Cell-adhesion molecules, glucocorticoids and long-term-memory formation.
The transition from short- to long-term memory requires lasting modulations of synaptic connectivity. In a variety of species and learning tasks, enhanced synthesis of glycoprotein cell-adhesion molecules (CAMs), such as neural CAM (NCAM) and Ll, 5-8 h post-training is a necessary step in this process. If the training event is weak, this phase of glycoprotein synthesis does not occur and memory is not retained. Antibodies or fragments that bind to the extracellular domains of NCAM or Ll at this time produce amnesia for the task. Centrally administered corticosterone enhances retention of weak learning, and steroid-receptor antagonists are amnestic. The effects of corticosterone are mediated through synthesis of 'second-wave' glycoproteins. As 'nootropic' drugs such as piracetam only enhance long-term retention and are ineffective in adrenalectomized animals, the interaction between glucocorticoids and glycoproteins might provide a site for pharmacological intervention in alleviating the losses of memory that occur in neurodegenerative disorders.[1]References
- Cell-adhesion molecules, glucocorticoids and long-term-memory formation. Rose, S.P. Trends Neurosci. (1995) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg