Neuroethology of olfactory preference development

Leon, Michael

doi:10.1002/neu.480231012

Cited by 71 publications

(44 citation statements)

References 102 publications

(99 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our findings are consistent, however, with previous studies that suggest that olfactory learning occurs in utero when odorants are injected into amniotic fluid (31,32). Interestingly, we detected BL immunoreactivity in the locus coeruleus at E17.5, suggesting that noradrenergic inputs from this area to the MOB, which are required for olfactory learning postnatally (33), are also present prenatally.…”

Section: Discussionsupporting

confidence: 92%

A genetic approach to trace neural circuits

Horowitz

Montmayeur²,

Echelard³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Mammalian nervous system function involves billions of neurons which are interconnected in a multitude of neural circuits. Here we describe a genetic approach to chart neural circuits. By using an olfactoryspecific promoter, we selectively expressed barley lectin in sensory neurons in the olfactory epithelium and vomeronasal organ of transgenic mice. The lectin was transported through the axons of those neurons to the olfactory bulb, transferred to the bulb neurons with which they synapse, and transported through the axons of bulb neurons to the olfactory cortex. The lectin also was retrogradely transported from the bulb to neuromodulatory brain areas. No evidence could be obtained for adverse effects of the lectin on odorant receptor gene expression, sensory axon targeting in the bulb, or the generation or transmission of signals by olfactory sensory neurons. Transneuronal transfer was detected prenatally in the odorsensing pathway, but only postnatally in the pheromonesensing pathway, suggesting that odors, but not pheromones, may be sensed in utero. Our studies demonstrate that a plant lectin can serve as a transneuronal tracer when its expression is genetically targeted to a subset of neurons. This technology can potentially be applied to a variety of vertebrate and invertebrate neural systems and may be particularly valuable for mapping connections formed by small subsets of neurons and for studying the development of connectivity as it occurs in utero.

show abstract

Section: Discussionsupporting

confidence: 92%

A genetic approach to trace neural circuits

Horowitz

Montmayeur²,

Echelard³

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…This paradoxical learning presumably occurs because pups must learn the maternal odor, which is then used to approach the mother and nipple attach (Hofer et al 1976;Pedersen et al 1982;Leon 1992;Polan and Hofer 1999). Therefore, pups' survival is dependent on odorapproach learning, suggesting that evolutionary pressure may have selected for a neural circuit to ensure pups only learn to approach their caregiver, regardless of the quality of care received (Bowlby 1965;Hofer and Sullivan 2001).…”

Section: Ecological Significancementioning

confidence: 99%

Ontogeny of odor-LiCl vs. odor-shock learning: Similar behaviors but divergent ages of functional amygdala emergence

Raineki¹,

Shionoya²,

Sander³

et al. 2009

Learn. Mem.

View full text Add to dashboard Cite

Both odor-preference and odor-aversion learning occur in perinatal pups before the maturation of brain structures that support this learning in adults. To characterize the development of odor learning, we compared three learning paradigms: (1) odor-LiCl (0.3M; 1% body weight, ip) and (2) odor-1.2-mA shock (hindlimb, 1sec)-both of which consistently produce odor-aversion learning throughout life and (3) odor-0.5-mA shock, which produces an odor preference in early life but an odor avoidance as pups mature. Pups were trained at postnatal day (PN) 7-8, 12-13, or 23-24, using odor-LiCl and two odor-shock conditioning paradigms of odor-0.5-mA shock and odor-1.2-mA shock. Here we show that in the youngest pups (PN7-8), odor-preference learning was associated with activity in the anterior piriform (olfactory) cortex, while odor-aversion learning was associated with activity in the posterior piriform cortex. At PN12-13, when all conditioning paradigms produced an odor aversion, the odor-0.5-mA shock, odor-1.2-mA shock, and odor-LiCl all continued producing learning-associated changes in the posterior piriform cortex. However, only odor-0.5-mA shock induced learning-associated changes within the basolateral amygdala. At weaning (PN23-24), all learning paradigms produced learning-associated changes in the posterior piriform cortex and basolateral amygdala complex. These results suggest at least two basic principles of the development of the neurobiology of learning: (1) Learning that appears similar throughout development can be supported by neural systems showing very robust developmental changes, and (2) the emergence of amygdala function depends on the learning protocol and reinforcement condition being assessed.Even in utero, infant rats rapidly learn to avoid odors paired with malaise (LiCl) as expressed by learning an odor aversion (Garcia et al. 1966(Garcia et al. , 1974Hennessey et al. 1976;Haroutunian and Campbell 1979;Smotherman 1982;Stickrod et al. 1982;Rudy and Cheatle 1983;Kucharski and Spear 1984;Smotherman and Robinson 1985, 1990;Alleva and Calamandrei 1986;Miller et al. 1990b; Best 1992, 1993;Richardson and McNally 2003;Gruest et al. 2004;Shionoya et al. 2006). In contrast to adult odor-LiCl learning, which relies on the amygdala (Touzani and Sclafani 2005), this early-life, odoraversion learning relies on the olfactory bulb until the pup approaches weaning age, when the amygdala is incorporated into the learning circuitry (Shionoya et al. 2006). In contrast, if infant rats receive an odor paired with a moderately painful stimulus (0.5-mA foot or tail shock, or tail pinch) the amygdala appears to be incorporated into this learning circuitry around postnatal day Here we expand assessment of the developing pups' odoraversion learning circuit by including the anterior and posterior piriform cortex, which have previously been demonstrated to be important for both pup and adult odor learning (Litaudon et al. 1997;Barkai and Saar 2001;Mouly et al. 2001;Mouly and Gervais 2002;Tronel and Sara 2002;Moriceau and Su...

