Membrane properties and synaptic responses of the guinea pig nucleus accumbens neurons in vitro

Uchimura, Naohisa; Higashi, H.; Nishi, S.

doi:10.1152/jn.1989.61.4.769

Cited by 50 publications

(29 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In agreement with other studies (Chang and Kitai 1986;Uchimura et al 1989b) the HPSP can be identified as a GABAA receptor-mediated IPSP and the DPSP as a glutamate receptor-mediated EPSP. The EPSP component is likely to be due to monosynaptic activation considering its constant onset latency in spite of varying stimulation intensity.…”

Section: Postsynaptic Potentsupporting

confidence: 92%

“…This observation is in agreement with the slow rise time of NMDA receptormediated activity recorded in cultured neurons from the hippocampus and the spinal cord (Forsythe and Westbrook 1988). Since low-affinity glutamate receptor antagonists were used in previous studies on synaptic responses in the ventral and dorsal striatum (Cordingley and Weight 1986;Cherubini et al 1988;Uchimura et al 1989b;Walsh et al 1989), the present investigations are the first to suggest that fast EPSPs evoked by local or callosal stimulation are almost completely mediated by Q/K receptors.…”

Section: Postsynaptic Potentsupporting

confidence: 90%

“…It has been proposed that a major part of the EPSP evoked in the Acb is mediated by NMDA receptors (Uchimura et al 1989b). Our previous extracellular recordings, however, suggested that Q/K instead of NMDA receptors mediate most of the EPSP (Pennartz et al 1990).…”

Section: Introductionmentioning

confidence: 69%

“…In about half of the neurons tested, depolarization to -65 to -45 mV revealed a biphasic response pattern, consisting of a shortened DPSP followed by a hyperpolarizing postsynaptic potential (HPSP) that lasted 80 to 150 ms (not illustrated, but see Kitai 1986 andUchimura et al 1989b). The reversal potential of the HPSP could not be accurately estimated since the tail of 193 the preceding DPSP component partially overlapped the HPSP.…”

Section: Postsvnaptic Potentialsmentioning

confidence: 99%

“…Likewise, the enlargement of the NMDA receptor mediated component in the presence of GABAA antagonists may be explained by a decreased shunting inhibition and thus a stronger depolarization at the subcellular sites of afferent input. Uchimura et al (1989b) suggested that a major portion of the postsynaptic potential, evoked under normal conditions in the Acb, is mediated by NMDA receptors. The difference between their results and the findings reported here may be ascribed to (1) a difference in the Acb subregion that was investigated (dorsomedial part vs. core of the Acb); (2) a smaller influence of IPSPs in their study, or (3) aspecific effects of high concentrations of DL--APV (250 ~tM) and D-~-aminoadipic acid (1 mM) used in their study.…”

Section: Postsynaptic Potentmentioning

confidence: 99%

See 4 more Smart Citations

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

et al. 1991

View full text Add to dashboard Cite

Summary. The principal aim of this study was to characterize the transmitter mechanisms mediating fast postsynaptic potentials in identified neurons of the rat nucleus accumbens. Using the biocytin-avidin labeling technique, impaled neurons were identified as medium spiny neurons. The basic membrane characteristics of these neurons were determined. Local electrical stimulation or stimulation of the corpus callosum elicited a depolarizing postsynaptic potential consisting of an EPSP often followed by an IPSP. The quisqualate/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (4 gM) abolished most of the depolarizing postsynaptic potential. The N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid depressed a small part of the decay phase of the depolarizing postsynaptic potential. Paired-pulse facilitation of postsynaptic potentials was found using interstimulus-intervals between 10 and 150 ms. N-methyl-D-aspartate receptors were found to contribute only slightly to the facilitation of the decay phase of the depolarizing postsynaptic potential, but not to its rising phase. This contribution was particularly clear under conditions of reduced GABAA receptor mediated inhibition. The present study indicates that postsynaptic responses of medium spiny neurons in the nucleus accumbens to local stimulation or stimulation of neocortical afferents are primarily mediated by quisqualate/kainate receptors. The contribution of NMDA receptors is normally limited to a portion of the decay phase of these responses, but is enlarged in the absence of GABAergic inhibition and following paired-pulse stimulation.

show abstract

Section: Postsynaptic Potentsupporting

confidence: 92%

Section: Postsynaptic Potentsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 69%

