Table 1. Selection of representative applications of DRG cultures for the study of peripheral neuropathies.

NRTI: Nucleoside reverse transcriptase inhibitors; RANTES: regulated upon activation normal T-cell expressed and secreted; rc: receptor; JNK: c-Jun N-terminal kinase; STZ: streptozotocin, SC: Schwann cells, ROS: reactive oxygen species; NO: nitric oxide

	Cell culture model	Major findings	References
HIV-related neuropathies
Anti-retroviral toxic neuropathy (ATN)	Rat E15 dissociated DRG neurons	NRTIs cause direct mitochondrial damage leading to axonal damage and non-apoptotic cell death.	Keswani et al., 2003[5]
Distal symmetric polyneuropathy (DSP)	Rat E15 dissociated DRG neurons	Gp120 induces RANTES in Schwann cells through CXCR4. RANTES induce TNF-α in neurons through CCR5 causing neuronal apoptosis.	Keswani et al, 2003[19]
ATN and DSP	Rat Post-natal dissociated DRG neurons	NRTIs and gp120 cause neuronal apoptosis through JNK pathway and inhibitors of the mixed lineage kinases prevents it.	Bodner et al., 2004[22]
DSP	Rat E15 dissociated DRG neurons in Campenot chambers	Gp120 causes neuronal apoptosis mediated by Schwann cells when applied to cell bodies and causes local axonal damage through caspases activation.	Melli et al., 2006[10]
Diabetic neuropathies
Diabetic neuropathy	Adult STZ treated mice dissociated DRG neurons	Improvement of neuronal survival and neurite growth from diabetic mice when exposed to insulin or high glucose	Sotelo et al., 1991[37]
Diabetic neuropathy	Rat E15 dissociated DRG neurons	High glucose induces ROS production, mitochondrial damage and apoptosis.	Russell et al., 2002[49]
Diabetic neuropathy	Adult STZ treated rat dissociated DRG neurons	Loss of insulin-dependent neurotrophic support contributes to mitochondrial membrane depolarization induced by diabetes.	Huang et al., 2003 [46]
Diabetic neuropathy	Rat E15 dissociated DRG neurons + rat Schwann cells/myelination	Myelinated SC/DRG cocultures provide a physiologically relevant model for studying demyelination observed in diabetic nerves in vivo.	Yu et al, 2008 [13]
Diabetic neuropathy	Rat sciatic nerve derived SC and adult mice DRG explants and dissociated cells	High glucose impairs proliferation and migration of Schwann cells, higher glucose impairs neurite elongation, no substantial apoptosis has been detected.	Gumy et al., 2008[56]
Diabetic neuropathy	Normal or 3-5 month STZ rats dissociated DRG neurons	Diabetic DRG neurons express low MnSOD and high ROS in axons, associated with impaired axonal outgrowth and aberrant dystrophic structures.	Zherebitskaya et al, 2009[58]
Chemoterapy-associated neuropathies
Paclitaxel associated neuropathy	Rat E15 dissociated DRG neurons	rhEPO prevents axonal degeneration in sensory neurons and is associated with downregulation of detyrosinated tubulin, further confirmed in the animal model.	Melli et al., 2006[6]
Paclitaxel and cisplatin associated neuropathies	Rat E15 dissociated DRG neurons	Alpha-lipoic acid protects sensory neurons through its anti-oxidant and mitochondrial regulatory functions, and induces the expression of frataxin.	Melli et al., 2008[7]
Demyelinating neuropathies
CMT1A	Transgenic PMP22 rat E15 dissociated neurons/myelination	Reproduction in vitro of dysmyelinated internodes and focal myelin swellings, pathological hallmarks of CMT1A.	Nobbio et al., 2001[63]
CMTIA	Transgenic PMP22 rat E15 dissociated neurons/myelination	Molecular and morphological signs of axonal damage following persistent demyelination.	Nobbio et al., 2006[65]
Inflammatory neuropathies	Rat E15 dissociated DRG neurons/myelination	NO causes demyelination secondary to axonal injury, no damage to Schwann cells viability.	Lehmann et al., 2007[66]