The effects of metabotropic glutamate receptors in NMDA receptor dependent long-term potentiation in hippocampus

 

Zhou Su-ya

 

The previous study has showed that LTP in CA1 region of hippocampus is NMDA receptor dependent. It is evoked by extracellular calcium enter into pyramidal neuron and the further responds is caused by calcium as second messenger.

Metabotropic glutamate receptor (mGluR) has been reported participate in LTP in dentate gyrus of hippocampus

Both NMDA receptor and mGlu receptor participate in many physiologic and pathologic processes. Such as: synaptic plasticity, study and memory, neuron excitory toxin, etc.

Recent experiments have shown that repetitive synaptic activation evokes regenerative calcium waves in the apical dendrites of hippocampal CA1 pyramidal neurons. Pharmacological experiments established that these increases are due to Ca2+ released from intracellular stores. The primary mechanism for opening these stores is activation of IP3 receptors by mGluR.

The requirement for repetitive stimulation

resembles one protocol for evoking LTP in these

cells. Our research has shown repetitive

stimulation from 20-100 Hz can induce LTP and

can evoke calcium release from internal store as

well.

15%

F

/F10

mv

1S

100Hz 15 pulses

-burst stimulation, another common protocol used to evoke LTP in pyramidal neurons can also evoke calcium release

30 %

F

/F20

mv

1 S

Stimulating frequency of 5 Hz, a parameter to induce LTD, could not induce the intracellular calcium release.

We hope to know :

What is the function of calcium released from internal store in LTP in CA1 region? 

Whether mGluR can increase the responses of NMDA receptor in LTP and what is the mechanism?

What are effects of mGluR in LTP which is evoked between two neurons?