SIGNAL-PROCESSING IN THE BRAIN
see
Patent US6172941:
Method
to Generate Self-Organizing Processes in Autonomous
(pages 9 - 17)
Figs.
4a - d illustrate a model for the acquisition and processing of STQ(d)
and STQ(v) elapse times
(see also Figs.
3a-g) and for temporal and motoric auto-adaptation in a molecular/biological
context.
The
basic elements of the model have already been described in the neurophysiology
literature by
KATZ,
GRAY, KELLY, REDMAN,
J. ECCLES and others. The present invention is of special
originality
because temporal and motoric auto-adaptation is effected here by means
of STQ quanta,
which are described
for the first time here. Such systems consist mainly of numerous neurons
(nerve
cells). The
neurons are interconnected with receptors (sensory neurons), which enables
the recording
and
recognition of
the neurons' physical surroundings. In addition, the neurons cooperate
with effectors
(e.g.muscles)
which serve as command executors for the motoric activity. The expression
"receptor"
or
"sensory neuron"
corresponds to the mechanistic term "sensor". An "effector" is the same
as an
"actuator",
which is a known term in the cybernetics literature. Each neuron consists
of a cell membrane
that encloses
the cell contents and the cell nucleus. Varying numbers of branches from
the neurons
(axons,
dendrites etc.) process information off to effectors or other neurons.
The junction of a dendritic
or
axional ending with another cell is called a synapse. The neurons themselves
can be understood as
complex
biomolecular sensors and time pulse generators; the synapses are time data
analyzers which
continually
compare the currently recorded elapse time sequences with prior recorded
elapse time
patterns that
were produced by the sensory neurons and were propagated along nerve fibers
towards the
synapses.
In turn, a type of "covariance analysis" is carried out there, and adequate
probability density
signals
are generated that propagate to other neighboring neural systems or to
effectors.
Fig.
4a shows a so-called "action potential" AP that is produced at the
cell membrane by an abrupt
alteration
of the distribution of sodium and potassium ions in the intra and extra-cellular
solution, which
works like
a capacitor. These ionic concentrations keep a certain balance as long
as no stimulus is
produced
by the receptor cell. In this equilibrium state, a constant negative potential
12, termed the "rest
potential",
exists at the cell membrane. As soon as a receptor perceives a stimulus
from an external
signal
source, Na+ ions flow into the neutral cell, which causes the distribution
of positive and negative
ions to be
suddenly inverted, and the cell membrane " depolarizes". Depending on the
intensity of the
receptor stimulus,
several effects are produced:
(a) If the
threshold P1 is not exceeded, then a so-called "electrotonic potential"
EP is produced which
propagates
passively along the cell membrane (or axon fiber), and which decreases
exponentially
with respect
to time and distance traveled. The production of EP is akin to igniting
an empty fuse
cord. The flame
will stretch itself along the fuse, becoming weaker as it goes along, before
finally
going out.
EP's originate with each stimulation of a neuron.
(b) If the
threshold P1 is exceeded, then an "action potential" AP (as in Fig. 4a)
is produced which
propagates
actively along the cell membrane (or axon fiber) with a constant amplitude
in a self-
regenerating
manner. The production of AP is akin to a spark incident at a blasting
fuse: the fiercely
burning
powder heats neighboring parts of the fuse, causing the powder there to
burn, and so on,
thus propagating
the flame along the fuse.
AP's are used
in the quantization of STQ(d) and STQ(v) elapse times. They are practically
equivalent to
identification
pulses IP with periods t(P1), t(P2), t(Pn)..., which are shown in Fig.
3a. AP's signal
the
occurrence of the phase transitions from which STQ(d) and STQ(v) elapse
times derive. In addition,
the
AP' indirectly
activate the molecular/biological "timers" that are used for recording
these elapse
times.
But AP's do not represent deterministic sampling rates for amplitude scanning;
and they do not
correspond
to electronic voltage/frequency converters. Moreover, their amplitude is
independent of the
stimulation
intensity at the receptor, and they do not represent the time counting
pulses used in the
measurement
of elapse times. Rather, the recording of STQ elapse times is effected
and modulated by
the
velocity with which the action potentials propagate along the nerve fibers
(axons) and membrane
regions.
The time measuring
properties of AP's are described in detail in the following section:
If an EP, in
answer to a receptor stimulus, exceeds a certain threshold value (P1) 13,
then an AP is
triggered.
The amplitude trace of an AP begins with the upstroke 14 and ends
with the repolarisation 15,
or
with the so-called "refractory period", respectively. At the end of this
process, the membrane potential
decreases again
to the resting potential P0, and the ionic distribution returns to equilibrium.
Not each
receptor
stimulus generates sufficient electric conductivity to produce an AP. As
long as it remains under
a
minimal threshold value P1, it generates only the electrotonic potential
EP (introduced above). (For a
better
understanding of elapse time measurements in biological/chemical structures,
see Fig. 2c and
Fig.
3a). The first AP, which is triggered after a receptor is stimulated, generates
initially (indirectly) the
impulse that
activates the first timer that records the first STQ(d) elapse time, when
the signal amplitude
W
passes through the threshold value of the potential P1 at phase transition
iTw(1.1). This signal
represents
simultaneously an identification pulse IP. The first AP corresponds to
the first IP in a
sequence
of IP's that represents the respective threshold value status or perception
zone in which the
stimulation
amplitudes were just found. As long as the stimulus at the receptor persists,
an AP 16a,
16b...
is triggered in temporal intervals whose duration depends on the respective
thresholds in which
the
stimulus intensities have just been found.
