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5. Global transcriptomic profile of dorsal root ganglion and physiological correlates of cisplatin-induced peripheral neuropathy

Author

Lessans, S, Lassiter, C, Carozzi, V, Heindel, P, Semperboni, S, Oggioni, N, Chiorazzi, A, Thompson, C, Wagner, M, Holden, J, Rahn, E, David Sweatt, J, Cavaletti, G, Renn, C, Dorsey, S, Lessans, Sherrie, Lassiter, Cameron B, Carozzi, Valentina, Heindel, Patrick, Semperboni, Sara, Oggioni, Norberto, Chiorazzi, Alessia, Thompson, Carleveva, Wagner, Monica, Holden, Janean, Rahn, Elizabeth, Cavaletti, Guido, Renn, Cynthia L, Dorsey, Susan G, Lessans, S, Lassiter, C, Carozzi, V, Heindel, P, Semperboni, S, Oggioni, N, Chiorazzi, A, Thompson, C, Wagner, M, Holden, J, Rahn, E, David Sweatt, J, Cavaletti, G, Renn, C, Dorsey, S, Lessans, Sherrie, Lassiter, Cameron B, Carozzi, Valentina, Heindel, Patrick, Semperboni, Sara, Oggioni, Norberto, Chiorazzi, Alessia, Thompson, Carleveva, Wagner, Monica, Holden, Janean, Rahn, Elizabeth, Cavaletti, Guido, Renn, Cynthia L, and Dorsey, Susan G

Abstract

Background Multiple cell signaling pathways are implicated in the development, progression, and persistence of cisplatin-induced peripheral neuropathy. Although advances have been made in terms of understanding specific neurotoxic mechanisms, there are few predictive factors identified that can help inform the clinician approach to symptom prevention or management. Objective We investigate the differential sensitivity to cisplatin-induced peripheral neuropathy and examine the contribution of dorsal root ganglion (DRG) transcriptional profiles across two inbred strains of mice. Methods Cisplatin (4 mg/kg intraperitoneal or vehicle control) was administered twice a week for 4 weeks to adult female C57BL/6J and A/J mice - the C57BL/6J strain of mice characterized by a robust mechanical allodynia and the A/J with a mild largely resistant allodynia phenotype. Peripheral nerve conduction velocities (NCVs), electrophysiological evaluation of wide dynamic range (WDR) neurons, morphological examination of DRG neurons, and microarray analysis of spinal cord tissues were compared across the 4 weeks. Results The A/J strain presents with an early, mild nocifensive response to cisplatin with reduced neuronal activity in WDR neurons and small changes in cross-sectional nucleus size in DRG neurons at 4 weeks. The more nocifensive-sensitive C57BL/6J strain presents with no early changes in WDR neuron responsiveness; however, there were significant changes in DRG size. Both strains demonstrate a drop in NCV after 4 weeks of treatment, with the greatest reduction present in the A/J strain. Transcriptome data implicate neuroimmune modulation in the differential response to cisplatin in the DRGs of A/J and C57BL/6J mice. Discussion Nocifensive responses in both strains implicate involvement of small myelinated and unmyelinated fibers in neurotoxic cisplatin response, whereas reductions in NCV reflect involvement of the largest myelinated fibers in the peripheral nerves. Microarray data

Published
2019

8. Annual Research Review: Epigenetic mechanisms and environmental shaping of the brain during sensitive periods of development.

Author

Roth, Tania L. and David Sweatt, J.

Subjects
*CENTRAL nervous system physiology, *MENTAL illness genetics, *MENTAL illness risk factors, *ETIOLOGY of mental illnesses, *BRAIN, *CHILD abuse, *CHILD development, *DNA, *ECOLOGY, *GENE expression, *GENETICS, *GENOMES, *HIPPOCAMPUS (Brain), *INFANT development, *LIFE change events, *MOTHER-child relationship, *MOTHERHOOD, *NERVE growth factor, *PARENTING, *CHILDREN
Abstract

