Kainate receptor activation potentiates GABAergic synaptic transmission in the nucleus accumbens core

• Published in: Brain research 2006-05, Vol.1088 (1), p.73-82
• Main Authors: Crowder, Tara L., Ariwodola, Olusegun J., Weiner, Jeff L.
• Format: Article
• Language: English
• Subjects: Animals; Animals, Newborn; Bicuculline - pharmacology; Biological and medical sciences; Calcium - pharmacology; Central nervous system; Dose-Response Relationship, Drug; Drug Interactions; Electrophysiology; Excitatory Amino Acid Agonists - pharmacology; Excitatory Amino Acid Antagonists - pharmacology; Fundamental and applied biological sciences. Psychology; GABA; GABA Antagonists - pharmacology; gamma-Aminobutyric Acid - metabolism; gamma-Aminobutyric Acid - pharmacology; In Vitro Techniques; IPSC; Kainic Acid - pharmacology; Male; Neural Inhibition - drug effects; Neural Inhibition - physiology; Neurons - drug effects; Neurons - physiology; Nucleus accumbens; Nucleus Accumbens - cytology; Patch-clamp; Patch-Clamp Techniques - methods; Presynaptic; Rats; Rats, Sprague-Dawley; Receptors, Kainic Acid - metabolism; Synaptic transmission; Synaptic Transmission - drug effects; Synaptic Transmission - physiology; Synaptic Transmission - radiation effects; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2005.12.133

Inhibitory synaptic transmission plays an important role in regulating the activity of medium spiny neurons (MSNs) in the nucleus accumbens (NAcc). The kainate (KA) subtype of ionotropic glutamate receptor has been shown to potently modulate GABAergic synaptic transmission in several brain regions. Although KA receptor subunits are expressed in the NAcc, KA receptor modulation of GABAergic synaptic transmission in this brain region has not been previously examined. In the current study, we sought to determine if KA receptor activation could alter inhibitory synaptic transmission in the NAcc as it has been shown to do in other brain regions. Using the whole cell patch-clamp technique, we demonstrate that KA receptor activation potentiates evoked GABAergic synaptic transmission and increases the frequency of spontaneous, but not miniature, GABA A-receptor-mediated IPSCs in the NAcc. In contrast, KA has no effect on currents evoked by exogenous application of GABA onto MSNs. Taken together, these data suggest that activation of KA receptors in the NAcc core potently facilitates action-potential-dependent GABAergic synaptic transmission, likely via an excitation of presynaptic GABAergic interneurons.