These temporal
intervals correspond to those IP periods t(P1), t(P2),... that are required
for serial
allocation
and processing of STQ elapse times (see Fig. 3a). The AP frequency is stabilised
through the
so-called
"relative refractory period" (i.e. downtime) after each AP, during which
no new depolarisation
is possible.
Because the relative refractory period shortens itself adaptively in proportion
to the increase
in
stimulation intensity at the receptor (e.g. if the EP reaches a higher
threshold value P2 (or perception
zone)
13a), there is a similarity here with "programmable bi-stable multivibrators"
found in the usual
mechanistic
electronics. The downtime (refractory period) after an AP is shown as the
divided line 19.
Fig. 4a illustrates
an "absolute refractory period" t(tot) following a repolarisation. No new
AP can be
created
during this time, irrespective of the stimulation intensity at the receptor
rises. The maximum
magnitude
of a recognizable receptor stimulus is programmed in this way. Of importance
is the fact that
both
the duration of the relative refractory period as well as character of
the absolute refractory period
are
subordinate to auto-adaptive regularities, and are therefore continually
adapting to newly appearing
conditions
in the organism. Consequently, the threshold values P0, P1, P2.... from
which STQ quanta
are
derived are themselves not absolute values, but are subject to adaptive
alteration like all other
parameters;
including, in particular, the physical "time".
We shall now
elaborate upon what happens after the first STQ(d) elapse time at P1 is
recorded via the
first
AP: If the stimulation intensity (with a theoretical amplitude W) increases
from the lower threshold
P1
to the next higher threshold P2, then the following AP triggers indirectly
the recording of the second
STQ(d)
elapse time as soon as a phase transition occurs through the next higher
threshold P2. The same
process is
repeated in turn for the threshold values P3, P4, ... and so on. In each
case, the AP functions
simultaneously
as an identification pulse IP, as described in Fig. 3a. It therefore recurs
in threshold-
dependent
periods as long as a perception acts upon the receptor (i.e. for as long
as the receptor is
perceiving
something).
As an example,
consider also Fig. 3a: As long as the stimulation intensity remains in
the zone P2, the
AP 17, 17a,
17b.... recurs in short temporal periods. These periods (or intervals)
are similar to those
periods
of IP identification pulses (with period t(P2)) that are required for serial
recording of the STQ
elapse
times Td(2) and Tw(2). When the increasing stimulation intensity reaches
the threshold value P3
(or
perception zone 3) 13b, the AP's recur in even shorter time periods
18a, 18b, 18c... This
corresponds
to the IP identification pulses with the period t(P3), shown in the figure,
which are indirectly
required for
serial timing of the STQ elapse times Td(3) and Tw(3). An even larger stimulation
intensity,
for
example in P4 (perception zone 4), would generate an even shorter period
for the AP's. This would
correspond
approximately to t(P4) in Fig. 3a. The maximum possible AP pulse frequency
is determined
by
t(tot). Shorter refractory periods, after the depolarization of APs, also
produce smaller AP-
amplitudes.
This property simplifies the allocation of AP's in addition.
In the following,
the generation of the actual time counting pulses for STQ quantization
is detailed. These
pulses are
either invariable ITPC or vm-proportional VTCP, as illustrated in Fig.
3a. The time counting
pulses for
the quantization of elapse times are dependent on the velocity with which
the AP propagate
along an axon.
This velocity is in turn dependent on the "rest potential" and on the concentration
of Na+
flowing into
the intracellular space at the start of the depolarization process, as
soon as perception at the
receptor cell
causes an electric current to influence the extra/intra-cellular ionic
equilibrium.
With the commencement
of stimulation of a receptor (at the outset of a perception), only capacitive
current
flows from the extra-cellular space into the intracellular fluid. This
generates an "electrotonic
potential"
EP, which propagates passively. If this EP exceeds the threshold P1, then
an AP, which
propagates
in a self-regenerating manner along the membrane districts, is produced.
The greater the
capacitive
current still available after depolarisation (or "charge reversal") of
the membrane capacitor,
the greater
the Na+ ion flow into the intracellular space, and the greater the available
EP current that can
flow
into still undepolarized areas. The rate of further depolarization processes
in the neuronal fibres,
and
consequently the propagation speeds of further AP's, are thus increased
proportionally.
The charge
reversal time of the membrane capacitor is therefore the parameter that
determines the value
12 of
the resting potential P0. When a stimulus ("excitation") starts from the
lowest resting potential 12,
then
the Na+ influx is the largest, the EP-rise is steepest and the electrotonic
flux is maximum. If an AP
is
triggered, then its propagation speed is in this case also maximum. But
when a receptor stimulus starts
from
a higher potential 12a, 12b, 12c...., then the Na+ influx is partially
inactivated, and the steepness
of
the EP-rise as well as its electrotonic flux velocity is decreased. Therefore,
the propagation speed of
an AP decreases
too.These specific properties are used in molecular/biologic organisms
to produce
either
invariant time
counting impulses ITCP, with periods tscan, or variable time counting impulses
VTCP
with
periods t.vscan. In the latter case, the VTCP's are modulated in accordance
with the relative speeds
vm
(via the STQ(v) parameters), and therefore have shorter intervals (see
Figs. 3b, 3c). The STQ(v)-
quantum
is determined by the deviation of the respective starting-potential from
the lowest resting-
potential P0,
which serves as a reference value, and is measured by the duration of the
capacitive
charging
of a cell membrane when a stimulus occurs at the receptor.
