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Postnatal phenotype and localization of spinal cord V1 derived interneurons

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Alvarez, Francisco J., Jonas, Philip C., Sapir, Tamar, Hartley, Robert, Berrocal, Maria C., Geiman, Eric J., Todd, Andrew J., Goulding, Martyn·2005·Journal of Comparative Neurology
DOI 10.1002/cne.20711PMC PMC2997483
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Abstract

Developmental studies identified four classes (V0, V1, V2, V3) of embryonic interneurons in the ventral spinal cord. Very little is known, however, about their adult phenotypes. Therefore, we characterized the location, neurotransmitter phenotype, calcium‐buffering protein expression, and axon distributions of V1‐derived neurons in the adult mouse spinal cord. In the mature (P20 and older) spinal cord, most V1‐derived neurons are located in lateral LVII and in LIX, few in medial LVII, and none in LVIII. Approximately 40% express calbindin and/or parvalbumin, while few express calretinin. Of seven groups of ventral interneurons identified according to calcium‐buffering protein expression, two groups (1 and 4) correspond with V1‐derived neurons. Group 1 are Renshaw cells and intensely express calbindin and coexpress parvalbumin and calretinin. They represent 9% of the V1 population. Group 4 express only parvalbumin and represent 27% of V1‐derived neurons. V1‐derived Group 4 neurons receive contacts from primary sensory afferents and are therefore proprioceptive interneurons. The most ventral neurons in this group receive convergent calbindin‐IR Renshaw cell inputs. This subgroup resembles Ia inhibitory interneurons (IaINs) and represents 13% of V1‐derived neurons. Adult V1‐interneuron axons target LIX and LVII and some enter the deep dorsal horn. V1 axons do not cross the midline. V1‐derived axonal varicosities were mostly (>80%) glycinergic and a third were GABAergic. None were glutamatergic or cholinergic. In summary, V1 interneurons develop into ipsilaterally projecting, inhibitory interneurons that include Renshaw cells, Ia inhibitory interneurons, and other unidentified proprioceptive interneurons. J. Comp. Neurol. 493:177–192, 2005. © 2005 Wiley‐Liss, Inc.

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  • Inhib-23 was identified by expression of Gm26673 and Pvalb, which may suggest that this cluster included Ia-inhibitory neurons.

    “They were identified by expression of Gm26673 and Pvalb in Inhib-23, which may suggest that this cluster included Ia-inhibitory neurons89.”

    From A harmonized atlas of mouse spinal cord cell types and their spatial organization (2021) · cites this paper as [89]

  • Inhib-26 was the most robust ventral cluster and expressed the Renshaw marker genes Chrna2, Chrna7, and Calb1, suggesting it corresponded to Renshaw cells.

    “Inhib-26 was the most robust ventral cluster and expressed the Renshaw marker genes Chrna2, Chrna7, and Calb1, suggesting that this cluster corresponded to Renshaw cells89,90.”

    From A harmonized atlas of mouse spinal cord cell types and their spatial organization (2021) · cites this paper as [89]

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Research works printed but not linked: 4

  1. Alvarez FJ, Dewey DE, Harrington DA, Fyffe RE. Cell-type specific organization of glycine receptor clusters in the mammalian spinal cord. J Comp Neurol. 1997;379:150–170. [PubMed] [Google Scholar]
  2. Alvarez FJ, Jonas P, Sapir T, Geiman EJ, Hartley R, Todd AJ, Goulding M. Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience; 2003. Postnatal phenotype and localization of spinal cord V1 derived interneurons. Program No. 39.3. Online. [Google Scholar]
  3. Pillai AM, Wang Z, Arber S, Brandon E, Gage R, Jessell T, Alvarez F, Frank E, Goulding M. Abstract Viewer/Itinerary Planner. Washington, DC: Society for Neuroscience; 2003. Specification and early development of Renshaw cells. Program No. 39.9. 2003. Online. [Google Scholar]
  4. Philpot BD, Lim JH, Brunjes PC. Activity-dependent regulation of calcium-binding proteins in the developing rat olfactory bulb. J Comp Neurol. 1997;387:12–26. [PubMed] [Google Scholar]

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Authors
Alvarez, F. J., Jonas, P. C., Sapir, T., Hartley, R., Berrocal, M. C., Geiman, E. J., Todd, A. J., & Goulding, M.
Affiliations
  • Wright State University (US)
  • Salk Institute for Biological Studies (US)
  • University of Glasgow (GB)
ORCID
Venue
Journal of Comparative Neurology
Publisher
Wiley
Published
2005-10-27
Volume
493
Issue
2
Pages
177-192
ISSN
  • 0021-9967 (ISSN-L)
  • 1096-9861
DOI
10.1002/cne.20711
PMC
PMC2997483
OpenAlex
W2075444384
Cited by
243
References
72
Citations by year
2026: 6 · 2025: 10 · 2024: 15 · 2023: 15 · 2022: 13 · 2021: 16 · 2020: 6 · 2019: 13 · 2018: 10 · 2017: 8 · 2016: 11 · 2015: 13 · 2014: 5 · 2013: 11 · 2012: 15
FWCI
3.14
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • The Journal of Comparative Neurology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • Journal of Bioresource Management (submittedVersion)
Funders
National Institute of Neurological Disorders and Stroke (NS047357, R56NS047357, R01NS047357)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
Keywords
Renshaw cells, calbindin, parvalbumin, calretinin, calcium-binding proteins, axonal projections, interneuron classification
MeSH terms
Animals, Anterior Horn Cells, Cell Count, Cell Differentiation, Cell Movement, Interneurons, Mice, Transgenic, Motor Neurons, Parvalbumins, Spinal Cord, Mice, Calbindins, S100 Calcium Binding Protein G, Calbindin 2

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