Localization of AMPA receptors in the hippocampus and cerebellum of the rat using an anti-receptor monoclonal antibody

Hampson, David R.; Huang, Xi‐Ping; Oberdorfer, M. D.; Goh, Joanne W.; Auyeung, Anthony; Wenthold, RJ

doi:10.1016/0306-4522(92)90378-f

Cited by 77 publications

(42 citation statements)

References 38 publications

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“…An argument against the role of ␦1 as an autoreceptor or an efferent receptor is that ␦1 immunoreactivity does not appear to be concentrated near the base of the hair cell, where the synaptic contacts are made. But the distribution of ␦1 throughout the hair cells may reflect a relatively large intracellular receptor pool, which seems to be a characteristic of glutamate receptors in neurons (Hampson et al, 1992;Petralia and Wenthold, 1992;Petralia, 1997). At the ultrastructural level, glutamate receptors are shown to be concentrated at the synapse (Mayat et al, 1995;Petralia et al, 1996;Petralia, 1997), and such studies may show a similar concentration of ␦1 at the base of the hair cells.…”

Section: Discussionmentioning

confidence: 87%

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

Safieddine

Wenthold

1997

J. Neurosci.

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In the inner ear, fast excitatory synaptic transmission is mediated by ionotropic glutamate receptors, including AMPA, kainate, and NMDA receptors. The recently identified ␦1 and ␦2 glutamate receptors share low homology with the other three types, and no clear response or ligand binding has been obtained from cells transfected with ␦ alone or in combination with other ionotropic receptors. Studies of mice lacking expression of ␦2 show that this subunit plays a crucial role in plasticity of cerebellar glutamatergic synapses. In addition, these mice show a deficit in vestibular compensation. These findings and the nature of glutamatergic synapses between vestibulocochlear hair cells and primary afferent dendrites suggest that ␦ receptors may be functionally important in the inner ear and prompted us to investigate the expression of ␦ receptors in the cochlea and peripheral vestibular system. Reverse transcription and DNA amplification by PCR combined with immunocytochemistry and in situ hybridization were used. Our results show that the expression of ␦1 in the organ of Corti is intense and restricted to the inner hair cells, whereas ␦1 is expressed in all spiral ganglion neurons as well as in their satellite glial cells. In the vestibular end organ, ␦1 was highly expressed in both hair cell types and also was expressed in the vestibular ganglion neurons. The prominent expression of ␦1 in inner hair cells and in type I and type II vestibular hair cells suggests a functional role in hair cell neurotransmission. Key words: cochlea; vestibular end organ; hair cells; spiral ganglion neurons; PCR; in situ hybridization; Western blot; immunocytochemistryAuditory and vestibular stimuli are detected by hair cells in the inner ear and are transmitted to the brain by way of the auditory and vestibular nerves. Of the two types of hair cells found in the organ of Corti, inner hair cells (IHC s) and outer hair cells (OHC s), IHC s are the primary transducers of sensory information. IHC s form chemical synapses with dendrites of type I spiral ganglion neurons (SGNs) that constitute 90 -95% of the SGNs. OHC s synapse on the remaining type II SGNs (Spoendlin, 1972;Berglund and Ryugo, 1987). The vestibular epithelium contains two types of sensory hair cells. T ype I cells (V HCI) are flaskshaped and surrounded by an afferent nerve caly x, whereas type

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Section: Discussionmentioning

confidence: 87%

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

Safieddine

Wenthold

1997

J. Neurosci.

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“…ANOVA indicated a main effect of group (F (3,20) ϭ 29.6; p Ͻ 0.0001), with D-APV rats showing significantly higher GluR1 levels than vehicle and extinction rats ( p Ͻ 0.001) as well as equivalent GluR1 levels to paired controls ( p Ͼ 0.1). Similar experimental procedures were performed to determine GluR1 levels in the synaptic sites using synaptoneurosomes that resemble isolated glutamatergic synapses located on the dendritic spines with resealed presynaptic and postsynaptic compartments (Hollingsworth et al, 1985;Hampson et al, 1992;Heynen et al, 2000). The GluR1 level was significantly increased after conditioning (F (2,15) ϭ 19.6; p Ͻ 0.0001), and the increase was reversed by extinction training.…”

Section: Light-alone Trials Conducted 1 H But Not 24 H After Trainimentioning

confidence: 99%

Extinction Training in Conjunction with a Partial Agonist of the Glycine Site on the NMDA Receptor Erases Memory Trace

