Abstract:
:GABAergic, somatostatin-containing bitufted interneurons in layer 2/3 of rat neocortex are excited via glutamatergic excitatory postsynaptic potentials (EPSPs) by pyramidal neurons located in the same cortical layer. Pair recordings showed that short bursts of backpropagating dendritic action potentials (APs) reduced the amplitude of unitary EPSPs. EPSP depression was dependent on a rise in dendritic [Ca2+]. The effect was blocked by the GABA(B) receptor (GABA(B)-R) antagonist CGP55845A and was mimicked by the GABA(B)-R agonist baclofen. As presynaptic GABA(B)-Rs were activated neither by somatostatin nor by GABA released from axon collaterals of the bitufted cell, we conclude that GABA(B)-Rs were activated by a retrograde messenger, most likely GABA, released from the dendrite. Because synaptic depression was prevented by loading bitufted neurons with GDP-beta-S, it is likely to be caused by exocytotic GABA release from dendrites.
journal_name
Neuronjournal_title
Neuronauthors
Zilberter Y,Kaiser KM,Sakmann Bdoi
10.1016/s0896-6273(00)81044-2subject
Has Abstractpub_date
1999-12-01 00:00:00pages
979-88issue
4eissn
0896-6273issn
1097-4199pii
S0896-6273(00)81044-2journal_volume
24pub_type
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