Paradoxical effects of ketamine on the memory of fetuses of different ages

Mickley, G. Andrew; Remmers-Roeber, Dawn R.; Dengler, Christine; Kenmuir, Cynthia L.; Crouse, Carrie

doi:10.1016/s0165-3806(01)00119-5

Cited by 16 publications

(22 citation statements)

References 25 publications

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“…The effect of ketamine on habituation, which is a form of learning and memory, may be coupled to the ability of ketamine to act as a NMDA receptor antagonist and the NMDA system is important learning. Animals neonatally exposed to ketamine and other NMDA-antagonists show spatial learning deficits in adulthood (Gorter and de Bruin, 1992) and can demonstrate taste aversion learning and taste recognition memory (Mickley et al, 2001), which further supports our present findings.…”

Section: Discussionsupporting

confidence: 90%

Neonatal ketamine exposure results in changes in biochemical substrates of neuronal growth and synaptogenesis, and alters adult behavior irreversibly

et al. 2008

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Section: Discussionsupporting

confidence: 90%

Neonatal ketamine exposure results in changes in biochemical substrates of neuronal growth and synaptogenesis, and alters adult behavior irreversibly

et al. 2008

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“…Although brain areas may presumably become incorporated into different behavioral circuits at different ages, at least in odor-0.5mA shock fear conditioning, the amygdala does not appear to be incorporated into the learning until around PN10 (Sullivan et al 2000;Roth and Sullivan 2005;. The developmental changes in pharmacological attenuation/potentiation of taste aversion also suggest that the underlying neural circuitry supporting taste/odor aversion may change (glutamate, Mickley et al 2001) (opioids, Stickrod et al 1982a). However, the molecular cascade of intracellular event associated with learning and memory appears rather consistent between pups and adults for both taste/odor aversion learning and odor learning in general (McLean et al 1999;Gruest et al 2004b).…”

mentioning

confidence: 99%

Development switch in neural circuitry underlying odor-malaise learning

Shionoya¹,

Moriceau²,

Lunday³

et al. 2006

Learn. Mem.

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Fetal and infant rats can learn to avoid odors paired with illness before development of brain areas supporting this learning in adults, suggesting an alternate learning circuit. Here we begin to document the transition from the infant to adult neural circuit underlying odor-malaise avoidance learning using LiCl (0.3 M; 1% of body weight, ip) and a 30-min peppermint-odor exposure. Conditioning groups included: Paired odor-LiCl, Paired odor-LiCl-Nursing, LiCl, and odor-saline. Results showed that Paired LiCl-odor conditioning induced a learned odor aversion in postnatal day (PN) 7, 12, and 23 pups. Odor-LiCl Paired Nursing induced a learned odor preference in PN7 and PN12 pups but blocked learning in PN23 pups. 14C 2-deoxyglucose (2-DG) autoradiography indicated enhanced olfactory bulb activity in PN7 and PN12 pups with odor preference and avoidance learning. The odor aversion in weanling aged (PN23) pups resulted in enhanced amygdala activity in Paired odor-LiCl pups, but not if they were nursing. Thus, the neural circuit supporting malaise-induced aversions changes over development, indicating that similar infant and adult-learned behaviors may have distinct neural circuits.Animals rapidly learn to avoid tastes, smells, and textures of foods associated with malaise, and this learning process produces conditioned taste and odor aversions (Garcia et al. 1966(Garcia et al. , 1974 Best 1992, 1993). This learning has been demonstrated early in development, including both the embryonic day (ED) 18 rat and mouse fetuses, with retention time lasting weeks Haroutunian and Campbell 1979;Smotherman 1982;Stickrod et al. 1982b;Rudy and Cheatle 1983; Robinson 1985, 1990;Alleva and Calamandrei 1986;Molina et al. 1986;Hoffmann et al. 1987Hoffmann et al. , 1990Miller et al. 1990;Hunt et al. 1991Hunt et al. , 1993Abate et al. 2001;Richardson and McNally 2003;Gruest et al. 2004a). Taste/odor aversion acquisition shows some specific differences between pups and adults. First, nursing during acquisition disturbs taste-aversion learning, although this diminishes as pups approach weanling (Martin and Alberts 1979;Gubernick and Alberts 1984;Melcer et al. 1985;Kehoe and Blass 1986). Second, in contrast to the long temporal parameters permitted between the odor/taste (conditioned stimulus, CS) and illness (unconditioned stimulus, US) in adult taste aversion, the temporal constraints between the CS and the malaise producing US for pup learning are very limited (Rudy and Cheatle 1983;Kraemer et al. 1988Kraemer et al. , 1989Hoffmann et al. 1990Hoffmann et al. , 1991.There is evidence that the neural basis of odor/taste aversion learning may change over development. In adults, the amygdala is thought to support taste-aversion learning, though there are discrepancies in the literature (Nachman and Ashe 1974;Burt and Smotherman 1980;Dunn and Everitt 1988;Yamamoto and Fujimoto 1991;Kesner et al. 1992;Yamamoto et al. 1994;Bures et al. 1998;Schafe et al. 1998;Sakai and Yamamoto 1999;Wilkins and Bernstein 2006). When the taste and smell component...

