| PFC |
1 |
Joffe (88) |
Activation of mGlu3 promotes AMPA receptor internalization on pyramidal cells. LTD occurs at long-range inputs from BLA, but not VH, and does not occur on fast-spiking interneurons. |
|
2 |
Di Menna/Joffe (84) |
mGlu3 enhances mGlu5-mediated signaling, including phosphoinositide production and Ca2+ mobilization. mGlu5 activity is also required for the induction of mGlu LTD. |
|
3 |
Walker (99) |
Genetic deletion of mGlu3, but not mGlu2, blocks LTD induced by group II agonists. Inhibition of mGlu3 disrupts extinction of cued fear. |
|
4 |
Joffe (100) |
mGlu3 LTD does not require the mobilization of intracellular Ca2+ stores. Instead, mGlu3 LTD proceeds through activation of PI3K and Akt. mGlu3 LTD is impaired by acute restraint stress. |
|
5 |
Joffe (97) |
Glutamate release is enhanced by acute application of a group II mGlu receptor antagonist or mGlu2 NAM. Acute application of an mGlu3 NAM does not affect basal release probability. |
|
6 |
Zhang (104) |
Application of a group III mGlu receptor agonist reduces glutamate released by serotonin. The specific mGlu receptor subtype mediating this effect is not known. |
|
7 |
Lafourcade (44) |
Synaptic or pharmacologic stimulation of mGlu5 induces the production of 2-AG. 2-AG activates presynaptic CB1 receptors to induce LTD. |
|
8 |
Cannady (21) |
mGlu5 activation inhibits SK channels, which normally act to inhibit NMDA receptor function. This mechanism promotes the induction of NMDA receptor LTP and extinciton of alcohol seeking. |
| NAC |
9 |
McCutcheon (50) |
mGlu5 induces eCB LTD. Following extended cocaine exposure, mGlu5 function is impaired, and mGlu1 induces postsynaptic PKC-dependent LTD instead. |
|
10 |
Loweth (61) |
Abstinence from cocaine exposure upregulates GluA2-lacking AMPA receptors. Activating mGlu1 depotentiates these synapses and reduces incubation of cocaine craving. |
|
11 |
Turner (51) |
In the NAC shell, mGlu5 induces LTD at MDT inputs onto D1-expressing neurons. In contrast, mGlu1 activation generates LTD at PFC inputs onto both D1(+) and D1(−) MSNs. |
|
12 |
Robbe (86) |
Group II mGlu receptor agonists induce presynaptic LTD. The mechanism involves cAMP, PKA, and the inhibition of P/Q type Ca2+ channels. |
|
13 |
Robbe (48) |
mGlu5 induces canonical eCB LTD through intracellular Ca2+ mobilization and activation of presynaptic CB1 receptors. |
|
14 |
Fourgeaud (98) |
A single administration of cocaine impairs mGlu5 LTD. This impairment requires in vivo activation of D1 and is associated with enhanced Homer expression and mGlu5 internalization. |
|
15 |
Grueter (47) |
In the NAC core, mGlu5 LTD occurs specifically on D2-expressing neurons. AEA is released to activate CB1 as well as postsynaptic TRPV1, which promotes AMPA receptor internalization. |
| BNST |
16 |
Grueter (28, 29) |
Activation of mGlu5 promotes the internalization of AMPA receptors. The mechanism requires the activation of ERK1 and is disrupted by repeated cocaine administration. |
|
17 |
McElligott (30) |
mGlu5 LTD is distinct from LTD induced by aradrenergic receptor activation. mGlu5 LTD does not involve GluA2-lacking AMPA receptors and is not impaired by stress. |
|
18 |
Grueter (113) |
Group II and group III mGlu receptor agonists depress excitatory transmission. Prolonged activation of group II mGu receptors induces LTD. |
|
19 |
Gosnell (112) |
An mGlu8−specific agonist induces a transient depression of excitatory transmission, and mGlu4 does not appear to modulate presynaptic release probability. |
