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Unique neural circuitry for neonatal olfactory learning.

Stephanie Moriceau1, Regina M Sullivan

  • 1Department of Zoology, University of Oklahoma, Norman, Oklahoma 73019, USA. smoriceau@ou.edu

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|February 6, 2004
PubMed
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Maternal imprinting in rats relies on norepinephrine (NE) release, which declines after postnatal day 10. This study reveals that changes in locus ceruleus (LC) autoreceptors, not olfactory bulb changes, cause this sensitive period to end.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Behavioral Science

Background:

  • Caregiver attachment is crucial for altricial species survival, with imprinting facilitating this bond.
  • Neonatal rats exhibit rapid odor-based maternal attachment, dependent on norepinephrine (NE) release from the locus ceruleus (LC) into the olfactory bulb.
  • This sensitive period for imprinting concludes around postnatal day 10 (P10), marked by reduced NE release.

Purpose of the Study:

  • To investigate if functional changes in LC alpha2 inhibitory and alpha1 excitatory autoreceptors cause the reduction in NE release that terminates the imprinting sensitive period.
  • To determine if alterations in LC autoreceptor activity underlie the termination of neonatal olfactory imprinting.

Main Methods:

  • Post-sensitive period rat pups (P12) received LC or olfactory bulb cannulas for classical conditioning (P14) involving intracranial drug infusions.

Related Experiment Videos

  • Conditioning paired a novel odor with either olfactory bulb infusion of isoproterenol (to mimic NE effects) or direct LC cholinergic stimulation.
  • LC stimulation involved alpha2 antagonists and alpha1 agonists to reinstate neonatal LC autoreceptor activity, assessing NE release source.

    • Main Results:

    • Pups successfully learned an odor preference when the odor was paired with olfactory bulb isoproterenol infusion.
    • Odor preference was also learned when neonatal LC autoreceptor activity was reinstated via direct LC stimulation.
    • These findings indicate that the termination of the imprinting sensitive period is linked to LC autoreceptor function.

    Conclusions:

    • Functional changes in LC autoreceptors, specifically the emergence of alpha2 inhibition and downregulation of alpha1 excitation, are responsible for the decline in NE release.
    • These autoreceptor modifications, rather than changes within the olfactory bulb, underlie the termination of the sensitive period for olfactory imprinting.