The neurobiology of infant maternal odor learning

Infant rats must learn to identify their mother’s diet-dependent odor. Once learned, maternal odor controls pups’ approach to the mother, their social behavior and nipple attachment. Here we present a review of the research from four different laboratories, which suggests that neural and behavioral responses to the natural maternal odor and neonatal learned odors are similar. Together, these data indicate that pups have a unique learning circuit relying on the olfactory bulb for neural plasticity and on the hyperfunctioning noradrenergic locus coeruleus flooding the olfactory bulb with norepinephrine to support the neural changes. Another important factor making this system unique is the inability of the amygdala to become incorporated into the infant learning circuit. Thus, infant rats appear to be primed in early life to learn odors that will evoke approach responses supporting attachment to the caregiver.

The neurobiology of infant maternal odor learning.

Infant rats must learn to identify their mother's diet-dependent odor. Once learned, maternal odor controls pups' approach to the mother, their social behavior and nipple attachment. Here we present a review of the research from four different laboratories, which suggests that neural and behavioral responses to the natural maternal odor and neonatal learned odors are similar. Together, these data indicate that pups have a unique learning circuit relying on the olfactory bulb for neural plasticity and on the hyperfunctioning noradrenergic locus coeruleus flooding the olfactory bulb with norepinephrine to support the neural changes. Another important factor making this system unique is the inability of the amygdala to become incorporated into the infant learning circuit. Thus, infant rats appear to be primed in early life to learn odors that will evoke approach responses supporting attachment to the caregiver.

Lateral olfactory tract input to dentate gyrus is depressed by prior noradrenergic activation using nucleus paragigantocellularis stimulation.

Nucleus paragigantocellularis stimulation potentiates the medial perforant path population spike in the dentate gyrus via beta-receptor activation. In this study, the same paragigantocellularis stimulation preceding lateral olfactory tract pulses depressed the lateral perforant path mediated synaptic potential in dentate gyrus. Depression of the lateral olfactory tract input was blocked by a beta-antagonist. These in vivo results confirm in vitro reports that norepinephrine induces potentiation of medial perforant path input and depression of lateral perforant path input to dentate gyrus.

Paragigantocellularis stimulation induces beta-adrenergic hippocampal potentiation.

The nucleus paragigantocellularis (PGi) is the major excitatory glutamatergic input to the locus coeruleus (LC). Glutamate activation of the LC has previously been shown to produce beta-adrenergic-dependent potentiation of the perforant path- (PP) evoked population spike in the dentate gyrus (DG). The present study asks if electrical stimulation of the PGi, by activating the LC endogenously, can produce a parallel beta-receptor-dependent potentiation of the PP-evoked population spike. An optimal interstimulus interval (ISI) was determined for PGi-PP stimulation in urethane-anesthetized rats and propranolol was used to assess the role of noradrenergic beta-receptors. PGi stimulation potentiated the PP-evoked population spike at an optimal ISI of 30 ms. The population synaptic response slope and spike latency were not affected. Propranolol blocked the PGi-induced potentiation, as would be expected for beta-receptor-dependent modulation. The parallels between PGi- and LC-induced effects on the PP-evoked population spike suggest PGi stimulation offers an alternate method of LC activation for studies of LC's role in behavior.