New antidepressant drugs that do not cross the blood-brain barrier

Med Hypotheses. 2002 Jan;58(1):83-4. doi: 10.1054/mehy.2001.1462.

Abstract

Stimulation of neurogenesis in the adult brain (i.e. in the hippocampus) has recently been proposed as a putative mechanism of antidepressant action of drugs. This effect of antidepressants may not be achieved by their primary action on proliferating cells, but may involve the drug-triggered mobilization of trophic factors, such as brain-derived neurotrophic factor (BDNF), glia-derived protein S100 beta, or insulin-like growth factor I (IFG-I). Whereas BDNF and S100 beta are produced in the brain, IGF-I is primarily released from peripheral tissues. Administered peripherally, IGF-I increases hippocampal neurogenesis in the adult rat. Because synthesis and release of IGF-I appear to be stimulated by serotonergic mechanisms, we propose that antidepressants that affect serotonergic mechanisms might be rendered more effective by mobilizing IGF-I. Moreover, we suggest that new antidepressant drugs could be designed that would not enter into the brain but would stimulate peripheral mediators such as IGF-I.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antidepressive Agents / pharmacokinetics*
  • Blood-Brain Barrier
  • Brain-Derived Neurotrophic Factor / metabolism
  • Insulin-Like Growth Factor I / metabolism
  • Rats

Substances

  • Antidepressive Agents
  • Brain-Derived Neurotrophic Factor
  • Insulin-Like Growth Factor I