Ontogeny of synaptic transmission in the rat hippocampus

Kudryashov, I. E.; Kudryashova, I. V.

doi:10.1016/s0006-8993(00)03157-7

Cited by 14 publications

(9 citation statements)

References 30 publications

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“…From this we conclude that activation of the NMDA-receptor, either in neurons, glia cells or both, is required to produce the observed biphasic patterns in the energy metabolism. Moreover, the similarity of the developmental patterns of the activity of neurons [15][16][17] and the NMDA-evoked metabolic responses in our cultures indicate that both phenomena might reflect reorganization of neurons and their synaptic circuits. Consequently, we suggest that the decrease of neuronal connections at 7 DIV and 16 DIV could account for the decrease in NMDA-induced NADPH-response due to dampened neurometabolic coupling between neurons and glia cells, thereby reducing metabolic response towards NMDA.…”

Section: Developmental Changes Of the Energy Metabolismsupporting

confidence: 51%

“…Such windows have been detected for other neuronal parameters during hippocampal development. For example, Kudryashov et al [15,16] showed that population spike (PS) amplitude increased until postnatal day (PND) 19, but decreased thereafter to a minimum between PND 21-PND 24, before it finally increased to adult levels. A study by…”

Section: Developmental Changes Of the Energy Metabolismmentioning

confidence: 99%

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NMDA-induced stimulation of glycolysis in developing hippocampal cell cultures

Luengviriya¹,

Helmeke

Braun

et al. 2009

Open Life Sciences

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Developmental changes in energy metabolism of primary hippocampal cell cultures from newborn rats were investigated during the first 3 weeks. These changes were measured by intensity of and number of cells exhibiting NAD(P)H fluorescence in response to NMDA-induced activation of neuronal activity. We observed gradual changes of stimulation-evoked NAD(P)H signaling over the first 3 weeks, such that at day 7 and 16, this stimulation is minimal, while at 5 and 12 days, it is maximal. These results describe a biphasic pattern that was similar to earlier findings from experiments investigating developmental changes in population spike amplitudes or glutamate release in young rats. Inhibition of mitochondrial respiration by KCN revealed that the NMDA-evoked stimulation of energy metabolism is mainly due to increased glycolytic activity.

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Section: Developmental Changes Of the Energy Metabolismsupporting

confidence: 51%

Section: Developmental Changes Of the Energy Metabolismmentioning

confidence: 99%

NMDA-induced stimulation of glycolysis in developing hippocampal cell cultures

Luengviriya¹,

Helmeke

Braun

et al. 2009

Open Life Sciences

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“…For example, during the first postnatal weeks, neuronal birth, differentiation and migration are ongoing (Altman and Bayer, 1990; Gould and Cameron, 1996). Based on slice physiology, both inhibitory and excitatory responses have been found in the infant hippocampus, although inhibitory responses are just beginning to develop around PN 9-12 and reach adult values between PN14-18 (Baudry et al, 1981; Michelson and Lothman, 1989; Muller et al, 1989; Bekenstein and Lothman, 1991a; DiScenna and Teyler, 1994; Kudryashov and Kudryashova, 2001). Neurogenesis of granule cells peaks just during the second week of life in rodents (Bayer, 1980a) with major synaptic maturation occurring later in the preweaning period (Crain et al, 1973; Muller et al, 1989).…”

Section: Discussionmentioning

confidence: 99%

“…Hippocampus development is protracted and continues through adolescence, although each subdivision has a distinct developmental time frame (Nurse and Lacaille, 1999; Swann et al, 1999; Tarazi and Baldessarini, 2000; Toscano et al, 2003; Crews et al, 2007), with long-term potentiation (LTP), which is a presumed measure of plasticity, emerging during the second postnatal week in CA1, and during the third postnatal week in DG (Harris and Teyler, 1984; Wilson, 1984; Swann et al, 1990; Bekenstein and Lothaman, 1991b). Neurotransmitter systems associated with plasticity, such as glutamatergic synapses, achieve maturity after PN14 (Michelson and Lothman, 1989; Kudryashov and Kudryashova, 2001), and GABAergic synaptic transmission has been observed at PN5-6 in CA3, though just at PN9 in CA1 (Swann et al, 1989, 1990). …”

Section: Introductionmentioning

confidence: 99%

Functional emergence of the hippocampus in context fear learning in infant rats

et al. 2010

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The hippocampus is a part of the limbic system and is important for the formation of associative memories, such as acquiring information about the context (e.g. the place where an experience occurred) during emotional learning (e.g. fear conditioning). Here, we assess whether the hippocampus is responsible for pups’ newly emerging context learning. In all experiments, postnatal day (PN) 21 and PN24 rat pups received 10 pairings of odor-0.5mA shock or control unpaired odor-shock, odor only and shock only. Some pups were used for context, cue or odor avoidance tests, while the remaining pups were used for c-Fos immunohistochemistry to assess hippocampal activity during acquisition. Our results show that cue and odor avoidance learning were similar at both ages, while contextual fear learning and learning-associated hippocampal (CA1, CA3 and dentate gyrus) activity (c-Fos) only occurred in PN24 paired pups. To assess a causal relationship between the hippocampus and context conditioning, we infused muscimol into the hippocampus, which blocked acquisition of context fear learning in the PN24 pups. Muscimol or vehicle infusions did not affect cue learning or aversion to the odor at PN21 or PN24. The results suggest that the newly emerging contextual learning exhibited by PN24 pups is supported by the hippocampus.

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“…At least based on extinction behavior, which involves the prefrontal cortex, this brain area emerges between PN12 and PN17 (Stanton et al 1984;Morgan et al 1993;Lilliquist et al 1999;Nair and Gonzalez-Lima 1999;Nair et al 2001;Milad and Quirk 2002). Hippocampus anatomical development is further delayed, and hippocampaldependent learning emerges near weaning Nadler et al 1974;Baudry et al 1981;Lobaugh et al 1989;Muller et al 1989;Bekenstein and Lothman 1991;Lilliquist et al 1993;DiScenna and Teyler 1994;Rudy 1994;Rudy and Morledge 1994;Nair and Gonzalez-Lima 1999;Kudryashov and Kudryashova 2001;Nair et al 2001). Thus, based on anatomical maturation of brain areas associated with coding hedonic value, the anterior and posterior piriform may indeed code hedonic value in early life.…”

Section: Piriform Cortex May Encode Olfactory Hedonic Valuementioning

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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Ontogeny of synaptic transmission in the rat hippocampus

Cited by 14 publications

References 30 publications

NMDA-induced stimulation of glycolysis in developing hippocampal cell cultures

NMDA-induced stimulation of glycolysis in developing hippocampal cell cultures

Functional emergence of the hippocampus in context fear learning in infant rats

Development switch in neural circuitry underlying odor-malaise learning

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