Grossman et al., A brain Adaptation View of Plasticity



Download 137.71 Kb.
Page2/4
Date conversion08.07.2018
Size137.71 Kb.
1   2   3   4

2 Plasticity of myelination


Although myelination is considered to be primarily a developmental phenomenon, studies of human autopsy tissue suggest that this process continues well into adulthood (Yakovlev and Lecours, 1967; Benes et al., 1994). In developing and adult animals, the process of myelination appears responsive to behavioral experience. The first evidence for experience effects on oligodendrocyte development came from Szeligo and Leblond (1977), who reported increased subcortical white matter in recently weaned rats following exposure to complex environment. It was subsequently observed that weanling (Juraska and Kopcik, 1988) and adult rats (Briones, et al., 1999) had more myelinated axons in the splenial corpus callosum after EC exposure than did IC rats. The effects of experience on oligodendrocytes are not restricted to white matter though as Sirevaag and Greenough (1987) found that the volume fraction of oligodendrocyte nuclei in the visual cortex was significantly greater for EC rats than their IC littermates.

In addition to the role oligodendroctyes play in responding to the increased demands placed on the brain by experience, these cells are critical for repair of neural tissue following damage. The glial environment surrounding regenerating axons is important for their successful growth into target tissues (Aguayo, et al., 1981). Much of the currently research effort on spinal cord injury repair is focused on the functional development of oligodendrocytes at the lesion site. Stem-cells that are implanted into the spinal cord, for example, can differentiate into oligodendrocytes and myelinate passing axons (Liu, et al., 2000) Although some Schwann cells in the peripheral nervous system exhibit plasticity by converting from non-myelinating to myelinating cells in response to local tissue damage (Kioussi and Gruss, 1996, [Akassoglou, 2002 #221], it is debated whether mature oligodendrocytes in the central nervous system exhibit such plasticity (Bruck, et al., 1994; Blakemore and Keirstead, 1999).



2 Plasticity of Vasculature


Despite long held beliefs that the brain’s capillary system is not plastic (Bar, 1980), and in contrast to earlier reports (e.g., Diamond et al., 1964; Rowan and Maxwell, 1981), the brain’s capillary system appears to increase in capacity in response to experience. Capillaries are both larger, on average, and more elaborately branched in rats placed in complex environments at weaning than in individually cages animals. As shown in Figure X, the volume fraction of capillaries per neuron, which combines diameter and density effects, increases by about 80% following exposure to EC, suggesting that capillaries exhibit seemingly far more plasticity than synapses in response to behavioral demands (Black et al., 1987; Sirevaag et al., 1988). Studies using functional magnetic resonance imaging indicate that the capacity of experientially enhanced vasculature to supply blood is increased in response to increased demand (reduced oxygen in anesthetized rats) (Swain et al, in press GET REF). While the greatest capillary response to EC housing is seen in weanlings, this experience-induced plasticity also continues into adulthood, although diminishing with age (Black, et al., 1989).

2 Persistence of non-neuronal changes


In general, the effects of plasticity on myelination appear to be relatively stable, while the effects on astrocytes seem to be more transient. The increased myelination observed in adults following 30 days of EC housing persists across a subsequent 30-day period of relative inactivity in an individual cage housing condition (Briones et al., 1999; Figure X). This stability parallels the synaptic effects discussed above (Camel et al., 1986; Kleim et al., 1997; Briones, et al., in preparation). Astrocytic changes, however, appear to fade rapidly once a specific behavioral experience is discontinued. As shown in Fig. X (Kleim et al., in revision), when rats were trained for 10 days and left idle for a subsequent 4 weeks, the astrocytic effects of training (compared to a group that simply traversed an alleyway) were no longer statistically evident, whereas the effects of training on synapses remained apparently as strong in the idle group as in animals examined at the end of 10 days of training or animals trained for all 38 (10 + 28) days of the experiment. One might speculate that added synapses and myelin are stable because they represent permanent additions to the “wiring diagram” of the brain that are important for survival, whereas astrocytic and possibly vascular (yet to be tested) changes are responses to immediate demands of experience that can be reset, conserving valuable metabolic resources in the absence of continued environmental pressure.

The overriding message from studies of both neuronal and non-neuronal plasticity is that the brain is an organ of adaptation — the interface between an individual and its environment. As such, the brain dynamically adjusts to the demands placed upon it. It does so not just by forming, strengthening, losing and weakening synapses but by altering non-neuronal elements such that neuron-glia relationships are altered, in some cases on a long-term basis. The persistence of many of the resulting morphological changes suggests that the brain assumes that the experiences of the past are good predictors of the future.

It is of interest to speculate upon the functional consequences of selective myelination of corpus callosal axons in response to complex environment exposure. Presumably those axons would more rapidly conduct action potentials. Assuming this is associated with functionally positive effects, the implication is that oligodendrocytes must follow some form of instruction in selecting particular axons for conduction enhancement (or, perhaps, retaining them from a larger set of initially myelinated axons). The clear implication is that there are means of neuronal-oligodendrocyte communication of which we are not now aware. Moreover, these communication mechanisms must be able to be activated by behavior.

1   2   3   4


The database is protected by copyright ©dentisty.org 2016
send message

    Main page