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J Neurophysiol (November 21, 2007). doi:10.1152/jn.00625.2007
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Submitted on June 5, 2007
Accepted on November 19, 2007

Developmental decrease in short-term facilitation at Schaffer collateral synapses in hippocampus is mGluR1-sensitive

Haley E. Speed1 and Lynn E. Dobrunz2*

1 Neurobiology, Univ of Alabama at Birmingham, Birmingham, Alabama, United States
2 Neurobiology, Univ Alabama @ Birmingham, Birmingham, Alabama, United States

* To whom correspondence should be addressed. E-mail: dobrunz{at}nrc.uab.edu.

Developmental changes can occur in the dynamic properties of synapses, known as short-term plasticity. Using rat acute hippocampal slices at room temperature, we have previously shown a decrease in short-term facilitation at Schaffer collateral synapses from young adults compared to juveniles in response to temporally complex natural stimulus patterns such as synapses receive in vivo. Here we show that this developmental decrease in facilitation is also seen at 32°C and investigate the underlying mechanism. Addition of the mGluR1 antagonist LY367385 increases short-term facilitation in response to the natural stimulus pattern, showing that mGluR1 is activated by synaptically released glutamate. While synaptic activation of mGluR1 occurs at both ages, the effect is larger in young adults. Furthermore, blocking mGluR1 eliminates most of the developmental decrease in short-term facilitation during the natural stimulus pattern. We investigated possible retrograde/downstream messengers involved after synaptic activation of mGluR1. Blocking cannabinoid receptors has no effect on the response during the natural stimulus pattern, indicating that the reduction in facilitation during synaptic activation of mGluR1 does not occur through release of endocannabinoids. We find that blocking GABAB receptors increases facilitation during the natural stimulus pattern and occludes the effect of the mGluR1 antagonist, indicating a role for the modulation of GABA release from inhibitory interneurons by mGluR1 activation. These data suggest a model where synaptic activation of mGluR1 on inhibitory interneurons causes an increase in GABA release by inhibitory interneurons, which activates GABAB receptors on Schaffer collateral synapses and inhibits short-term facilitation during the natural stimulus pattern.




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