The duration
of the charging is inversely proportional to the velocity of the Na+ influx
through the
membrane
channels into the intracellular space. A cell membrane can be understood
as an electric
capacitor,
in which two conducting media, the intracellular and the extracellular
solution, are separated
from one another
by the non-conducting layer, the membrane. The two media contain different
distributions
of Na/K/Cl ions. The greater the "stimulation dynamics" (see below) that
first influences
the
outer molecular media - corresponding to sensor 2 in Fig. 2a - and, subsequently,
the inner
molecular
media - which corresponds to sensor 1 in Fig. 2a - the faster is the Na+
influx and the
shorter
the charging time (which determines the parameter for the relative speed
vm), and the faster is
the AP propagation
velocity v(ap) in the neighbouring membrane districts. The signals at the
inner and
outer
sides, respectively, of the membrane, correspond to the signal amplitudes
V and W. The velocity
v(ap),
therefore, indirectly generates the invariant time counting pulses ITCP
or the variable vm-
proportional
time counting pulses VTCP.
These variable
VTCP pulses are self-adaptive modulated time pulses that are correlated
to the relative
length. As
explained in the following (contrary to the traditional physical sense),
no "invariant time"
exists -- only
"perceived time" exists. Of essential importance also is the difference
between "stimulation
intensity
" whose measurement is determined by the AP frequency and therefore by
the refractory period,
and
the "stimulation dynamics", whose measurement is defined by the charge
duration of the cell
membrane
and therefore also by the speed of the Na+ influx. "Stimulation dynamics"
is not the same as
"increase of
the stimulation intensity". It is a measure of the temporal/spatial variation
of the position of
the
receptor relative to the position of the stimulus source, and therefore
of the relative speed vm. The
stimulation
intensity corresponds to signal amplitudes, from which vm-adaptive STQ(d)
elapse times
Td
(1,2,3...) are derived, while the stimulation dynamics is defined by the
acquired STQ(v) parameters.
Fig. 4b
and Fig. 4c show the analysis of STQ elapse times in a molecular/biological
model in an easily
comprehensible
manner. The results of the analysis are used to generate redundancy-free
auto-adaptive
pattern
recognition as well as autonomous regulating and self-organization processes.
The organism in
the
particular example shown here is forced to distinguish certain types of
foreign bodies that press on
its
"skin". It must reply with a fast muscle reflex when it recognizes a pinprick.
But it should ignore the
stimulus
when it recognizes a blunt object. A continuous vm-adaptive recording of
STQ(d) elapse times
by
means of VTCP pulses is necessary to do this. The frequency of these time
counting impulses is
modulated in
accordance with the STQ(v) parameters of the stimulus dynamics (vm). These
STQ(v)
parameters
are required for the recording of the STQ(d) elapse times Td
(1,2,3...) from the signal
amplitude
at the current stimulus intensity. The difference between "stimulation
intensity" and
"stimulation
dynamics" is easily seen in this example. A stimulus can even show a different
intensity if
no
temporal-spatial change takes place between signal source and receptor.
A needle in the skin can
cause a different
sensory pattern even when its position is not changing if, for example,
it is heated. This
sensory
pattern is determined by the signal amplitude, and consequently by the
AP frequency and by the
STQ(d)
quanta. As long as the needle persists in an invariant position, the AP
propagation velocity is
constant,
because the membrane charging time is constant too. During the prick into
the skin, there is a
"dynamic
stimulation", and the STQ(d) quantization of the signal amplitude is carried
out in a manner
that depends
on the pricking speed vm. It should be noted that two temporally displaced
signal
amplitudes
(at the inner and outer membrane surface) always exist during this dynamic
process. The
STQ(v)
parameters are derived from this. The AP propagation velocities and the
acquired STQ(d) time
patterns
are adapted accordingly ("temporal auto-adaptation").
The STQ(d)
time patterns Td(1,2,3,4,.....),
measured adaptively according to the vm, are constantly
compared to
and analysed together with the previously measured and stored STQ(d) time
patterns
Td'(1,2,3...).
This time comparation process occurs continuously in the so-called synapses,
which are
the
junctions to axional endings of other neurons. The probability density
values that are produced at the
synapses,
and which are used to represent the convergence of both regression curves,
are communicated
for
further processing to peripheral neural systems, or to muscle fibres in
order to trigger motoric reflex.
Fig. 4b
shows the vm-dependent propagation of an AP from a sensory neuron (receptor)
20 along an
axon
to a synapsis, where a comparison of acquired time sequences takes place
through molecular
"covariance
analysis". This receptor functions like a "pressure sensor". If a needle
21 with a certain
dynamics
impinges on the outer side of the cell membrane, then this stimulation
causes triggering of
AP's
23 as described in Fig. 4a. The AP's propagate in the axon 22
with a STQ(v)-dependent speed vap.
The sequence
(a'.....v') represents the signal amplitude values that are produced by
the pinprick. The
sequence
begins with the phase transition at the first threshold value P1, continues
over P2, P3, P4 (at
which
point the stimulus maximum is attained), and finally to the phase transitions
through P3 and P2.
