmitter induced current alters
the membrane potential possibly leads to generation of new action potential in the
postsynaptic neuron. The action of the neurotransmitter is terminated by removal from the
cleft, either by enzymatic degradation or by re-uptake by glial cells.
, Neurotransmitters, of which over a 100 have been found, have the following properties:
- Present/stored in the presynaptic neuron.
- Released upon depolarization and calcium influx
- Specifically detected by receptors on the postsynaptic neuron
- Be temporarily present outside the cell, as the signal must also be stopped.
The two main classes of neurotransmitters described are the small-molecules (like ACh) and
the neuropeptides. Each neurotransmitter induces a specific type of response and each has
a different reaction speed. Small-molecule neurotransmitter propagate rapid synaptic
action, while the neuropeptides modulate slower, ongoing neuronal functions. There are
even neurons which may release two kinds of neurotransmitters, which can be differentially
released so signaling properties change dynamically according to the rate of activity.
Effective transmission requires close control over the neurotransmitter concentration – so,
there are sophisticated mechanisms to regulate the synthesis, packaging, release and
degradation of neurotransmitters. Synthesis occurs in the presynaptic terminal, whereby the
precursor molecule is taken to this site by transporter molecules. There are specific enzymes
in the terminal that subsequently synthesize the neurotransmitter, as are there selective
transporter enzymes to package vesicles with neurotransmitter. There actually are two
types of synaptic vesicles:
- Small clear-core vesicles are packaged with the small-molecule neurotransmitters
- Large dense-core vesicles are packaged with neuropeptides, which are actually
synthesized in the cell body and then, via axonal transport, they end up in the
terminal.
Removal of neurotransmitters is necessary so that the cell does not engage in another cycle
of synaptic transmission. This occurs via diffusion of neurotransmitter away from the cleft in
combination with re-uptake into nerve terminals or nearby glial cells, or, by enzymatic
degradation.
Understanding chemical synaptic transmission was done by investigating cholinergic
neurotransmission at neuromuscular junctions, where the specialized synapses occur at so-
called end plates. Whenever the membrane potential is raised above the threshold, an
active action potential in the postsynaptic element is produced, also known as the end plate
potential. This EPP causes the muscle fiber to contract. There is some time delay though
between the time the presynaptic neuron is stimulated and muscle contraction. Aside from
EPPs, which actually induce muscle contraction, there are also smaller spontaneous changes
in muscle membrane potential, known as miniature end plate potentials (MEPPs).
To study the EPP, calcium concentrations were lowered, which causes a lowered secretion
of neurotransmitters and hence a reduced magnitude of EPPs. A small EPP is similar to an
MEPP, whereby thus fluctuations can be seen. A full-blown EPP is comprised, along these
lines, of MEPP-like units, which correlates with the idea that the release of
neurotransmitters occurs in discrete packets. A presynaptic action potential causes a
postsynaptic EPP because then it synchronizes the release of many of these packets.
The source of the packets would be the synaptic vesicles loaded with transmitter, wherein
they thus reside in extremely high concentrations. Studies showed that the fusion of one
synaptic vesicle produces a single MEPP. This so, because if treated with drugs that enhance
the fusion potential of vesicles during an action potential, the number of vesicles released
can be varied. One would then compare the number of synaptic vesicles fusions (via
electron microscopy) with the number of ‘quanta’ released at the synapse.
HC 5
Communication between neurons is enabled by synapses, which are the functional contacts
between two neurons. Synaptic transmission depends on the type of synapse, the type of
neurotransmitter, the release mechanism of neurotransmitters, the type of receptor and the
summation to a new action potential or not. Essentially, there are two types of synapses,
which differ based on their transmission signals from the presynaptic to the postsynaptic
element. The two are:
- Electrical: permit the direct, passive flow of electrical current from one neuron to the
other, via the exchange of ions and small molecules through gap junctions. Current,
in the form of ions, may flow through these intercellular specializations at the
membranous interface between two communicating neurons. Gap junctions contain
connexons, which are transmembrane ion channels that create the pathway for the
flow of current. This type of exchange is really fast, bidirectional, and one-to-one
transmission, being used to synchronize cells in a network of fast responses.
- Chemical: features indirect transmission of an electrical signal through chemical
transduction, in the form of neurotransmitters, which in the end induce an electrical
in the postsynaptic neuron. The space between the pre- and postsynaptic
membrane, the synaptic cleft, is substantially bigger for chemical synapses. Here,
synaptic vesicles of the presynaptic element, may release their content;
neurotransmitters. The chemical agents are messengers between communicating
neurons. The exchange rate is relatively slow, one directional, but most importantly,
the transmission can be regulated.
