Related Experiment Video
Updated: Mar 30, 2026

Single Synapse Indicators of Glutamate Release and Uptake in Acute Brain Slices from Normal and Huntington Mice
Published on: March 11, 2020
Interneuronal Nitric Oxide Signaling Mediates Post-synaptic Long-Term Depression of Striatal Glutamatergic Synapses
Igor V Rafalovich1, Alexandria E Melendez1, Joshua L Plotkin2
1Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA.
Abstract:
Experience-driven plasticity of glutamatergic synapses on striatal spiny projection neurons (SPNs) is thought to be essential to goal-directed behavior and habit formation. One major form of striatal plasticity, long-term depression (LTD), has long appeared to be expressed only pre-synaptically. Contrary to this view, nitric oxide (NO) generated by striatal interneurons was found to induce a post-synaptically expressed form of LTD at SPN glutamatergic synapses. This form of LTD was dependent on signaling through guanylyl cyclase and protein kinase G, both of which are abundantly expressed by SPNs. NO-LTD was unaffected by local synaptic activity or antagonism of endocannabinoid (eCb) and dopamine receptors, all of which modulate canonical, pre-synaptic LTD. Moreover, NO signaling disrupted induction of this canonical LTD by inhibiting dendritic Ca(2+) channels regulating eCb synthesis. These results establish an interneuron-dependent, heterosynaptic form of post-synaptic LTD that could act to promote stability of the striatal network during learning.
Related Concept Videos
Long-term Depression
Calcium Ion Concentration Mechanism
If over...
Long-term Depression
Nitric Oxide Signaling Pathway
Long-term Potentiation
Hebbian LTP
LTP can occur when...
Long-term Potentiation
Ligand-Gated Ion Channel Receptor: Gating Mechanism