The intensity
zones for stimulus perception are designated with Z1, Z2, Z3 and Z4. The
periods t(P1),
t(P2),
t(P3), t(P4)......, and the magnitudes of the AP's serve to identify the
particular threshold in which
the stimulation
intensity is currently to be found. Their temporal sequence is therefore
a type of "code".
AP's
are not time counting pulses. Besides their coding function, they also
serve as (indirect) activating
and
deactivating pulses for the recording of STQ(d) elapse times. The actual
vm-dependent
measurement
of the STQ elapse times Td(1), Td(2), Td(3), Tw(4) and Td(4)... (see Fig.
2c), as well as
the
comparison of these with previously recorded elapse times, takes place
in the synapse 24.
At the presynaptic
terminal of the axons, the AP's 23 arrive with variable velocities
vm(n...), according to
the
dynamics of the needle prick as well as the measured STQ(v) parameters.
This variable arrival
velocity
at the synapses is the key to producing the adaptive time counting impulses
VTCP (see Fig. 3c)
with
vm-modulated frequency ƒscan. The synapse is separated from the postsynaptic
membrane by the
"synaptic
cleft", and the postsynaptic membrane, for its part, is interconnected
with other neurons; for
instance,
to a "motorneuron" 25. This neuron generates a so-called "excitatory
postsynaptic potential"
(EPSP) 27
that is approximately proportional to the convergence probability g. If
this EPSP (or,
equivalently,
the probability density g) exceeds a certain threshold value, then, in
turn, an action
potential
AP 28 is triggered. This AP is communicated via motoaxon 26
to the "neuromuscular
junction",
at which a muscle reflex is triggered. The incoming AP sequences 23
generate the release of
particular
amounts of molecular transmitter substance from their repositories - tiny
spherical structures
in the synapse,
termed "vesicles". In principle, a synapse is a complex programmable timedata
processor
and
analyzer that empties the contents of a vesicle into the presynaptic cleft
when the recurrence of any
prior
recorded synaptic structure is confirmed within a newly recorded key sequence.
The synaptic
structures
and vesicle motions are generated by the dynamics (vap) of the AP ionic
flux, as well as by
its frequency.
AP influx velocities v(ap) correspond to the STQ(v) elapse times, and AP
frequencies
correspond
to the STQ(d) elapse times. The transmitter substance is reabsorbed by
the synapse, and
reused
later, whereby the cycle continues uninterrupted.
We now present
a detailed description of Fig. 4b (referring also to Figs. 4e and 4f).
The ionic influx of
the
initial incoming AP 23 (a') activates the spherical structures (vesicles)
containing the ACh transmitter
molecules.
These molecules are released in the form of a "packet". The duration of
this ACh packaging
depends on
the dynamics (represented by the velocity v(ap)) of the AP ionic influx
at the presynaptic
terminal,
and therefore on the stimulus dynamics (represented by vm) at the receptor
20. Each
subsequent
incoming AP, namely b', c'..., in turn causes neurotransmitter substances
in the vesicle to be
released
toward the synaptic cleft. Each of the following are elapse time counting
and covariance
analyzing
characteristics:: the duration of accumulation of neurotransmitter substance
T(t); the velocities
v(t) with which
the neurotransmitter substances move in the direction of the synaptic cleft;
the effects
induced
by the neurotransmitter substances at the synaptic lattice at the synaptic
cleft; the duration of
pore
opening; and so on. By means of AP's acting on synaptic structures, not
only are the actual time
counting
frequencies ƒscan generated (to be used in vm-dependent measurement of
STQ(d) elapse times
as
described in Fig. 2c), but also time patterns are stored and analysed.
If the pattern
of a current temporal sequence is recognised by the synapse as matching
an existing stored
pattern,
a pore opens at the synaptic lattice, and all of the neurotransmitter content
of a vesicle is
released
into the subsynaptic cleft. The released transmitter molecules (mostly
ACh) combine at the
other
side of the cleft with specific receptor molecules of the sub-synaptic
membrane of the coupled
neuron.
Thus, a postsynaptic potential (EPSP) is generated, which then propagates
to other synapses,
dendrites,
or to a "neuromuscular junction". If the EPSP exceeds a certain amplitude,
then it triggers an
action
potential (AP) of the described type, which then triggers, for example,
a muscle reflex. If the
potential
does not reach this threshold, then the EPSP propagates in the same manner
as an EP (i.e. in
an
electrotonic manner); an AP is not produced in this case.
Of special
significance is the summing property of the subsynaptic membrane. This
characteristic,
termed "temporal
facility", results in the summation of amplitudes of the generated EPSP's,
if they arrive
in
short sequences within certain time intervals. Each release of neurotransmitter
molecules into the
synaptic
cleft designates an increased probability density occurring during the
comparison of
instantaneous
vm-proportionally acquired STQ time patterns to prior vm-proportionally
recorded STQ-
time
patterns. Increased probability density causes a higher frequency of transmitter
substance release
and
therefore a higher summation rate of the EPSP's, which in turn produces,
at a significantly increased
rate, postsynaptic
action potentials (AP). Therefore, a postsynaptic AP is effectively a confirmation
signal
that flags the fact that isomorphism between a previously and currently
recorded time data pattern
has
been recognized. On the basis of this time pattern comparison, the object
that caused the perception
at
the receptor cell is thereby identified as "needle"; and the command to
"trigger a muscle reflex" is
conveyed
to the corresponding muscle fibres.
Parallel and
more exact recognition processes are executed by the central nervous system
CNS (i.e. the
brain).
