Hebb's postulate of learning envisages that activation or inactivation of extant synaptic contacts in plastic neural networks depends on the synchronous impulse activity of pre- and postsynaptic nerve cells. The physiological mechanism proposed here for this process posits that at synapses acting according to Hebb's postulate, the receptors for the neurotransmitter are eliminated from the postsynaptic membrane by the transient reversals of the sign of membrane polarization that occur during action potential impulses in the postsynaptic cell. But, since the release of neurotransmitter drives the membrane potential of the synaptic zone towards a level about half-way between the negative-inside resting potential and the positive-inside action potential, it would follow that the membrane patches surrounding the receptors of a synapse whose activity has contributed to setting off the postsynaptic impulse would be spared the full extent of the noxious polarity reversal. This mechanism can account for a neurophysiologically documented example of the operation of Hebb's postulate, namely the plasticity of the connections between fourth- and fifth-order neurons in the visual cortex of cats.
The swimming movement of the leech is produced by an ensemble of bilaterally symmetric, rhythmically active pairs of motor neurons present in each segmental ganglion of the ventral nerve cord. These motor neurons innervate the longitudinal muscles in dorsal or ventral sectors of the segmental body wall. Their duty cycles are phase-locked in a manner such that the dorsal and ventral body wall sectors of any given segment undergo an antiphasic contractile rhythm and that the contractile rhythms of different segments form a rostrocaudal phase progression. This activity rhythm is imposed on the motor neurons by a central swim oscillator, of which four bilaterally symmetric pairs of interneurons present in each segmental ganglion appear to constitute the major component. These interneurons are linked intra- and intersegmentally via inhibitory connections to form a segmentally iterated and inter-segmentally concatenated cyclic neuronal network. The network appears to owe its oscillatory activity pattern to the mechanism of recurrent cyclic inhibition.
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