Is the brain hormonally imprintable?

Research output: Contribution to journalArticle

24 Citations (Scopus)

Abstract

Hormonal imprinting develops at the first encounter between the target hormone and its developing receptor in the perinatal critical period. This determines the binding and response capacity of the receptor-signal transduction system and hormone production of cells for life. Molecules similar to the hormone and excess or absence of the target hormone cause faulty imprinting with lifelong consequences. Prenatal or neonatal imprinting with opiates, other drugs and prenatal stress have harmful consequences on the adult brain. Perinatal imprinting with endorphin or serotonin decreases the serotonin level of the brain while increasing sexual activity and (as in the case of endorphin) aggression. Endorphin or serotonin antagonist treatment at weaning (late imprinting) also significantly reduces the serotonin content of the brain. Backed by literary data, these observations are discussed, and the possible consequences of medical treatments are shown. The paper concludes that an excess of molecules produced by the brain itself can provoke perinatal imprinting, and it points to the possibility of late imprinting of the brain by receptor level acting agents, including a brain product (endorphin).

Original languageEnglish
Pages (from-to)465-471
Number of pages7
JournalBrain and Development
Volume27
Issue number7
DOIs
Publication statusPublished - Oct 2005

Fingerprint

Endorphins
Brain
Hormones
Serotonin
Opiate Alkaloids
Serotonin Antagonists
Imprinting (Psychology)
Weaning
Aggression
Sexual Behavior
Signal Transduction
Pharmaceutical Preparations

Keywords

  • Drugs
  • Endorphin
  • Hormonal imprinting
  • Late imprinting
  • Perinatal imprinting
  • Serotonin

ASJC Scopus subject areas

  • Clinical Neurology
  • Pediatrics, Perinatology, and Child Health
  • Neurology

Cite this

Is the brain hormonally imprintable? / Csaba, G.; Tekes, K.

In: Brain and Development, Vol. 27, No. 7, 10.2005, p. 465-471.

Research output: Contribution to journalArticle

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