Academic journal article Canadian Journal of Experimental Psychology

Synaptic Plasticity and the Organization of Behaviour after Early and Late Brain Injury

Academic journal article Canadian Journal of Experimental Psychology

Synaptic Plasticity and the Organization of Behaviour after Early and Late Brain Injury

Article excerpt

Abstract Hebb proposed that synaptic change underlies behavioural and cognitive plasticity. When applied to recovery from brain injury, the general hypothesis is that if there is recovery following brain injury, then there ought to be a correlated synaptic change, which is presumed to be responsible for recovery. In contrast, if recovery fails to occur, or expected recovery is blocked in some manner, then the synaptic change will likely not be present. Systematic study of functional recovery and synaptic change following brain injury at different ages supports these predictions. Good recovery is always correlated with enhanced connectivity whereas poor recovery is always correlated with an absence of reorganized connectivity. Furthermore, factors that stimulate recovery, such as neurotrophins or experience, stimulate synaptic change and functional recovery. Factors that retard recovery, such as depletion of neuromodulators, also block synaptic change. These results thus support Hebb's general idea that synaptic plasticity is related to behavioural change.

Introduction

Hebb proposed that synaptic change underlies behavioural and cognitive flexibility. There was little evidence of this in 1949, and although the concept of the "Hebb synapse" has become popular in the last decade, there is still rather little direct evidence that synaptic plasticity is associated with processes such as learning or memory, except perhaps in the simplest model systems. Nonetheless, the concept has considerable appeal and remains a viable hypothesis for behavioural flexibility. I will present evidence from studies of the anatomical bases of recovery from brain injury that support the general hypothesis that synaptic change can support behavioural change.

ASSUMPTIONS

As I begin, I must first admit to several biases (see also Kolb, Forgie, Gibb, Gorny, & Rowntree, 1998). First, I assume that the nervous system is conservative. Thus, general mechanisms that are used for one type of behavioural change, such as learning and memory, may also be used for other types of behavioural change, such as in recovery from brain injury. (This assumption does not preclude separate mechanisms too, but it provides a rationale for what to look for and where to look for it.) Studies of functional recovery have the advantage that perturbations of the brain at different times from birth through to ageing produce consistent differences in behavioural outcome ranging from almost complete recovery of function after cortical injury to truly devastating behavioural loss. This variation in behaviour is useful for it is reasonable to suppose that these behavioural differences are related to differences in anatomico-physiological response(s) as well.

Second, I am a "cortex chauvinist" and assume that the changes in the cerebral cortex form the principal mechanism for cognitive change. This assumption comes from several lines of evidence. For instance, it is generally agreed that the relative increase in cortical volume across mammalian evolution is associated with increased cognitive capacity. It follows that changes in cognitive functions in a particular mammal likely will involve changes in cortical structure or organization. Furthermore, studies of decorticated rats show that although they are capable of a remarkable behavioural repertoire (e.g., Whishaw, 1990), there is virtually no recovery or sparing of function from decortication under conditions that would normally lead to marked recovery after restricted cortical removals. For example, Whishaw and I have found that whereas removal of frontal, motor, or parietal cortex at 7-10 days of age allows dramatic sparing of function relative to similar injury in adulthood, there is no sparing at all after complete neonatal neodecortication at 7 days (Kolb & Whishaw, 1981a, b). Further, there is no obvious evidence of anatomical reorganization in the neonatal decorticates (Kolb et al. …

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