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“…The number of mouthing and licking responses of our E18/E19 fetuses was approximately 10 to 11 per min. Our previous work with fetal animals at this stage of development has never revealed a rate of responding higher than this (Mickley et al, 2000;Mickley et al, 2001). Likewise, spontaneous FIGURE 1 Mean mouthing and licking responses (AESEM) of rats after a taste of 0.30% SAC (Taste Exposure 2: TE2) which followed oral lavage with either 0.15% SAC or 0.30% SAC administered on E18 or E19 (Taste Exposure 1: TE1).…”

Section: Discussionmentioning

confidence: 96%

“…Administration of the NMDA receptor-blocking drug ketamine before CS to US pairings potentiated CTA formation and conditioned motor responses in E18 fetuses (Mickley et al, 1995;Mickley et al, 2001). However, when injected with equivalent doses of ketamine at the time of conditioning, E19 and older rats later failed to exhibit a CTA or conditioned motor responses (Mickley et al, 1998;Mickley et al, 2001). Thus, there may be critical periods in the developmental process when the NMDA receptor blockade produces very different effects on learning and memory.…”

Section: Figurementioning

confidence: 98%

“…Infants and fetuses are now recognized as having a diverse behavioral repertoire and intellectual abilities to perceive and interact with their environment (Smotherman & Robinson, 1988b). Because the gustatory and olfactory systems are somewhat functional late in gestation (Teicher & Blass, 1977), our laboratory has been studying conditioned taste aversion (CTA) formation, taste recognition memory formation, and other gustatory memory phenomena in fetal and neonatal rats (Mickley, Lovelace, Farrell, & Chang, 1995;Mickley, Remmers-Roeber, Crouse, & Peluso, 2000a, 2000bMickley, Remmers-Roeber, Crouse, Walker, & Dengler, 2000;Mickley, Remmers-Roeber, Dengler, Kenmuir, & Crouse, 2001;Mickley et al, 1998). The studies reported here extend this work to a different behavioral paradigm designed to assess behavioral indicators of gustatory positive contrast and long-term habituation in fetal and neonatal rats.…”

Section: Introductionmentioning

confidence: 94%

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Repeated exposures to gustatory stimuli produce habituation or positive contrast effects in perinatal rats

Mickley

Kenmuir

Crish

et al. 2004

Developmental Psychobiology

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Adult rats exhibit a decrease in consummatory responses following repeated presentations of a taste (habituation) and an increase in consummatory responses if they experience an upward shift in the magnitude or intensity of a gustatory stimulus (e.g., sucrose or saccharin). These responses do not represent a direct sensorimotor reaction to a gustatory cue, but rather reflect a change in responding based on the memory of a previous taste. Here, we sought to determine if fetal rats could (like adults) adjust their orofacial motor responses based on a memory of recent gustatory experience. Embryonic Day 18 (E18) or Day 19 (E19) rat fetuses received oral lavage with either 0.15 or 0.30% saccharin (SAC). Subsequently, observations of orofacial movements (mouthing and licking) following oral lavage with 0.30% SAC were made 50 min later, 24 hr later, or on postnatal Day 3 (P3). Thus, some animals were in a "shifted" condition in which they first experienced a relatively low concentration of SAC and then a higher one while control rats ("nonshifted") received 0.30% SAC during both taste exposures. Fetuses exhibited evidence of both habituation (with repeated presentation of the 0.30% SAC) and positive contrast effects (PCEs) (following an upward shift in SAC concentration) when retested 50 min after their first exposure to SAC on E19. However, these animals did not exhibit PCEs 24 hr later or 5 days later (on P3). Contrast effects were not observed when the initial SAC exposure was on E18, and habituation responses were variable depending on the time interval between the taste presentations to these animals. Rats with a 5- to 6-day latency between the two taste presentations showed neither PCEs nor habituation. Our data indicate that PCEs and habituation effects emerge at different ages, and their demonstration is dependent upon the latency between the taste presentations.

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Paradoxical effects of ketamine on the memory of fetuses of different ages

Cited by 16 publications

References 25 publications

Neonatal ketamine exposure results in changes in biochemical substrates of neuronal growth and synaptogenesis, and alters adult behavior irreversibly

Neonatal ketamine exposure results in changes in biochemical substrates of neuronal growth and synaptogenesis, and alters adult behavior irreversibly

Development switch in neural circuitry underlying odor-malaise learning

Repeated exposures to gustatory stimuli produce habituation or positive contrast effects in perinatal rats

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