From the sensitive skin-receptor neuron 20, a further axonal branching
29 is connected via a
synapse
30 to a "CNS neuron". In contrast to the "motorneuron" which actuates
the motoric activity of
the
organism directly, a CNS neuron serves for the conscious recognition of
a receptoric stimulation
sequence.
An AP 31, produced at the postsynaptic cell membrane 30, can spread out
along dendrites in
the axon
30a, as well as to several other CNS neurons; or, alternatively, indirectly
via CNS neurons to
a motorneuron,
then on to a neuromuscular junction.
The parameters
controlling the recording of STQ time quanta in the synapses 25
and 30 can differ with
different
synaptic structures. (Indeed, the synaptic structures themselves are generated
by continuous
"learning"
processes). This explains how it is possible for a needle prick to be registered
by the brain,
while eliciting
no muscular response; or how a fast muscle reflex can be produced while
a cause is
hardly
perceived by the brain. The first case shows a conscious reflex, the other
case an instinctive
reflex.
The former occurs when the CNS synapse 30 cannot find enough isomorphic
structures (in
contrast
to the synapse 25), transmitter molecules are not released with
sufficient frequency, and
subsequently
no postsynaptic AP 31 and no conscious recognition of the perceived
stimulus can take
place. Numerous
functions of the central nervous system can be explained in such a monistic
way; as
well
as phenomena such as "consciousness" and "subconscious". Generally, auto-adaptive
processes
are
deeply interlaced
in organisms, and are therefore extremely complex. In order to be capable
of
distinguishing
a needle prick from the pressure of a blunt eraser, essentially more time
patterns are
necessary;
in addition, more receptors and synapses must be involved in the recognition
process.
Fig. 4c
illustrates the process by which moderate pressure from a blunt object
(e.g. a conical eraser on a
pin)
is recognized, resulting in no muscle reflex. The blunt object 32
presses down with a certain
relative
velocity vm onto a series of receptors in neural skin cells 33, 34,
35, 36 and 37. Several
sequences
of AP's 39, 40, 41, 42 and 43 are produced after the individual
adjacent receptors (see also
Fig.
4b) are stimulated. These action potentials propagate along the collateral
axons 38 with variable
periods t(P1,2,3..)
and velocities vap(1..5), which result on the one hand from the prevailing
stimulation
intensity,
and on the other hand from the respective stimulation dynamics. Since each
receptor stimulus
generates
a different pattern of STQ(v) and STQ(d) quanta, various AP sequences a'.....m'
emerge from
each
axon. All sequences taken together represent the pattern of STQ elapse
times which characterises
the
pressure of the eraser on the skin. These variable AP ionic fluxes reach
the synapses 44, 45, 46, 47
and 48,
which are interconnected via the synaptic cleft with the motoneuron 49.
As soon as the currently
acquired
STQ time data pattern shows a similarity to a prior recorded STQ time data
pattern, each
individual
synapse releases the contents of a vesicle into the subsynaptic cleft.
Simultaneously, this
produces
an EPSP at the subsynaptic membrane of the neuron. These EPSP potentials
are mostly below
the
threshold. The required threshold value for the release of an AP is reached
only when a number of
EPSP's
are summed. This happens only when a so-called "temporal facilitation"
of such potentials
occurs, as
described in the previous paragraph.
In the model
shown, the individual EPSP's 50, 51, 52, 53 and 54 effect
this summing property of the
subsynaptic
membrane. These potentials correspond to receptor-specific probability
density parameters
g1,
g2, g3, g4 and g5, that represent the degree of isomorphity of time patterns.
Simultaneous
neurotransmitter
release in several synapses, for example in 45 and 47, causes
particular EPSP's to be
summed to a
total potential 56, which represents the sum of the particular probability
densities
G
= g1+g3. This property of the neurons (i.e. the summing of spatially separated
subliminal EPSP's
when
release of neurotransmitter substance appears simultaneously at a number
of parallel synapses on
the
same subsynaptic membrane) is termed "spatial facilitation".
In the described
model case, the summed EPSP 56 does not, however, reach the marked
threshold (gt),
and therefore
no AP is produced. Instead, the EPSP propagates in the sub-synaptic membrane
region 49
of
the neuron, or in the following motoaxon 55, respectively, as a
passive electrotonic potential (EP).
Such
an EP attenuates
(in contrast to a self-generating active AP) a few millimetres along the
axon, and
therefore
has no activating influence on the neuromuscular junction, and consequently
no activating
influence
on the muscle. The stimulation of the skin by pressing with the eraser
is therefore not
sufficient
to evoke a muscle reflex.
It would be
a different occurance if the eraser would break off and the empty pin meet
the skin receptors
with
full force. In this case, neurotransmitter substances would be released
simultaneously in all five
synapses
50, 51, 52, 53 and 54, because the acquired STQ time patterns
Td(1,2,3..),
with very high
probability,
would be similar to those STQ time patterns Td'(1,2,3...
) already stored in the synaptic
structures
that pertain to the event "needle prick". The EPSP's would be summed, because
of their
temporal
and spatial "facilitation", to a supraliminal EPSP 56, and a postsynaptic
AP would be
produced
that propagates along the motoaxon 55 in a self-regenerating manner
(without temporal and
spatial
attenuation) up to the muscle, producing a muscle reflex.
As in Fig.