show abstract

“…The second study focused on the likelihood that ethanol odor processing in utero can be associated with behaviorally activating tactile stimulation occurring soon after birth. The latter US mimics a portion of the maternal stimulation routinely experienced by newborn rats and also can promote olfactory preference learning in newborn rats (97,99,(166)(167)(168). When paired with tactile activation in the second study (99), prenatal exposure to ethanol odor facilitated subsequent neonatal learning comprising temporally contiguous presentations of ethanol odor and tactile stimulation.…”

Section: Interactions Between Prenatal and Postnatal Experiences Withmentioning

confidence: 99%

Fetal Learning About Ethanol and Later Ethanol Responsiveness: Evidence Against “Safe” Amounts of Prenatal Exposure

Abate

Pueta

Spear

et al. 2008

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Near-term fetuses of different mammalian species, including humans, exhibit functional sensory and learning capabilities. The neurobiological literature indicates that the unborn organism processes sensory stimuli present in the amniotic fluid, retains this information for considerable amounts of time, and is also capable of associating such stimuli with biologically relevant events. This research has stimulated studies aimed at the analysis of fetal and neonatal learning about ethanol, a topic that constitutes the core of the present review. Ethanol has characteristic sensory (olfactory, taste, and trigeminal) attributes and can exert pharmacologic reinforcing effects. The studies under examination support the hypothesis that low to moderate levels of maternal ethanol intoxication during late pregnancy set the opportunity for fetal learning about ethanol. These levels of prenatal ethanol exposure do not generate evident morphologic or neurobehavioral alterations in the offspring, but they exert a significant impact upon later ethanol-seeking and intake behaviors. Supported by preclinical and clinical findings, this review contributes to strengthening the case for the ability of prenatal ethanol exposure to have effects on the postnatal organism. Keywords ethanol; fetal learning; associative conditioningThis review analyzes the impact of low to moderate prenatal levels of exposure to ethanol on later responding to ethanol and stimuli associated with ethanol. These levels of ethanol exposure might be viewed as "safe" but nevertheless have negative effects that might not be noticed for many years.We previously reviewed the literature, examining possible associations between early ontogenetic experiences with alcohol and subsequent affinity for ethanol ingestion and sensitivity to its reinforcing effects (postabsorptive consequences that increase behaviors aimed at obtaining ethanol or that generate preferences to stimuli signaling such consequences) (1). This review took into account fetal and infantile experiences involving acute or chronic exposure to ethanol and how they exerted significant effects upon subsequent ethanol 1To whom correspondence should be addressed at Instituto Ferreyra,

show abstract

Neuroethology of olfactory preference development

Cited by 71 publications

References 102 publications

A genetic approach to trace neural circuits

A genetic approach to trace neural circuits

Ontogeny of odor-LiCl vs. odor-shock learning: Similar behaviors but divergent ages of functional amygdala emergence

Fetal Learning About Ethanol and Later Ethanol Responsiveness: Evidence Against “Safe” Amounts of Prenatal Exposure

Contact Info

Product

Resources

About