Summary

1. Following neuronal apoptosis, another regressive process is the loss of many synapses during synapse rearrangement. The loss of some synapses is usually accompanied by the production of new synapses, so depending on the system and stage of development, there may be a net gain or loss of total synapses.
2. Neuronal activity plays a role in early developmental events such as neuronal apoptosis, as when motor neuron death occurs only if the target muscles are electrically active. See Figure 8.1
3. In newborn muscles, every fiber is polyneuronally innervated, but most of the initial contacts from each motor neuron are retracted over time until each fiber is innervated by one and only one neuron. This is a competitive process that occurs only if the junctions are electrically active. Presynaptic terminals that activate the muscle fiber are more likely to remain than those that are ineffective. See Figures 8.2–8.5
4. In autonomic ganglia, an initially exuberant pattern of polyneuronal innervation is followed by a loss of most inputs until each neuron receives extensive synaptic input from a relatively small number of afferents, sometimes a single afferent. See Figures 8.8–8.10
5. Hebbian synapses are strengthened or duplicated when they effectively drive the postsynaptic cell to fire, and they are weakened or withdrawn when they are ineffective. See Figure 8.11
6. Several pathways in the hippocampal formation function in a Hebbian fashion, as when driving excitatory afferents though a tetanus results in a long-lasting enhancement of the synapses, called long-term potentiation (LTP). See Figures 8.12 and 8.13
7. In several hippocampal pathways, LTP is mediated by NMDA-type glutamate receptors. When the postsynaptic neuron is depolarized, as happens after a tetanus, a magnesium block on the NMDA receptor’s channel is lifted, such that glutamate triggers an inrush of Ca²⁺ ions, which leads to insertion of additional AMPA-type glutamate receptors in the postsynaptic site and eventually an increase in glutamate release from the presynaptic terminal. See Figures 8.14 and 8.15
8. In the mammalian fetus, both eyes innervate wide regions of the lateral geniculate nucleus (LGN) of the thalamus, but as development proceeds, each eye comes to innervate separate, monocular domains of the LGN. The process of segregation of inputs to the LGN depends on waves of spontaneous activity that cross the retinas, which drive synaptic competition, following Hebbian rules, between the eyes. See Figures 8.16, 8.17, and 8.21
9. Similarly, information from both eyes is broadly distributed across all of layer IV in primary visual cortex (V1) at first but then becomes segregated such that ocular dominance bands result, with each cortical neuron in layer IV receiving monocular input. The segregation of ocular dominance bands in layer IV may also depend on a Hebbian-type synaptic competition between the two eyes, but if so, it would be in response to spontaneous activity, not visual experience, because it occurs before birth in primates. In the next chapter we’ll see that almost all neurons in visual cortex outside layer IV receive binocular input, a process that depends on Hebbian-like competition driven by visual experience. See Figures 8.18–8.20, and 8.22
10. The number of synapses in the human cortex increases rapidly until the first few years of life, then declines sharply until adulthood. The loss of synapses from adulthood to old age is much more gradual. See Figures 8.23 and 8.24
11. The net loss of synapses from childhood to adulthood can be gauged by the thickness of the gray matter, which becomes progressively thinner until about 20 years of age. Among cortical regions, the last to complete the thinning of gray matter is the prefrontal cortex. The prefrontal cortex has been implicated in executive control and inhibition, so its late development may account for the relatively impulsive behavior of adolescents. Myelination of the cortex increases during adolescence, and there is evidence that neuronal activity regulates this process. See Figures 8.25 and 8.26