4b, in the present example a recognition process takes place in the central
nervous system
(CNS) that
proceeds in parallel. From the skin receptor cells 33, 34, 35, 36 and
37, collateral axonal
branches
extend to CNS synapses that are connected to other neurons 58. Such
branches are termed
"divergences".
The subdivision of axons into collateral branches in different neural CNS
districts, and
the
temporal and spatial combination of many postsynaptic EPSP's, allows conscious
recognition of
complex
perceptions in the brain (for example, the fact of an eraser pressing onto
the skin). Since this
recognition
has to take place independent of the production of a muscle reflex, the
sum of individual
EPSP's
must be supraliminal in the CNS. Otherwise, no postsynaptic AP - i.e. no
signal of
confirmation
- can be produced.
As an essential
prerequisite for this, it is necessary that auto-adaptive processes have
already occurred
which
have formed certain pre-synaptic and sub-synaptic STQ time structures in
the parallel synapses
58.
These structures hold information (time sequences; i.e. patterns) pertaining
to similar sensory
experiences
(e.g. "objects impinging on the skin" - amongst these, a conical eraser).
Obviously the
threshold
for causing an AP in the postsynaptic membrane structure of the ZNS Neurons
58 (and
therefore
also in the brain) has to be lower than in the motoneuron membrane 49
described previously.
Therefore
also the sum of these EPSP's must be larger than the sum of the EPSP's
g1, g2, g3, g4 and
g5.
Isomorphisms of STQ time patterns in the CNS synapses of the brain have
to be more precisely
marked out
than those in the synapses of motoneurons, which are only responsible for
muscle reflexes.
The
structure of the CNS synapses must be able to discern finer information,
so it must be more subtle.
The production
of a sub-synaptic AP represents a confirmation of the fact that a currently
acquired
Td(1,2,3...)
time pattern is virtually isomorphic to a prior recorded reference time
pattern Td'(1,2,3...),
which,
for example, arose from a former sensory experience with an eraser impinging
at a certain
location on
the skin. If such a former experience has not taken place, the consciousness
has no physical
basis
for the recognition, since the basis for time pattern comparison is missing.
In such a case, therefore,
a
learning process would first have to occur. Most of the time, however,
sensory experiences of a visual,
acoustic
or other type, arising from a variety of receptor stimulation events, are
co-ordinated with the
pressure
sensing experience.
This explains
why CNS structures are extremely intensively interlaced. CNS neurons, as
well as moto-
neurons,
have up to 5000 coupled synapses, which are interconnected in a multifarious
manner with
receptor
neurons and axonal branches. There are complex time data patterns for lower
and higher task
sites,
which are structured in a hierarchical manner. We have already described
simple Td(1,2,3....)
and
Td'(1,2,3...)
analysis operations. Blood circulation, respiration, co-ordination of muscle
systems, growth,
seeing, hearing,
speaking, smelling, and so on, necessitate an extremely large number of
synaptic
recorded
"landscapes" of the organism's STQ time patterns, produced by a variety
of receptors; and
which
continually have to be analysed for isomorphism with time patterns currently
being recorded.
Accordingly,
temporal and motoric auto-adaptation occurs in deeper and higher hierarchies
and at
various
levels.
Fig. 4d
illustrate the counterpart to the EPSP (Excitatory Postsynaptic Potential):
the "Inhibitory
Postsynaptic
Potential " , or IPSP. As seen in the figure, the IPSP potentials 61,
62, 63, 64 and 65 at
the
subsynaptic membrane 60 are negative compared to the corresponding
EPSP's. IPSP's are produced
by
a considerable proportion of the synapses to effect pre-synaptic inhibition
instead of activation. The
example
here shows an IPSP packet 67 propagating from the motoaxon 66
to a neuromuscular junction
(or muscle
fibre, respectively) which prevents this muscle from being activated -
even if a supraliminal
EPSP
were to reach the same muscle fibre at the same time via a parallel motoaxon.
Positive EPSP's
ion fluxes and negative IPSP's ion fluxes counterbalance each other. The
main function
of
the IPSP's is to enable co-ordinated and homogeneous changes of state in
the organism, e.g. to enable
exact
timing of motion sequences. In order to ensure, for example, a constant
arm swing, it is necessary
to activate
the bicep muscles, which then flex the elbow with the aid of EPSP's; but
to inhibit the
antagonistic
tricep muscles (which extend the elbow) with the aid of IPSP's. Antagonist
muscles must be
inhibited
via so-called "antagonistic motoneurons", while the other muscle is activated
via "homonym
motoneurons".
The complex synergism of excitatory (EPSP) synapses and inhibitory (IPSP)
synapses
act
like a feedback system (servoloop) and enables optimal timing and efficiency
in the organism. One
can compare
this process with a servo-drive, or with power-steering, which ensures
correct co-ordination
and
execution of current motion through data-supported operations and controls.
If data are missing, the
servoloop
collapses. Disturbances in a molecular biological servoloop that is supported
by STQ time
data
structures lead to tetanic twitches, arbitrary contractions, chaotic cramps
and so on.
From the point
of view of cybernetics, each excitatory synapse generates a "motoric impulse"
(EPSP),
while
each inhibitory synapse generates a "brake impulse" (IPSP). The continued
tuning of the
complicated
servoloops, and the balance which results from continuous comparison of
prior sensory
experiences
(the stored reference time patterns) with current sensory experiences (the
time patterns
currently
being recorded), creates "perfect timing" in the organism.
