I've just done some further reading[1]...
<READING>
Apparently the Purkinje cell of the cerebellum may have 100,000
dendritic synapses.
The ribosomes (protein synthesis sites) are many in the dendrites and
few (if any) in the axon.
The axon usually emerges from an "axon hillock".
Some soma and dendrites transmit information directly to the dendrites
and cell bodies of another neuron.
Neurons "feed" on glucose, although they have the enzymes for
metabolising other sugars, ketone fats, acetoacetate, lactate and
3-hydroxybutyrate. The latter chemicals are less likely to pass through
the blood-brain barrier, although infants may use them.
Vitamin B1 (thiamine) is necessary to the use of the glucose and neurons
will eventually die in its absence.
Glia cells occupy as much space as neurons. Some construct the myelin
sheaths. They also keep unmyelinated axons apart. They form a sewage
disposal function, occupy the space left by a deceased neuron and
sometimes form scar tissue. They may provide structural support which
holds "connections" in place against external shocks.
Neuron migration is guided by long-fibred radial glia. (Possibly by
secreting neurotrophin, semaphorin or the controlling cyclic
nucleotides?)
Glia retain the ability to divide but most neurons lose it. Dendrite
growth and shrinkage is always possible. Larger animals and those kept
in more extensive environments develop more dendritic branches and glia
cells. These changes have limited persistence. (I wonder what putting a
human in a prison cell for X years does to dendritic branching?)
Dendrites appear to be constantly changing.
Potassium, sodium, chloride, bicarbonate (and other?) ions can pass
through the polarised neuron cell membrane via pores in embedded
proteins. At rest, sodium pores are closed. Potassium and chloride pores
allow a constant, small flow of ions (and the occasional sodium ion) to
flow.
A sodium-potassium pump pulls two potassium ions into the cell for every
three sodium ions ejected. The potassium ions can diffuse out again,
faster than the sodium ions can return. The result is a concentration
gradient, an electrical gradient and the neuron's resting potential. The
electrical gradient encourages potassium ions to bunch together in the
centre of the neuron.
The sodium ion concentration gradient allows the neuron to be ready for
a rapid response. On excitation, the neuron opens the sodium pores and a
faster inrush of soodium ions than would otherwise be possible, is
achieved.
Stimulation of any amount beyond a threshhold (generally 15 mV above the
resting potential), causes the sodium gates to be opened.
</READING>
Presumably, the spike amplitude is dependent upon the sodium
concentration outside the cell. If this is depressed by any factor, the
intensity of the spike may be diminished. Again, if anything slows the
opening of the sodium gate, or alters the resting potential or
threshold, then the spike may be delayed. If anything ties up the
potassium in the neuron, the reestablishment of the resting potential
will be delayed as will any subsequent spikes.
<READING>
The depolarisation of the membrane due to the spike, opens the sodium
and potassium gates. Sodium ions flood in faster and potassium ions
depart. Eventually a reversed polarity is achieved although, at the
spike's (action potential's) peak, the sodium ion concentration int the
neuron is still lower than that outside. Despite the concentration
gradient, the electrical gradient is reversed to the point where further
sodium entry is virtually halted. The resting state is reached as the
sodium-potassium pump restores the previous balance.
</READING>
<SPECULATION>
If slightly more sodium ions remain, it is conceivable that the
excitation of the neuron will be marginally faster (few ions need to
enter the cell), hence leading to a "more expert" response. (I'm still
looking for the mechanism that explains skill-fluency and its temporary
loss and recovery).
</SPECULATION>
<READING>
The refractory period (during which the neuron recovers from excited
state to resting), determines the possible firing frequency of the cell.
Action potentials arise in the axon hillock. They are transmitted along
the axon as sodium ions, but some diffuse through the membrane.
Polarisation results, leading to ion exchange, regenerating the signal.
The result can be viewed as a wave along the axon. Different axons
propagate this wave at different rates. Thin axons may achieve 1 m/s.
Thicker, unmyelinated axons may propagate action potentials at 10 m/s.
The fastest myelinated axons may achieve 120 m/s. Axons in some larger
animals may exceed a metre in length.
Action potentials may not be generated in small neurons. Instead a
graded potential is generated which is conducted to areas adjacent ot
the cell. Decay over distance limits this to local cellular
intercommunication, but, the communication can be in any direction.
At the presynaptic ending of an axon, neurotransmitters are released
across a synapse. Each such release contributes to the excitation or
inhibition of the "connected" dendrite. But, there are some "electrical"
synapses used for synchronisation. Repeated stimulation of an axon may
be sufficient to generate an action potential in the postsynaptic
neuron. This has to overcome the steady decay of the graded potential
invoked in the post-synaptic dendrite.
Neurotransmitters include Dopamine, Epinephrine, Acetylcholine,
Norepinephrine, Serotonin, aspartate, glutamate, glycine, some amino
acide metabolites, the enkephalins and many hormone peptides.
Calcium pores in the presynaptic membrane are opened by the arrival of
the action potential. The resulting increase in calcium concentration
triggers the release of an amount of neurotransmitter. Sometimes this
release occurs periodically without an action potential.
The neurotransmitter diffuses across to the postsynaptic membrane (less
than 0.5 microns in under 10 microseconds) and attaches to a receptor.
The inhibitory or excitatory effect of the neurotransmitter depends upon
the type of receptor it finds.
Some neurotransmitters attaching to a receptor open sodium, chloride or
potassium gates for an a fixed period ionic effect. The others cause a
metabolic effect by stimulating an enzyme. This will convert an existing
resource to some other chemical. This may cause chemical changes in
proteins, affecting gate operation or even neuron structure. Some
resulting molecules themselves act as secondary transmitters.
Ionic effects may last a few milliseconds, but peptide transmitters may
have an effect lasting hours.
Some neurotransmitters need to be dismantled after use and the products
can diffuse back to the presynaptic neuron. Others are detached from
their receptors and reabsorbed directly, or broken down into products
that diffuse into the blood stream.
</READING>
[1] James W. Kalat, Biological Psychology, 3rd Edition, 1988, Wadsworth
Inc.
I hope this compensates for the earlier, uninformed speculation <g>
--
Jeff Best
jeffb at jtbest.demon.co.uk
Windows 95 [win'doze], n. a Linux configuration utility.
