The role of autophagy in Parkinson's disease: rotenone-based modeling

Table 1 Rotenone-induced ultrastructural changes in SNc (semi-quantification)

	Normal	Mitochondrial swelling	Mitochondrial crest fracture	Mitochondrial vacuolar degeneration	Dilated and broken rough endoplasmic reticula	Lipofuscin deposition	Perinular space augmentation	increase of autophagic vacuoles/lysosomes	Degeneration of medullary sheathes
Contralateral SNc (Figure 6A)	Mitochondrial complex ribosomes, medullary sheathes
One day after surgery (Figure 6B)		+	+	+	+			+
Two day after surgery (6C)		++	++	++	++			++
One week after surgery (Figure6E)		+++	+++	+++		++
Two weeks after surgery (6F)		+++	+++	+++		++
Four weeks after surgery (Figure 6G,H)		+++	+++	+++	++		++	+	++

Rotenone-administrated animals were sacrificed 1 day, 2 days, 1 week, 2 weeks or 4 weeks after the stereological surgery. A 1-mm3 tissue block from the ipsilateral and contralateral SNc regions (−4.5 to −6.2 mm caudal to the bregma) was micro-punched for TEM assessment. “+”, frequency of rotenone-induced ultrastructural changes in SNc, including mitochondrial swelling, mitochondrial crest fracture, mitochondrial vacuolar degeneration, dilated and broken rough endoplasmic reticula, lipofuscin deposition, perinuclear space augmentation and increase in autophagic vacuoles.

ISSN: 1744-9081