Fig. 4e
shows the basic construction of a synapse. Axon 68 ends at the pre-synaptic
terminal 69, which
is
also termed "bouton". The serial incoming AP's cause the vesicles to be
filled with neurotransmitter
molecules.
When the filling process is finished, the vesicles begin to move in the
direction of the pre-
synaptic
lattice 71. If a currently acquired time pattern is approximately
isomorphic to an existing time
pattern
(see also Fig. 4b), then a small canal opens at an attachment site on the
lattice, which releases
the
entire contents
of the vesicle into the narrow synaptic cleft 72. This process is
termed "exocytosis".
The
sub-synaptic neural membrane 73 supports specific
molecular receptors 73a, to which the released
transmitter
molecules bind themselves.
For a certain
period, a pore opens, through which the transmitter substance diffuses.
The conductivity of
the
postsynaptic membrane increases and the EPSP (following postsynaptic depolarisation)
is triggered.
The
duration of opening of the pores and the recognition of complementary receptors
by the molecules
are
likewise determined by auto-adaptive processes and evaluation of STQ time
pattern structures.
However, these
molecular processes represent deeper sub-phenomena in comparison to synaptic
processes.
Structures for temporal and motoric auto-adaptation, which depend on quantization
of STQ-
elapse
times, also exist at the molecular and atomic levels.
Fig. 4f
shows the filling of a vesicle 70 with neurotransmitting substances,
and its subsequent motion
towards
a pre-synaptic dense projection at the lattice 71. The start of
the filling process 74 can be seen as
the
activation of a stopwatch. The rate v(t) of the filling is proportional
to the dynamics of the AP ionic
flux
into the synapse. The periods T(t...) of the filling follow the periods
t(P1,P2,...) of the arriving AP's;
these
times, therefore, represent vm-adaptive quantized STQ(d) elapse times Td(1,2,3...).
The direction
of
filling is shown at 75. The direction of motion of a vesicle is
shown at 76. If the current velocity v(t),
the
duration of the vesicle packaging T(t), the quantity of transmitter molecules,
the current vesicle
motion and
other currently significant STQ parameters have characteristics which correlate
to an
existing
synaptic STQ structure, then a filled vesicle binds itself onto an "attachment
site" 77 at the
lattice.
Ca++ ions flow into the synapse, a pore at the para-crystalline vesicle
lattice opens, and the entire
molecular
neurotransmitter content is released into the synaptic cleft 72.
At the postsynaptic membrane
of
the target neuron, these molecules are fused with specific receptor molecules.
Such receptors have
verification
tasks. They prevent foreign transmitter substances (that originate from
other synapses) from
producing
wrong ESPS's at this neuron.
To complete
the discussion of Fig. 4, we relate the descriptions of Figs. 4a, 4b, 4e
and 4f to the STQ-
configurations
of Figs. 3a - g. For argument's sake, we assume once again that a pinprick
impinges onto
a
receptor cell (see also Fig. 4b).
The IP sequences
shown in Fig. 3a correspond to the AP's 23 which are produced by
stimulating a
receptor
cell 20 with a needle 21. Their periods t(P1), t(P2),...
serve to classify the respective zones of
stimulation
intensity (P1, P2...) or perception intensity (Z1, Z2... ). Each AP 23,
arriving into a synapse
69,
activates the adaptive quantization of STQ(d) elapse times, depending on
the velocity vap of the
propagation
of the AP along the axon. Elapse timing with modulated time base is triggered
as soon as a
vesicle
begins to fill. Finished filling (packaging) signifies "elapse timing stop,
STQ(d)- quantum
recorded".
The elapse times Td(1),
Td(2),
Td(3),
Td(4)....
thus recorded generate the significant synaptic
structures.
Invariant time counting pulses ITCP (see Fig. 3b) with frequency fscan
correspond to
constant
axonal AP propagation with velocity vap, if no dynamic stimulus appears
at the skin receptor
cell
(for example, if a needle remains in a fixed position and generates a constant
stimulation intensity).
In
this case, the receptor membrane senses no relative speed vm; the AP's
propagate with constant
velocity vap
along the axon 22; and the synapse quantizes the STQ(d) elapse times with
invariant time
counting
frequency fscan.
Time counting
pulses VTCP (see Fig. 3c) with variable frequency ƒscan are then applied,
if dynamic
stimulation
affects the receptor. The AP's propagate along the axon with STQ(v)-dependent
velocities
vap(n...),
modulated by the variable dynamics vm(n...) which are measured as an STQ(v)
parameter by
the membrane.
Adaptive alteration of all of the following processes occurs in a similar
manner: the
variation
of time counting periods t(P1... .n) corresponding to the points 2.1, 3.1,
4.1 in Fig. 3c; the
velocities
v(t....) of AP ionic flux into the synapse; the vesicle filling times T(t...);
the amounts of
transmitter
molecules contained in the vesicles; the motion of these molecules in the
direction of the
vesicle
lattice; the structure of this lattice; and many other parameters of the
presynaptic and subsynaptic
structures.
