scholarly journals Somatostatin-Expressing Interneurons Co-Release GABA and Glutamate onto Different Postsynaptic Targets in the Striatum

2019 ◽  
Author(s):  
Stefano Cattaneo ◽  
Mattia Ripamonti ◽  
Francesco Bedogni ◽  
Alessandro Sessa ◽  
Stefano Taverna

SummaryThe functional contribution of somatostatin-expressing interneurons (SST-INs) to the synaptic organization of the striatum is poorly understood. Using electrophysiological recordings, optogenetic stimulation, and single-cell PCR analysis, we investigated functional patterns of synaptic connectivity in striatal SST-INs expressing channelrhodopsin-2. Photostimulation of these cells induced both glutamatergic excitatory postsynaptic currents (EPSCs) and GABAergic inhibitory postsynaptic currents (IPSCs) in striatal spiny projection neurons (SPNs) and fast-spiking interneurons (FSIs). The two synaptic components showed equally fast onset latencies, suggesting a mechanism of co-transmission. Accordingly, single-cell PCR analysis revealed that individual striatal SST-INs expressed mRNAs for both glutamate and GABA vesicular transporters (VGLUT1 and VGAT, respectively). During relatively prolonged optical stimuli (0.5-1s), IPSC arrays consistently outlasted EPSCs. As a result, photostimulation of SST-INs caused a transient burst of action potentials followed by a prolonged inhibition in postsynaptic cells.These data suggest that striatal SST-INs are specialized to locally project synapses exerting a composite excitatory and inhibitory effect through GABA/glutamate co-transmission onto different postsynaptic targets.

Immunity ◽  
1996 ◽  
Vol 4 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Janet L. Maryanski ◽  
C.Victor Jongeneel ◽  
Philipp Bucher ◽  
Jean-Laurent Casanova ◽  
Paul R. Walker

2006 ◽  
Vol 59 (2) ◽  
pp. 104-114 ◽  
Author(s):  
T. Yuasa ◽  
O. Takahashi ◽  
J.K. Dolven ◽  
S. Mayama ◽  
A. Matsuoka ◽  
...  

2010 ◽  
Vol 32 (3) ◽  
pp. 247-254 ◽  
Author(s):  
Seung-Won Jung ◽  
Chang-Soo Kim ◽  
Jae-Won Yoo ◽  
Young-Ok Kim ◽  
Jin-Hwan Lee ◽  
...  

2000 ◽  
Vol 156 (3) ◽  
pp. 1067-1071 ◽  
Author(s):  
Axel Roers ◽  
Martin Leo Hansmann ◽  
Klaus Rajewsky ◽  
Ralf Küppers

1999 ◽  
Vol 36 (11-12) ◽  
pp. 745-753 ◽  
Author(s):  
Janet L Maryanski ◽  
Valérie Attuil ◽  
Philipp Bucher ◽  
Paul R Walker

2014 ◽  
Vol 307 (6) ◽  
pp. C508-C520 ◽  
Author(s):  
Max F. Oginsky ◽  
Ningren Cui ◽  
Weiwei Zhong ◽  
Christopher M. Johnson ◽  
Chun Jiang

Rett syndrome is an autism-spectrum disorder resulting from mutations to the X-linked gene, methyl-CpG binding protein 2 (MeCP2), which causes abnormalities in many systems. It is possible that the body may develop certain compensatory mechanisms to alleviate the abnormalities. The norepinephrine system originating mainly in the locus coeruleus (LC) is defective in Rett syndrome and Mecp2-null mice. LC neurons are subject to modulation by GABA, glutamate, and acetylcholine (ACh), providing an ideal system to test the compensatory hypothesis. Here we show evidence for potential compensatory modulation of LC neurons by post- and presynaptic ACh inputs. We found that the postsynaptic currents of nicotinic ACh receptors (nAChR) were smaller in amplitude and longer in decay time in the Mecp2-null mice than in the wild type. Single-cell PCR analysis showed a decrease in the expression of α3-, α4-, α7-, and β3-subunits and an increase in the α5- and α6-subunits in the mutant mice. The α5-subunit was present in many of the LC neurons with slow-decay nAChR currents. The nicotinic modulation of spontaneous GABAA-ergic inhibitory postsynaptic currents in LC neurons was enhanced in Mecp2-null mice. In contrast, the nAChR manipulation of glutamatergic input to LC neurons was unaffected in both groups of mice. Our current-clamp studies showed that the modulation of LC neurons by ACh input was reduced moderately in Mecp2-null mice, despite the major decrease in nAChR currents, suggesting possible compensatory processes may take place, thus reducing the defects to a lesser extent in LC neurons.


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