Development of glutamate binding sites and their regulation by calcium in rat hippocampus

Baudry, Michel; Arst, Denise; Oliver, Michael W.; Lynch, Gary

doi:10.1016/0165-3806(81)90092-4

Cited by 150 publications

(40 citation statements)

References 18 publications

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“…Extensive work, using binding techniques, has been done on the development of NMDA receptors in the hippocampus [Baudry, et al, 1981;Tremblay et al, 1988;Morin et al, 1989;Insel et al, 1990;Wright et al, 1994] and visual cortex [Bode-Greuel and Singer, 1989;Erdö and Wolff, 1990;Gordon et al, 1991;Reynolds et al, 1991;Kumar et al, 1994]. In general, NMDA receptor binding is present at birth and increases during the first 2-3 weeks of postnatal development.…”

Section: Discussionmentioning

confidence: 99%

Postnatal Development of Glutamate Receptor-Mediated Responses in the Neostriatum

et al. 1998

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Three experimental approaches were used to examine the maturation of N-methyl-D-aspartate (NMDA) receptors in the neostriatum and compare their developmental profile to that of the non-NMDA receptors [α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) and kainate (KA)]. The first, and least conventional approach utilized infrared videomicroscopy to measure NMDA-induced swelling in single cells in a brain slice. The results demonstrated that NMDA receptors display an incremental pattern of postnatal development with no responses at postnatal day (PND) 3, weak responses at PND 7, the largest responses by PND 14 and slight decreases at PNDs 21 and 28. At PNDs 3 and 7, KA-induced cell swelling was proportionately greater than NMDA-induced cell swelling suggesting earlier maturation of this non-NMDA receptor subtype. The second approach used whole-cell patch clamp analysis to examine NMDA currents and compare their maturation to AMPA/KA-induced currents. Though the data are still preliminary, a very similar developmental pattern emerged. NMDA-induced currents were small and developed slowly after PND 7. In contrast, AMPA/KA-induced currents were larger and appeared to develop earlier. Finally, dizocilpine (MK-801) binding was measured in homogenates of neostriatal tissue. The ontogeny of binding resembled a step function with increases between PNDs 3 and 7 and PNDs 14 and 21. Binding peaked at PND 28 and then declined slightly in the adult (PND 60). The affinity of MK-801 for the receptor did not change during postnatal development. These findings demonstrate the pattern of functional development of glutamate receptors in the neostriatum. The NMDA receptor subtype displays minimal functional development until PND 14. In contrast, neostriatal AMPA/KA receptor function appears to precede NMDA receptor function.

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Section: Discussionmentioning

confidence: 99%

Postnatal Development of Glutamate Receptor-Mediated Responses in the Neostriatum

et al. 1998

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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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“…LTP is an enduring enhancement of synaptic transmission that results from appropriate stimulation of presynaptic axons and is considered to be a good candidate for a cellular mechanism of learning and memory (Baudry and Davis,199 1). During development, LTP is first enduring (beyond 2 hr posttetanus) at PNDl5; however, for up to 4 hr posttetanus the magnitude of potentiation can be high before declining to a lower stable level or to the pretetanus baseline (Baudry et al, 1981;Harris and Teyler, 1984;Muller et al, 1989;Jackson et al, 1991). This pattern contrasts with adults, where the lower stable potentiation is reached within 30 min posttetanus (Harris and Teyler, 1984;Malenka, 199 1).…”

mentioning

confidence: 99%

Three-dimensional structure of dendritic spines and synapses in rat hippocampus (CA1) at postnatal day 15 and adult ages: implications for the maturation of synaptic physiology and long-term potentiation [published erratum appears in J Neurosci 1992 Aug;12(8):following table of contents]

1992

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It has long been hypothesized that changes in dendritic spine structure may modify the physiological properties of synapses located on them. Due to their small size, large number, and highly variable shapes, standard light microscopy of Golgi impregnations and electron microscopy (EM) of single thin sections have not proved adequate to identify most spines in a sample or to quantify their structural dimensions and composition. Here we describe a new approach, the series sample, that was developed to classify by shape and subcellular composition all of the spines and synapses in a sample of neuropil by viewing them through serial EM sections. Spines in each class are then randomly selected for serial reconstruction and measurement in three dimensions. This approach was used to assess whether structural changes in hippocampal CA1 spines could contribute to the enhanced synaptic transmission and the greater endurance of long-term potentiation (LTP) that occur with maturation. Our results show a near doubling in the total density of synapses in the neuropil and along reconstructed dendrites between postnatal day 15 (PND 15) and adult ages. However, this doubling does not occur uniformly across all spine and synapse morphologies. Thin spines, mushroom spines containing perforated postsynaptic densities (PSDs) and spine apparatuses, and branched spines increase by about four-fold in density between PND 15 and adult ages. In contrast, stubby spines decrease by more than half and no change occurs in mushroom spines with macular PSDs or in dendritic shaft synapses. The stubby spines that remain are smaller in adults than at PND 15 and the mushroom spines are larger, while no change occurs in the three-dimensional structure of thin spines. Only a few spine necks at either age are constricted or long enough to attenuate charge transfer; therefore, the doubling in synapses should mediate the enhancement of synaptic transmission that occurs with maturation. In addition, LTP is not likely to be mediated by widening of spine necks at either age. However, the constricted spine necks could serve to concentrate specific molecules at activated synapses, thereby enhancing the specificity and endurance of LTP with maturation. These results demonstrate that the new series sample method combined with three- dimensional reconstruction reveals quantitative changes in the frequency and structure of spines and synapses that are not discernable by other methods and are likely to have dramatic effects on synaptic physiology and plasticity.

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Development of glutamate binding sites and their regulation by calcium in rat hippocampus

Cited by 150 publications

References 18 publications

Postnatal Development of Glutamate Receptor-Mediated Responses in the Neostriatum

Postnatal Development of Glutamate Receptor-Mediated Responses in the Neostriatum

Development switch in neural circuitry underlying odor-malaise learning

Three-dimensional structure of dendritic spines and synapses in rat hippocampus (CA1) at postnatal day 15 and adult ages: implications for the maturation of synaptic physiology and long-term potentiation [published erratum appears in J Neurosci 1992 Aug;12(8):following table of contents]

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