Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury

Ruifeng Cao; Hiroshi Hasuo; Satomi Ooba; Takashi Akasu; Xiang Zhang

doi:10.1016/j.neulet.2006.03.005

Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury

Ruifeng Cao, Hiroshi Hasuo, Satomi Ooba, Takashi Akasu, Xiang Zhang

Biomedical Sciences

Research output: Contribution to journal › Article › peer-review

16 Scopus citations

Abstract

We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8 atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.

Original language	English (US)
Pages (from-to)	136-141
Number of pages	6
Journal	Neuroscience Letters
Volume	401
Issue number	1-2
DOIs	https://doi.org/10.1016/j.neulet.2006.03.005
State	Published - Jun 19 2006

Bibliographical note

Funding Information:
This work was supported by a Grant-in-Aid for Scientific Research (C) (17500279) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. This research was also supported from the Ministry of Education, Culture, Sports, Science and Technology as a part of a project for establishing open research centers in private universities.

Keywords

Excitability
Glutamate release
Hippocampal CA1
Intracellular recording
Synaptic transmission
Traumatic brain injury

Publisher link

10.1016/j.neulet.2006.03.005

Find It

Find It at U of M Libraries

Cite this

@article{ef18a3227d2a46a8885e37dd9f668e79,

title = "Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury",

abstract = "We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8 atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.",

keywords = "Excitability, Glutamate release, Hippocampal CA1, Intracellular recording, Synaptic transmission, Traumatic brain injury",

author = "Ruifeng Cao and Hiroshi Hasuo and Satomi Ooba and Takashi Akasu and Xiang Zhang",

note = "Funding Information: This work was supported by a Grant-in-Aid for Scientific Research (C) (17500279) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. This research was also supported from the Ministry of Education, Culture, Sports, Science and Technology as a part of a project for establishing open research centers in private universities.",

year = "2006",

month = jun,

day = "19",

doi = "10.1016/j.neulet.2006.03.005",

language = "English (US)",

volume = "401",

pages = "136--141",

journal = "Neuroscience Letters",

issn = "0304-3940",

publisher = "Elsevier Ireland Ltd",

number = "1-2",

}

TY - JOUR

T1 - Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury

AU - Cao, Ruifeng

AU - Hasuo, Hiroshi

AU - Ooba, Satomi

AU - Akasu, Takashi

AU - Zhang, Xiang

N1 - Funding Information: This work was supported by a Grant-in-Aid for Scientific Research (C) (17500279) from the Ministry of Education, Culture, Sports, Science and Technology of Japan. This research was also supported from the Ministry of Education, Culture, Sports, Science and Technology as a part of a project for establishing open research centers in private universities.

PY - 2006/6/19

Y1 - 2006/6/19

N2 - We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8 atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.

AB - We investigated the effects of traumatic brain injury (TBI) on the glutamatergic synaptic transmission in the hippocampal CA1 area. A moderate impact (3.8-4.8 atm) was applied onto the left parietal cerebral cortex by a fluid percussion injury (FPI) device. Conventional intracellular recordings were made from hippocampal CA1 pyramidal neurons in vitro. Electrophysiological properties of these neurons were compared between three groups (control, FPI-ipsilateral, and FPI-contralateral). The excitability of postsynaptic membrane of CA1 pyramidal neurons was not altered by the moderate FPI; however, the evoked glutamatergic excitatory synaptic transmission in the pyramidal neurons of post-FPI-CA1 was enhanced. Paired-pulse facilitation (PPF) was significantly suppressed in both the FPI-ipsilateral and FPI-contralateral groups and the frequencies of mEPSPs in neurons from the bilateral FPI groups were greater than the frequency in the control group. These results suggest that the glutamatergic synaptic transmission in the hipppocampal CA1 area is facilitated through presynaptic mechanisms after TBI.

KW - Excitability

KW - Glutamate release

KW - Hippocampal CA1

KW - Intracellular recording

KW - Synaptic transmission

KW - Traumatic brain injury

UR - http://www.scopus.com/inward/record.url?scp=33646538488&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33646538488&partnerID=8YFLogxK

U2 - 10.1016/j.neulet.2006.03.005

DO - 10.1016/j.neulet.2006.03.005

M3 - Article

C2 - 16574323

AN - SCOPUS:33646538488

SN - 0304-3940

VL - 401

SP - 136

EP - 141

JO - Neuroscience Letters

JF - Neuroscience Letters

IS - 1-2

ER -

Facilitation of glutamatergic synaptic transmission in hippocampal CA1 area of rats with traumatic brain injury

Abstract

Bibliographical note

Keywords

Publisher link

Find It

Other files and links

Fingerprint

Cite this