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Morphological Changes in the Geniculocortical Pathway Associated with Monocular Deprivationa

Suzannah Bliss Tieman

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Abstract

To summarize (Fig. 10), the structural consequences of monocular deprivation include the following changes: the relay cells in the binocular segments of the deprived geniculate layers shrink and contain less of the possible neurotransmitter NAAG. These changes appear to be secondary to a loss of terminal synaptic arbor. Certainly, deprived geniculocortical cells project to smaller ocular dominance patches in layer IV of visual cortex, where they make fewer and abnormal synapses. As a result, they activate ocular activation columns that, in addition to being small, are faint and usually fail to extend into extragranular layers. This failure to extend to other layers probably results from a failure of the poorly activated deprived-eye cells in layer IV to compete successfully with neighboring experienced-eye cells in layer IV, resulting in a loss of connections from layer IV to other layers (Fig. 11). Thus, the primary effect of monocular deprivation is probably the disruption of the geniculocortical synapse, with the other changes, such as cell size, and possibly the change in neurotransmitter content, being secondary. The disrupted synapse would result in poorly driven cortical cells and faint ocular activation columns, which in turn would bias a secondary competition for access to cells in extragranular layers. There are certain general principles that unite the findings presented in this chapter with the others in this session. First, there are similarities in the types of morphological changes observed, for example, changes in the number and size of synaptic terminals, as well as mitochondrial changes. This implies that there are similar changes during development and adult plasticity and also similar changes in vertebrates and invertebrates. Second, it is not so much the amount of activity that determines these changes, but the pattern of activity. In my results, the relative imbalance in activity is important, but not the absolute amount (for example, the columns activated by the 8-hr eye of an AME 8/1 are different from those activated by the 8-hr eye of an AME 8/8). Similarly, the binocular segment, where there was an imbalance and competition could occur, was affected, whereas the monocular segment, where there was no imbalance and competition could not occur, was not. Finally, the recent results of Reiter and Stryker suggest that monocular deprivation produces changes only when the activity of the presynaptic cell and the postsynaptic cell are correlated.(ABSTRACT TRUNCATED AT 400 WORDS)

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To summarize (Fig. 10), the structural consequences of monocular deprivation include the following changes: the relay cells in the binocular segments of the deprived geniculate layers shrink and contain less of the possible neurotransmitter NAAG. These changes appear to be secondary to a loss of terminal synaptic arbor. Certainly, deprived geniculocortical cells project to smaller ocular dominance patches in layer IV of visual cortex, where they make fewer and abnormal synapses. As a result, they activate ocular activation columns that, in addition to being small, are faint and usually fail to extend into extragranular layers. This failure to extend to other layers probably results from a failure of the poorly activated deprived-eye cells in layer IV to compete successfully with neighboring experienced-eye cells in layer IV, resulting in a loss of connections from layer IV to other layers (Fig. 11). Thus, the primary effect of monocular deprivation is probably the disruption of the geniculocortical synapse, with the other changes, such as cell size, and possibly the change in neurotransmitter content, being secondary. The disrupted synapse would result in poorly driven cortical cells and faint ocular activation columns, which in turn would bias a secondary competition for access to cells in extragranular layers. There are certain general principles that unite the findings presented in this chapter with the others in this session. First, there are similarities in the types of morphological changes observed, for example, changes in the number and size of synaptic terminals, as well as mitochondrial changes. This implies that there are similar changes during development and adult plasticity and also similar changes in vertebrates and invertebrates. Second, it is not so much the amount of activity that determines these changes, but the pattern of activity. In my results, the relative imbalance in activity is important, but not the absolute amount (for example, the columns activated by the 8-hr eye of an AME 8/1 are different from those activated by the 8-hr eye of an AME 8/8). Similarly, the binocular segment, where there was an imbalance and competition could occur, was affected, whereas the monocular segment, where there was no imbalance and competition could not occur, was not. Finally, the recent results of Reiter and Stryker suggest that monocular deprivation produces changes only when the activity of the presynaptic cell and the postsynaptic cell are correlated.(ABSTRACT TRUNCATED AT 400 WORDS)

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Available abstract

To summarize (Fig. 10), the structural consequences of monocular deprivation include the following changes: the relay cells in the binocular segments of the deprived geniculate layers shrink and contain less of the possible neurotransmitter NAAG. These changes appear to be secondary to a loss of terminal synaptic arbor. Certainly, deprived geniculocortical cells project to smaller ocular dominance patches in layer IV of visual cortex, where they make fewer and abnormal synapses. As a result, they activate ocular activation columns that, in addition to being small, are faint and usually fail to extend into extragranular layers. This failure to extend to other layers probably results from a failure of the poorly activated deprived-eye cells in layer IV to compete successfully with neighboring experienced-eye cells in layer IV, resulting in a loss of connections from layer IV to other layers (Fig. 11). Thus, the primary effect of monocular deprivation is probably the disruption of the geniculocortical synapse, with the other changes, such as cell size, and possibly the change in neurotransmitter content, being secondary. The disrupted synapse would result in poorly driven cortical cells and faint ocular activation columns, which in turn would bias a secondary competition for access to cells in extragranular layers. There are certain general principles that unite the findings presented in this chapter with the others in this session. First, there are similarities in the types of morphological changes observed, for example, changes in the number and size of synaptic terminals, as well as mitochondrial changes. This implies that there are similar changes during development and adult plasticity and also similar changes in vertebrates and invertebrates. Second, it is not so much the amount of activity that determines these changes, but the pattern of activity. In my results, the relative imbalance in activity is important, but not the absolute amount (for example, the columns activated by the 8-hr eye of an AME 8/1 are different from those activated by the 8-hr eye of an AME 8/8). Similarly, the binocular segment, where there was an imbalance and competition could occur, was affected, whereas the monocular segment, where there was no imbalance and competition could not occur, was not. Finally, the recent results of Reiter and Stryker suggest that monocular deprivation produces changes only when the activity of the presynaptic cell and the postsynaptic cell are correlated.(ABSTRACT TRUNCATED AT 400 WORDS)

Key concepts: Monocular deprivation, Ocular dominance column, Visual cortex, Neuroscience, Lateral geniculate nucleus, Geniculate, Synapse, Ocular dominance

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