Signaling transmission at electrical synapses works via the so-called gap junctions, which
contains connexons, which are composed of ion-channel proteins called connexins – the
subunits of connexons. The various types of connexins yield different connexons with
diverse physiological properties; six connexins come together to form one hemi-channel or
connexon. Two hemi-channels are aligned to form a pore that connects the two membranes
and permits the current to flow through. As indicated, transmission if extremely fast,
whereby communication occurs without delay. Also, transmission is bidirectional, as can
small molecules like second messengers pass through connexons; two properties which
permit electrical synapses to synchronize their activity.
Signal transmission at chemical synapses uses synaptic vesicles and neurotransmitters as
primary means of communication. In the presynaptic terminal, the so-called active zone is
where synaptic vesicles release their content, whereas in the postsynaptic terminal contains
the postsynaptic density, where many receptors reside and other structures to induce
excitation of the receiving neuron. Transmission actually has a distinct sequence of events;
synaptic vesicles are formed filled with neurotransmitters action potential invades the
presynaptic terminal voltage-gated calcium channels open calcium influx allows
synaptic vesicle to fuse with the presynaptic membrane exocytosis neurotransmitters
diffuse across the synaptic cleft bind to specific receptors on the postsynaptic membrane
binding changes the ion channel permeability neurotransmitter induced current alters
the membrane potential possibly leads to generation of new action potential in the
postsynaptic neuron. The action of the neurotransmitter is terminated by removal from the
cleft, either by enzymatic degradation or by re-uptake by glial cells.
, Neurotransmitters, of which over a 100 have been found, have the following properties:
- Present/stored in the presynaptic neuron.
- Released upon depolarization and calcium influx
- Specifically detected by receptors on the postsynaptic neuron
- Be temporarily present outside the cell, as the signal must also be stopped.
The two main classes of neurotransmitters described are the small-molecules (like ACh) and
the neuropeptides. Each neurotransmitter induces a specific type of response and each has
a different reaction speed. Small-molecule neurotransmitter propagate rapid synaptic
action, while the neuropeptides modulate slower, ongoing neuronal functions. There are
even neurons which may release two kinds of neurotransmitters, which can be differentially
released so signaling properties change dynamically according to the rate of activity.
Effective transmission requires close control over the neurotransmitter concentration – so,
there are sophisticated mechanisms to regulate the synthesis, packaging, release and
degradation of neurotransmitters. Synthesis occurs in the presynaptic terminal, whereby the
precursor molecule is taken to this site by transporter molecules. There are specific enzymes
in the terminal that subsequently synthesize the neurotransmitter, as are there selective
transporter enzymes to package vesicles with neurotransmitter. There actually are two
types of synaptic vesicles:
- Small clear-core vesicles are packaged with the small-molecule neurotransmitters
- Large dense-core vesicles are packaged with neuropeptides, which are actually
synthesized in the cell body and then, via axonal transport, they end up in the
terminal.
Removal of neurotransmitters is necessary so that the cell does not engage in another cycle
of synaptic transmission. This occurs via diffusion of neurotransmitter away from the cleft in
combination with re-uptake into nerve terminals or nearby glial cells, or, by enzymatic
degradation.
Understanding chemical synaptic transmission was done by investigating cholinergic
neurotransmission at neuromuscular junctions, where the specialized synapses occur at so-
called end plates. Whenever the membrane potential is raised above the threshold, an
active action potential in the postsynaptic element is produced, also known as the end plate
potential. This EPP causes the muscle fiber to contract. There is some time delay though
between the time the presynaptic neuron is stimulated and muscle contraction. Aside from
EPPs, which actually induce muscle contraction, there are also smaller spontaneous changes
in muscle membrane potential, known as miniature end plate potentials (MEPPs).
To study the EPP, calcium concentrations were lowered, which causes a lowered secretion
of neurotransmitters and hence a reduced magnitude of EPPs. A small EPP is similar to an
MEPP, whereby thus fluctuations can be seen. A full-blown EPP is comprised, along these
lines, of MEPP-like units, which correlates with the idea that the release of
neurotransmitters occurs in discrete packets. A presynaptic action potential causes a
postsynaptic EPP because then it synchronizes the release of many of these packets.
The source of the packets would be the synaptic vesicles loaded with transmitter, wherein
they thus reside in extremely high concentrations. Studies showed that the fusion of one
synaptic vesicle produces a single MEPP. This so, because if treated with drugs that enhance
the fusion potential of vesicles during an action potential, the number of vesicles released
can be varied. One would then compare the number of synaptic vesicles fusions (via
electron microscopy) with the number of ‘quanta’ released at the synapse.
