Skip to main content Accessibility help
×
Hostname: page-component-5db58dd55d-htx7c Total loading time: 0 Render date: 2026-05-26T22:47:25.918Z Has data issue: false hasContentIssue false

11 - Programmed cell death

Published online by Cambridge University Press:  22 August 2009

Rafael Linden
Affiliation:
Instituto de BiofÍsica da UFRJ, CCS, bloco G, Cidade Universitaria, 21949-900, Rio de Janeiro, Brazil
Benjamin E. Reese
Affiliation:
Neuroscience Research Institute and Department of Psychology, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA
Evelyne Sernagor
Affiliation:
University of Newcastle upon Tyne
Stephen Eglen
Affiliation:
University of Cambridge
Bill Harris
Affiliation:
University of Cambridge
Rachel Wong
Affiliation:
Washington University, St Louis
Get access

Summary

Introduction

Interest in programmed cell death (PCD) emerged over a century ago (reviewed in Clarke and Clarke, 1996), and such naturally occurring cell death in the developing nervous system has been extensively documented (Oppenheim, 1991 for review). More recently, the concept of PCD has been the subject of some controversy mainly due to the overwhelming interest in one of its forms, apoptosis (Sloviter, 2002). For the purpose of this chapter, PCD is defined simply as a sequence of events based on cellular metabolism that leads to cell destruction (Lockshin and Zakeri, 2001; Guimarães and Linden, 2004), without commitment to particular morphological types.

Programmed cell death has been identified using a variety of techniques, though each of them is prone to errors when estimating the magnitude of cell loss. Estimating the size of the population based on counts of axons in developing nerves or tracts may be confounded by the simultaneous occurrence of both cell death and axonal ingrowth, and by the transient contaminating presence of other axonal populations. Estimates based on cell counts may be influenced by the continuous migration of differentiating cells into spatially delimited cell populations, as well as by the inclusion of other types of cells that are not so readily discriminable at earlier developmental stages. And while great progress has been made in understanding the molecular mechanisms of apoptosis in the last decade, multiple alternative pathways of PCD add a further degree of complexity in understanding developmental cell death and estimating its magnitude.

Information

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

Book purchase

Temporarily unavailable

Save book to Kindle

To save this book to your Kindle, first ensure no-reply@cambridge.org is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

  • Programmed cell death
    • By Rafael Linden, Instituto de BiofÍsica da UFRJ, CCS, bloco G, Cidade Universitaria, 21949-900, Rio de Janeiro, Brazil, Benjamin E. Reese, Neuroscience Research Institute and Department of Psychology, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA
  • Edited by Evelyne Sernagor, University of Newcastle upon Tyne, Stephen Eglen, University of Cambridge, Bill Harris, University of Cambridge, Rachel Wong, Washington University, St Louis
  • Book: Retinal Development
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541629.013
Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

  • Programmed cell death
    • By Rafael Linden, Instituto de BiofÍsica da UFRJ, CCS, bloco G, Cidade Universitaria, 21949-900, Rio de Janeiro, Brazil, Benjamin E. Reese, Neuroscience Research Institute and Department of Psychology, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA
  • Edited by Evelyne Sernagor, University of Newcastle upon Tyne, Stephen Eglen, University of Cambridge, Bill Harris, University of Cambridge, Rachel Wong, Washington University, St Louis
  • Book: Retinal Development
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541629.013
Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

  • Programmed cell death
    • By Rafael Linden, Instituto de BiofÍsica da UFRJ, CCS, bloco G, Cidade Universitaria, 21949-900, Rio de Janeiro, Brazil, Benjamin E. Reese, Neuroscience Research Institute and Department of Psychology, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA
  • Edited by Evelyne Sernagor, University of Newcastle upon Tyne, Stephen Eglen, University of Cambridge, Bill Harris, University of Cambridge, Rachel Wong, Washington University, St Louis
  • Book: Retinal Development
  • Online publication: 22 August 2009
  • Chapter DOI: https://doi.org/10.1017/CBO9780511541629.013
Available formats
×