ULTIMATE COMPUTING - Quantum Consciousness Studies

From Brain to Cytoskeleton 75
ability to spatially and temporally integrate multiple converging signals to a
specific protein state, or “conformation.”
The second form of neuronal plasticity is long term potentiation (LTP). In
LTP, repeated use of a synapse makes transmission through that synapse
increasingly easy. In the synapses of mammalian brain hippocampus, the effect
endures for many hours and LTP has been classically related to learning and
memory. If two pathways share an interneuron, then LTP can enhance
transmission through the pathway not originally excited, a form of associative
memory and recall. The duration of LTP effect of many hours to days
corresponds with the morphological turnover and trophic maintenance of synaptic
membrane proteins by axoplasmic transport, a function of the neuronal
cytoskeleton.
The third form of neuronal plasticity is heterosynaptic potentiation in which
activity on one synapse changes efficiency of transmission in another on the same
postsynaptic membrane. This may occur either through change in sensitivity of
the post synaptic neuron to the transmitter, or by change in the amount of
transmitter released. There is some evidence that LTP may be due to increased
numbers of receptors in post synaptic membranes and a similar mechanism could
occur in heterosynaptic potentiation in which more then one neuron is involved.
Habituation, long term potentiation, and heterosynaptic potentiation can account
for synaptic plasticity and some aspects of learning and memory. Brain processes
related to representation, memory, learning, and consciousness thus focus on
molecular level alterations in synaptic membrane proteins which are regulated by
the neuronal cytoskeleton.
There is some evidence for direct cytoskeletal involvement in cognitive
processes. Activities of cytoskeletal microtubules and turnover of microtubule
subunits (“tubulin”) have been shown to be increased in the brain during specific
times of learning, memory and experience. Mileusnic, Rose, and Tillson (1980)
have utilized a learning model in baby chicks who can be readily trained not to
peck at a bright bead coated with an unpleasant tasting substance. These authors
have studied some of the neurochemical correlates of this “passive avoidance
learning” and point out that tubulin, the major constituent of microtubules, is
present in large amounts in the developing brain of young chicks. Significant
amounts of tubulin are associated with synaptic membranes leading the authors to
conclude that any model of learning and memory which postulates modulation of
synaptic structure, as consistent with Hebb’s postulates, must involve tubulin in
learning. Other work from their laboratory and others have shown that both
incorporation of precursor amino acids and total quantity of tubulin may be
enhanced by experience and learning during early development.
John Cronly-Dillon and co-workers (1974) of Britain’s Manchester
University have found that when baby rats first open their eyes, genes in visual
cortex suddenly begin producing vast quantities of tubulin which presumably
form microtubules involved in establishing new synaptic connections. When the
rats are 35 days old, the critical phase for learning is over and tubulin production
is drastically reduced. Their conclusion is that tubulin turnover and microtubule
activity are involved in synaptic plasticity aspects of learning and memory.
Another dynamic mode of synaptic plasticity focusing on dendritic spines has
been proposed by Francis Crick (1982). He suggested that dendritic spines can
“twitch” and change their shape, thereby altering their synaptic thresholds by
mechanical changes. The placement and architecture of dendritic spines are
determined by microtubules, but spines themselves are comprised mostly of
contractile actin (Matus, Ackermann, Pehling, Byers, and Fujiwara, 1982).
Dynamic spine plasticity, orchestrated by dendritic MT and cytoskeleton, may be