Experiences during early development profoundly affect development of the central nervous system (CNS) to impart either risk for or resilience to later psychopathology. Work in the developmental neuroscience field is providing compelling data that epigenetic marking of the genome may underlie aspects of this process. Experiments in rodents continue to show that experiences during sensitive periods of development influence DNA methylation patterns of several genes. These experience-induced DNA methylation patterns represent stable epigenetic modifications that alter gene transcription throughout the lifespan and promote specific behavioral outcomes. We discuss the relevance of these findings to humans, and also briefly discuss these findings in the broader contexts of cognition and psychiatric disorder. We conclude by discussing the implications of these observations for future research. [ABSTRACT FROM AUTHOR]

Published
2011
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10. Global Transcriptomic Profile of Dorsal Root Ganglion and Physiological Correlates of Cisplatin-Induced Peripheral Neuropathy

Author

Norberto Oggioni, S. Semperboni, Susan G. Dorsey, Carleveva Thompson, Cameron B Lassiter, Valentina Alda Carozzi, Guido Cavaletti, Janean E. Holden, Elizabeth J. Rahn, Monica A. Wagner, Patrick Heindel, Alessia Chiorazzi, Cynthia L. Renn, Sherrie Lessans, J. David Sweatt, Lessans, S, Lassiter, C, Carozzi, V, Heindel, P, Semperboni, S, Oggioni, N, Chiorazzi, A, Thompson, C, Wagner, M, Holden, J, Rahn, E, David Sweatt, J, Cavaletti, G, Renn, C, and Dorsey, S

Subjects
Microarray, Dorsal Root Ganglion, Cisplatin-Induced Peripheral Neuropathy, Cyclic Nucleotide-Gated Cation Channels, Antineoplastic Agents, Apoptosis, Receptors, Nerve Growth Factor, Pharmacology, Biology, 03 medical and health sciences, Mice, 0302 clinical medicine, Dorsal root ganglion, Inbred strain, Ganglia, Spinal, medicine, gene expression profiling, Premovement neuronal activity, Animals, 030212 general & internal medicine, CIPN, General Nursing, Cisplatin, cisplatin neuropathy, 030504 nursing, Peripheral Nervous System Diseases, medicine.disease, Spinal cord, Mice, Inbred C57BL, medicine.anatomical_structure, Peripheral neuropathy, Allodynia, Neuralgia, medicine.symptom, 0305 other medical science, microarray, medicine.drug
Abstract

Background Multiple cell signaling pathways are implicated in the development, progression, and persistence of cisplatin-induced peripheral neuropathy. Although advances have been made in terms of understanding specific neurotoxic mechanisms, there are few predictive factors identified that can help inform the clinician approach to symptom prevention or management. Objective We investigate the differential sensitivity to cisplatin-induced peripheral neuropathy and examine the contribution of dorsal root ganglion (DRG) transcriptional profiles across two inbred strains of mice. Methods Cisplatin (4 mg/kg intraperitoneal or vehicle control) was administered twice a week for 4 weeks to adult female C57BL/6J and A/J mice-the C57BL/6J strain of mice characterized by a robust mechanical allodynia and the A/J with a mild largely resistant allodynia phenotype. Peripheral nerve conduction velocities (NCVs), electrophysiological evaluation of wide dynamic range (WDR) neurons, morphological examination of DRG neurons, and microarray analysis of spinal cord tissues were compared across the 4 weeks. Results The A/J strain presents with an early, mild nocifensive response to cisplatin with reduced neuronal activity in WDR neurons and small changes in cross-sectional nucleus size in DRG neurons at 4 weeks. The more nocifensive-sensitive C57BL/6J strain presents with no early changes in WDR neuron responsiveness; however, there were significant changes in DRG size. Both strains demonstrate a drop in NCV after 4 weeks of treatment, with the greatest reduction present in the A/J strain. Transcriptome data implicate neuroimmune modulation in the differential response to cisplatin in the DRGs of A/J and C57BL/6J mice. Discussion Nocifensive responses in both strains implicate involvement of small myelinated and unmyelinated fibers in neurotoxic cisplatin response, whereas reductions in NCV reflect involvement of the largest myelinated fibers in the peripheral nerves. Microarray data analysis identifies neuropathy-relevant gene sets with differential activation of pathways, suggesting a role for antigen presentation in the differential neurotoxic response to cisplatin across strains. Further research is indicated to determine the relative contributions of each of these potential pathological mechanisms to both the neurotoxic response to cisplatin and to the potential for targeted therapy.

Published
2018

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