The organization of piriform cortex and the lateral olfactory tract following the loss of mitral cells in PCD mice

Homozygous Purkinje Cell Degeneration (PCD) mice exhibit a selective loss o f olfactory bulb mitral cells (MCs) after 4 months of age. This selective d egeneration leaves a subpopulation of denervated granule cells which establ ish new reciprocal dendro-dendritic synapses with unaffected tufted cells ( TCs) (14). This suggests a capacity for plasticity in TCs and raises the qu estion of whether a comparable degree of reorganization occurs in their axo nal terminals in piriform cortex (PC) following the loss of MCs. Homozygous (experimental) and heterozygous (control) PCD mice were routinely perfused and processed for electron microscopy. Aquantitative electron microscopic analysis was performed on radially oriented micrograph montages spanning fr om the pia into layer II of PC. After MC loss in the experimental animals t here was a decrease in density of larger myelinated axons in the lateral ol factory tract (LOT). Myelinated axons in the LOT had a mean cross-sectional diameter of 1.26 +/- 0.04, and 0.81 +/- 0.025 mu m in the control and expe rimental mice, respectively. In superficial layer I of PC, control mice had presynaptic axonal terminals from mitral and tufted cells with characteris tic electron lucent (light) profiles establishing asymmetric synapses with pyramidal cell dendrites. In contrast, the experimental mice showed a decre ase in electron lucent terminals and a robust increase in electron dense (d ark) presynaptic associational terminals. Although the overall synaptic den sity did not differ between the control and experimental mice (16.40 +/- 0. 94 and 18.10 +/- 0.96 synapses/100 mu m(2), respectively), an overall decre ase in the thickness of Layer 1 suggests that the total number of synapses decreases following MC loss. In addition to the apparent increase of associ ational terminals, the diameter of terminal enlargements increased as well as the number of multiple synaptic contact per terminals in the experimenta l animal, suggesting further compensatory mechanisms for the loss of MC pre synaptic terminals. (C) 1998 Academic Press.