Mao¹,

Hsiao²,

Gean³

2006

J. Neurosci.

108

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Much evidence indicates that extinction training does not erase memory traces but instead forms inhibitory learning that prevents the expression of original memory. Fear conditioning induces long-term potentiation and drives synaptic insertion of AMPA receptors into the amygdala. Here we show that extinction training applied 1 h after training reversed the conditioning-induced increase in surface glutamate receptor subunit 1 (GluR1) in parallel with the inhibition of startle potentiation. However, if applied 24 h after training, extinction training reduced startle potentiation without influencing the GluR1 increase. We infused D-cycloserine (DCS), a partial agonist of the glycine site on the NMDA receptor, bilaterally into the amygdala 30 min before extinction training. This augmented the extinction training-elicited reduction in startle and reversed the conditioning-induced increase in GluR1. Delivery of five sets of tetanic stimulation (TS) to the external capsule produced a robust enhancement of synaptic responses in the lateral amygdala neurons that persisted for Ͼ2 h. Low-frequency stimulation applied 1 h after TS had no long-lasting effect on synaptic responses. The same treatments, however, induced depotentiation in the presence of DCS and reversed TS-induced increase in surface GluR1. Together, this study has two important findings: (1) whether a memory trace remains intact or is erased depends on the interval between conditioning and extinction training and (2) DCS facilitates the reversal of memory trace. DCS-induced augmentation of extinction and reversal of GluR1 surface expression are likely mediated by DCS-facilitated endocytosis of AMPA receptors.

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“…Synaptoneurosomes resemble isolated glutamatergic synapses located on the dendritic spines, with resealed pre-and postsynaptic compartments (Hollingsworth et al, 1985;Hampson et al, 1992;Heynen et al, 2000). We examined whether regulation of glutamate receptor availability after fear conditioning at the synaptoneurosomes occurred as that measured with biotin labeling.…”

Section: Fear Conditioning Increases Surface Expression Ofmentioning

confidence: 99%

Synaptic Expression of Glutamate Receptor after Encoding of Fear Memory in the Rat Amygdala

et al. 2005

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Fear conditioning has been ascribed to presynaptic mechanisms, particularly presynaptic facilitation of transmission at thalamo-and cortico-amygdala synapses. Here, by labeling surface receptors with biotin or using membrane fractionation approaches, we report that fear conditioning resulted in an increase in surface expression of GluR1 subunit of ␣-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors in the amygdala, whereas total GluR1 mRNA and protein levels were unchanged. The control group that received conditioned stimulus (CS) and unconditioned stimulus in an unpaired fashion did not present any increase, indicating that GluR1 increase was specific to the learning component of the task. Conditioninginduced increase in surface expression of GluR1 depended on the activation of N-methyl-D-aspartate receptors and protein kinases and required the synthesis of new proteins. CS-alone trials applied 24 h before training attenuated fear-potentiated startle and prevented conditioning-induced increase in surface expression of GluR1. Increase in GluR1 was also observed in the amygdala slices after delivery of tetanic stimulation that elicited long-term potentiation of synaptic transmission. Proteasome inhibitor increased surface expression of GluR1 in a time-and dose-dependent manner. Furthermore, pretraining administration of proteasome inhibitor into the amygdala facilitated the fear-potentiated startle. These results suggest that long-term memory formation is correlated with the change in synaptic expression of GluR1, and trafficking of GluR1 to the synaptic sites contributes at least in part to the expression of fear memory.Fear conditioning, an animal model of emotional learning and post-traumatic stress disorder, is initiated by a cue (conditioned stimulus, CS) that is previously paired with an aversive stimulus (unconditioned stimulus, US) such as footshock. Neuronal changes mediating the association between the CS and US occur in the lateral (LA) and basolateral (BLA) amygdala (McKernan and Shinnick-Gallagher, 1997;Rogan et al., 1997;Pare, 2003). It is generally recognized that consolidation of long-term memory in vertebrate and invertebrate brains requires transcription and translation of new proteins (Dudai, 1996;McGaugh, 2000). Newly synthesized proteins are believed to deposit at the synapses that encode the persistent changes in synaptic strength. Despite the signal cascades that have been identified to be responsible for the consolidation of fear memory, little is known about the downstream effectors leading to the expression of memory. Previous study has showed that conditioned fear is associated with a reduction in paired-pulse facilitation and an enhancement in the probability of transmitter release in the thalamo-amygdala pathway (McKernan and Shinnick-Gallagher, 1997). Quantal analysis of unitary synaptic responses in cortico-amygdala pathway after induction of long-term potentiation (LTP) revealed a marked decrease in the fraction of failures, with no change in potency of CV of the...

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Localization of AMPA receptors in the hippocampus and cerebellum of the rat using an anti-receptor monoclonal antibody

Cited by 77 publications

References 38 publications

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

The Glutamate Receptor Subunit δ1 Is Highly Expressed in Hair Cells of the Auditory and Vestibular Systems

Extinction Training in Conjunction with a Partial Agonist of the Glycine Site on the NMDA Receptor Erases Memory Trace

Synaptic Expression of Glutamate Receptor after Encoding of Fear Memory in the Rat Amygdala

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