Section: Postsvnaptic Potentialsmentioning

confidence: 99%

Section: Postsynaptic Potentmentioning

confidence: 99%

See 3 more Smart Citations

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

et al. 1991

View full text Add to dashboard Cite

show abstract

Physiological and morphological properties of accumbens core and shell neurons recorded in vitro

O’Donnell

Grace

1993

Synapse

149

111

View full text Add to dashboard Cite

The morphology and electrophysiological properties of neurons in the nucleus accumbens were studied using intracellular recording techniques in rat brain slices maintained in vitro. Neurons were subdivided according to their location in the shell or core region of the nucleus accumbens. Most of the cells in both regions had small to medium-sized (15.8 +/- 2.8 microns) somata with densely spinous dendrites, somewhat similar to the striatal medium spiny neuron. However, minor morphological differences between neurons from accumbens core and shell regions were found, such as fewer primary dendrites in shell neurons than in the core (3.8 +/- 0.8 vs. 4.4 +/- 1.0) and the spatial organization of their dendritic trees. In general, the passive membrane properties of neurons in each region were similar. However, shell neurons appeared to be less excitable in nature, as suggested by (1) a faster time constant, (2) the absence of TTX-insensitive events resembling low-threshold spikes, and (3) the lower probability of evoking spikes in shell neurons by stimulation of amygdaloid or cortical afferents in comparison to the responses of core neurons to cortical afferent stimulation. In most nucleus accumbens neurons the action potentials evoked by membrane depolarization were preceded by a slow Ca(2+)-dependent depolarization and showed firing-frequency adaptation. Following TTX administration, all-or-none spike-like events resembling high-threshold calcium spikes were observed in both regions. In summary, except for minor differences, most of the properties of core and shell neurons are similar, supporting their characterization as subdivisions of a single structure. Therefore, differences in the functional properties of these neuronal populations are likely to be due to their distinct connectivity patterns.

show abstract

Handbook of Neurochemistry and Molecular Neurobiology

2008

View full text Add to dashboard Cite

Additionally, the whole set will be available upon completion under The electronic version of the whole set will be available under The print and electronic bundle of the whole set will be available under ISBN: 978-0-387-35478-1 ß 2008 Springer Science+Business Media, LLC.All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, LLC., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. springer.comPrinted on acid-free paper SPIN: 11416593 2109 -5 4 3 2 1 0 PrefaceThe brain is the organ that collects information from the environment, processes and stores the information, and generates behavior as and when needed. In essence, the brain makes us who we are. For this reason, understanding the biology of brain function is a great challenge and a major goal of modern science. The brain is one of the last great frontiers in science, and the unraveling of its mysteries is comparable in complexity to efforts in space exploration. Therefore, it was not a surprise that the U.S. Congress proclaimed the 1990s the ''Decade of the Brain,'' a movement also introduced by several other countries, thereby giving a chance for neuroscientists to focus on this topic and to have better conditions for their research.A fundamental goal of neuroscience is to understand how neurons generate behavior and the pathophysiology of different mental and neurological diseases. This requires, among other things, information about where these neurons are located, how they are connected, and how they communicate with each other in various physiological and pathophysiological conditions.At the end of the nineteenth century, the great neuroanatomist Santiago Ramon y Cajal recognized that neurons are the individual signaling elements of the brain. In this book, we focus on these nerve cells of the brain and the chemical molecules that allow them to talk to each other. The discovery of intercellular communication through endogenous molecules is a milestone in the history of science. It makes the brain a unique organ.Our aim is to describe recent discoveries about the basic operations of the brain and to provide an introduction to the adaptations for specific types of information processing. For example, at a chemical synapse, the presynaptic terminal liberates a transmitter substance that acts on the postsynaptic process. Thus, a synapse converts a presynaptic electrical signal into a chemical signal and back into a postsynaptic electrical signal.Cur...

show abstract

Membrane properties and synaptic responses of the guinea pig nucleus accumbens neurons in vitro

Cited by 50 publications

References 0 publications

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

Contribution of NMDA receptors to postsynaptic potentials and paired-pulse facilitation in identified neurons of the rat nucleus accumbens in vitro

Physiological and morphological properties of accumbens core and shell neurons recorded in vitro

Handbook of Neurochemistry and Molecular Neurobiology

Contact Info

Product

Resources

About