Format

Send to

Choose Destination
Sci Rep. 2018 Oct 2;8(1):14679. doi: 10.1038/s41598-018-32762-y.

Developmental transitions in amygdala PKC isoforms and AMPA receptor expression associated with threat memory in infant rats.

Author information

1
Emotional Brain Institute, Nathan Kline Institute, Orangeburg, 10962, USA. maya.opendak@nyulangone.org.
2
Child Study Center, Child & Adolescent Psychiatry, New York University School of Medicine, New York, 10016, USA. maya.opendak@nyulangone.org.
3
Department of Psychology, CUNY Hunter College, New York, 10016, USA.
4
The Graduate Center of CUNY, New York, 10016, USA.
5
Child Study Center, Child & Adolescent Psychiatry, New York University School of Medicine, New York, 10016, USA.
6
Emotional Brain Institute, Nathan Kline Institute, Orangeburg, 10962, USA.

Abstract

Although infants learn and remember, they rapidly forget, a phenomenon known as infantile amnesia. While myriad mechanisms impact this rapid forgetting, the molecular events supporting memory maintenance have yet to be explored. To explore memory mechanisms across development, we used amygdala-dependent odor-shock conditioning and focused on mechanisms important in adult memory, the AMPA receptor subunits GluA1/2 and upstream protein kinases important for trafficking AMPAR, protein kinase M zeta (PKMζ) and iota/lambda (PKCι/λ). We use odor-shock conditioning in infant rats because it is late-developing (postnatal day, PN10) and can be modulated by corticosterone during a sensitive period in early life. Our results show that memory-related molecules did not change in pups too young to learn threat (PN8) but were activated in pups old enough to learn (PN12), with increased PKMζ-PKCι/λ and GluA2 similar to that observed in adult memory, but with an uncharacteristic decrease in GluA1. This molecular signature and behavioral avoidance of the conditioned odor was recapitulated in PN8 pups injected with CORT before conditioning to precociously induce learning. Blocking learning via CORT inhibition in older pups (PN12) blocked the expression of these molecules. PN16 pups showed a more adult-like molecular cascade of increased PKMζ-PKCι/λ and GluA1-2. Finally, at all ages, zeta inhibitory peptide (ZIP) infusions into the amygdala 24 hr after conditioning blocked memory. Together, these results identify unique features of memory processes across early development: AMPAR subunits GluA1/2 and PKC isoform expression are differentially used, which may contribute to mechanisms of early life forgetting.

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central Icon for NYU School of Medicine
Loading ...
Support Center