Enhanced quantal release of excitatory transmitter in anterior cingulate cortex of adult mice with chronic pain

doi:10.1186/1744-8069-5-4

Molecular Pain

Volume 5

Viewing options:

Abstract
Full text
PDF (1.9MB)

Associated material:

Related literature:

Articles citing this article
on BioMed Central
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Toyoda H
Zhao MG
Zhuo M

on PubMed

Toyoda H
Zhao MG
Zhuo M
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Research

Enhanced quantal release of excitatory transmitter in anterior cingulate cortex of adult mice with chronic pain

Hiroki Toyoda¹^,2 , Ming-Gao Zhao¹^,3 and Min Zhuo¹

¹Department of Physiology, Faculty of Medicine, Centre for the Study of Pain, University of Toronto, Toronto, Ontario, Canada

²Department of Neuroscience and Oral Physiology, Osaka University Graduate School of Dentistry, Suita, Japan

³Department of Pharmacology, Fourth Military Medical University, Xi'an, PR China

author email corresponding author email

Molecular Pain 2009, 5:4doi:10.1186/1744-8069-5-4


Published:	27 January 2009

Abstract

The anterior cingulate cortex (ACC) is a forebrain structure that plays important roles in emotion, learning, memory and persistent pain. Our previous studies have demonstrated that the enhancement of excitatory synaptic transmission was induced by peripheral inflammation and nerve injury in ACC synapses. However, little information is available on their presynaptic mechanisms, since the source of the enhanced synaptic transmission could include the enhanced probability of neurotransmitter release at existing release sites and/or increases in the number of available vesicles. The present study aims to perform quantal analysis of excitatory synapses in the ACC with chronic pain to examine the source of these increases. The quantal analysis revealed that both probability of transmitter release and number of available vesicles were increased in a mouse model of peripheral inflammation, whereas only probability of transmitter release but not number of available vesicles was enhanced in a mouse model of neuropathic pain. In addition, we compared the miniature excitatory postsynaptic potentials (mEPSCs) in ACC synapses with those in other pain-related brain areas such as the amygdala and spinal cord. Interestingly, the rate and amplitude of mEPSCs in ACC synapses were significantly lower than those in the amygdala and spinal cord. Our studies provide strong evidences that chronic inflammatory pain increases both probability of transmitter release and number of available vesicles, whereas neuropathic pain increases only probability of transmitter release in the ACC synapses.