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There seems to be a paradox between results
showing that spontaneous retinal activity directs
synapse development (Stellwagen and Shatz, 2002),
and the observation that ocular dominance columns
can form even when both eyes are removed (Crowley
and Katz, 1999). Perhaps the spontaneous activity pat-
terns that arise in the thalamus and cortex will resolve
this question (Yuste et al., 1995; Weliky and Katz, 1999;
Garaschuk et al., 2000; Chiu and Weliky, 2001). The
influence of low levels of spontaneous activity may be
supported by local inhibitory projections which fur-
ther refine the spatial pattern. In fact, local GABAergic
circuits within the cortex regulate the binocular com-
petition between thalamic afferents, and establish the
precise dimensions of ocular dominance columns
(Iwai et al., 2003; Hensch and Stryker, 2004; Fagiolini
et al., 2004).
glion cell arbors have segregated into eye-specific
layers in the cat LGN, the response properties of
LGN neurons are nonetheless altered (Dubin et al.,
1986).
The critical period may occur during a very narrow
time window in some brain areas. One region of
rodent somatosensory cortex receives afferents from
each of the facial whiskers and contains an array of
barrel-shaped cell clusters that are activated selectively
by each of the whiskers. If the whiskers are destroyed
before postnatal day 5, their associated barrels do not
form, but if the whiskers are destroyed after that time,
then the manipulation has no effect (Van der Loos and
Woolsey, 1973). There are also extensive intracortical
connections between each of the whisker barrels, and
this connectivity is dependent on continued use. When
the sensory nerve to the whiskers is cut on postnatal
day 7, after the barrel fields are formed, there is a dra-
matic reduction in the number of local projections
(McCasland et al., 1992). In fact, whisker trimming sig-
nificantly decreases the motility of dendritic spines
and filopodia in rat barrel cortex only from postnatal
days 11 to 13 (Lendvai et al., 2000). This manipulation
also affects the development of whisker-evoked recep-
tive fields in cortical Layer 2/3 until day 14, but has
no effect on Layer 4 receptive fields (Stern et al., 2001).
Thus, the critical period for barrel cortex differs by
layer. Even adult cortex can exhibit changes following
deprivation. For example, monocular action potential
blockade with TTX results in a decreased expression of
GABA A receptor subunits in Layer IV of primate cortex
(Hendry et al., 1994).
MANY FORMS OF PLASTICITY
HAVE A TIME LIMIT
Synaptic activity begins to exert an influence soon
after synaptogenesis, but how long does this process
continue? If we embrace learning and memory in our
definition, then it lasts for our entire lifetime (Box:
Remaining Flexible). However, there are certain sig-
nificant changes in nervous system structure and
function that only occur during a limited period of
development (Berardi et al., 2000; Hensch, 2004). A
common example is language acquisition, which is
accomplished most easily before age 10 and becomes
a grueling task for most of us if attempted as adults
(see Chapter 10). At least some forms of neuronal plas-
ticity only last for a limited period during develop-
mental, often called a critical period . The influence of
visual experience on ocular dominance has been
explored in older animals to determine whether corti-
cal neuron function is always dependent on vision
(Hubel and Wiesel, 1970). Ocular dominance is most
susceptible to monocular deprivation after several
weeks of sight. The visual environment influences cor-
tical neuron function for roughly the first three months
of life in cats, but this critical period does not apply to
connections forming throughout the brain.
The term critical period is a very general expression,
and the neuronal property under discussion should
always be taken into account. In primates, monocular
deprivation affects the segregation of LGN afferents
in Layer IV for about two to three months, but con-
tinues to produce severe weakening of intrinsic corti-
cal synapses for up to a year (Figure 9.22). Similarly,
when retinal activity is blocked with TTX after gan-
SYNAPSES INTERACT OVER
A SHORT DISTANCE
The modification of synapse function involves both
pre- and postsynaptic signaling mechanisms, and the
neurotransmitter itself is likely to initiate the bio-
chemical cascade. But is it really possible that there is
a single mechanism to account for synaptic plasticity?
After all, most central neurons are innervated by a
wide variety of synapses: some release glutamate,
others GABA; still others release a neuromodulator
such as serotonin. Moreover, a single glutamate-releas-
ing synapse can activate receptors that open ion chan-
nels (cf, ionotropic) and others that activate second
messenger systems (cf, metabotropic). There are few
generalizations that can cover the plasticity of all these
systems. Therefore, we will focus on synapses that
have been studied thoroughly, such as the nerve-
muscle junction.
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