A synapse has
features that enable the conversion of the AP influx dynamics into vap-proportional
molecular
changes of states. This is like the variable VTCP time counting pulses
seen in Fig. 3c. The
process
can be compared with variable water pressure driving a turbine, through
which a generator
produces
variable frequencies depending on pressure and water speed: higher water
pressure is akin to
higher stimulation
dynamics vm at the receptor, higher AP propagation velocity vap along the
axon, and
higher
VTCP time pulse frequency ƒscan in the synapse (which in turn affects not
only the rate v(t) with
which
vesicles are filled, but also many other synaptic parameters). According
to these processes, the
STQ(d)
time sequence Td(1,
2, 3, 4...) is recorded in the synapse with vm-modulated time counting
frequencies
ƒscan(1,2,3...); as a consequence, the physical structure of the synapse
is determined by this
time sequence.
Fig. 3d shows
a currently acquired time data sequence 32 30 22 23 20 that is equivalent
to the recorded
time
pattern Td(1,2,3..),
and which leaves a specific molecular biological track in the synapse 24.
The
prior
acquired time data sequence 30 29 22 24 19 in Fig. 3e corresponds to the
synaptic structure that
has
been "engraved" through frequent repetition of particular stimulation events
and time patterns
Td'(1,2,3...).The
manifested synaptic Td'
structure can be considered also as a bootstrap sequence that
was
generatedby continuous
learning processes and perception experiences, and which, for example,
serves
as areference pattern for the event "pinprick".
If a newly acquired Td bootstrap sequence - which
is
given bythe current properties of the vesicle filling, as well as other
significant time dependent
parameters
- approximately keeps step with this existing Td'
(bootstrap sequence (or with a part of it ),
then"covariance"
is acknowledged in the synaptic structure. This opens a vesicle attachment
site at
thesynaptic
lattice and results in the release of all transmitter molecules that are
contained in a
vesicle,whereupon
an EPSP is generated at the sub-synaptic membrane 25.
The potential
of an EPSP
corresponds
to the probability density parameters shown in Fig. 3f, which are significant
for the
currently
evaluated covariance. If such "probability density parameters" sum within
a certain time
interval
to a certain threshold potential 27, an AP 26 is produced.
This AP serves as confirmation of
the
event "pin recognized", and produces a muscle reflex.
The comparison
of the current elapse time pattern with prior recorded elapse time patterns,
as shown in
Fig.
3c, takes place continuously in the synapses. Each recognized covariance
of a new time sequence,
that
is recorded by "temporal auto-adaptation", sets a type of "servoloop mechanism"
in motion. It
initiates a
process that we term "motoric auto-adaptation", and which can be understood
as the actual
"motor"
in biological chemical organisms, or life forms, respectively. Structures
of temporal and
motoric
auto-adaptation, which are based on STQ quantization, exist also at the
lowest molecular level.
Without
elapse time-supported servoloops, co-ordinated change in biological systems
would be
impossible.
This applies especially to the motion of proteins; to the recognition and
replication of the
genetic code;
and to other basic life processes. The creation of higher biological/chemical
order and
complex
systems such as synapses or neurons presupposes the existence of an STQ
quantization
molecular
sub-structure, from which simple acknowledgement and self-organization
processes at a
lower
level derive. Indeed, there are innumerable hierarchies of auto-adaptive
phenomena on various
levels.
Simple phenomena on a molecular level also include: fusion of receptor
molecules; the formation
of pores, ion
canals and sub-axonal transportation structures (microtubules); and the
formation of new
synapses
and axonal branchings.
By this token,
recognition of stimulation signal sequences by synaptic time pattern comparison
(as an
involuntary
reflex or as a conscious perception), as discussed in the description of
Figs. 4a - c, is an
STQ-epiphenomenon.
Each such auto-adaptive STQ-epiphenomenon, for its part, is superimposed
from
STQ-epiphenomena
of higher rankings; for example, the analysis of complex "time landscapes"
in order
to
find isomorphism. STQ-epiphenoma such as regulation of blood circulation,
body temperature,
respiration,
the metabolism, seeing, hearing, speaking, smell, the co-ordination of
motion, and so on, are
for
their parts superimposed from STQ-scenarios of higher complexity, including
consciousness,
thought,
free will, conscious action, as well as an organism's sensation of time.
In all these cases, the
central nervous
system looks after convergent time patterns that are placed like pieces
of a jigsaw puzzle
into
an integrated total sensory scenario.
If, in any
hierarchy, within a certain "latency time" (i.e. time limit) and despite
intensive "searching", no
time
subpattern covariant with the STQ time pattern can be found, then the organism
displays chaotic
behaviour.
This behaviour restricts itself to that synaptic part in which the non-convergence
has
appeared. As
soon as a covariant time pattern is found, the co-ordinated process of
temporal and motoric
auto-adaptation
(and auto-emulation) resumes. (This can be likened to servo-steering that
has collapsed
for
a short time.) However, the "chaotic behaviour" is itself quantized as
an STQ time pattern, and is
recorded
by the affected synapses in such a manner that no neurotransmitter substance
release occurs
despite
arriving AP's. Via subaxonal transportation structures (i.e. the microtubules)
such information
streams back
borne on transmitter molecules which travel in the inverse direction along
the axon.
Microtubules
are used to generate new synapses and synaptic connections at the neurons
and neural
networks
in which a collapse of an auto-adaptation process has occurred. The production
of new
synapses
proceeds to the generation of dendrites; i.e., axonal branches that carry
processing information
from
neurons. In this way the auto-adaptive neural feedback mechanism regenerates
itself, and the STQ
time
pattern that was acquired during the short termed "chaotic behaviour" becomes
a new reference
basis for the
recognition of future events. Thus, the CNS learns to record new events
and experiences;
and
learns to evaluate time patterns which were unknown previously.
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