GABAergic Circuitry in the Dorsal Division of the Cat Medial Geniculate Nucleus DIANA L. COOMES, MARTHA E. BICKFORD, AND BRETT R. SCHOFIELD * Department of Anatomical Sciences and Neurobiology, University of Louisville, Louisville, Kentucky 40202 ABSTRACT -Aminobutyric acid (GABA) is the main inhibitory neurotransmitter of the thalamus. We used postembedding immunocytochemistry to examine the synaptic organization of GABA-positive profiles in the dorsal superficial subdivision of the cat medial geniculate nucleus (MGN). Three groups of GABA-positive profiles participate in synapses: axon termi- nals, dendrites, and presynaptic dendrites. The presynaptic GABA-positive terminals target mainly GABA-negative dendrites. The GABA-positive postsynaptic profiles receive input primarily from GABA-negative axons. The results indicate that the synaptic organization of GABA-positive profiles in the dorsal superficial subdivision of the MGN nucleus is very similar to that in other thalamic nuclei. J. Comp. Neurol. 453:45–56, 2002. © 2002 Wiley-Liss, Inc. Indexing terms: auditory system; thalamus; inhibition; neuroanatomy; electron microscopy With the exception of olfaction, all sensory signals must pass through the dorsal thalamus en route to cortex. The convergence of a wide variety of inputs to the thalamus can amplify or dampen the response to ascending sensory signals. This allows the thalamus to regulate the transfer of sensory information to the cortex. -Aminobutyric acid (GABA)-ergic interneurons are one of the most important influences on thalamic activity. In the cat, interneurons constitute 20 –35% of the thalamic cells (LeVay and Ferster, 1979; Weber and Kalil, 1983; Madarasz et al., 1985; Huang et al., 1999). In the lateral geniculate nucleus (LGN) and ventroposterior nucleus (VP), the dendrites of interneurons receive ascending sen- sory input and form dendrodendritic connections with thalamocortical cells. This arrangement is thought to me- diate a “feed-forward” inhibition of thalamocortical cells (Ralston, 1971; Famiglietti and Peters, 1972; Dubin and Cleland, 1977). In other nuclei, such as the pulvinar and lateral posterior nucleus, interneurons are contacted by descending cortical inputs and may modulate the transfer of information from one cortical area to another through dendrodendritic connections with thalamocortical cells (Bickford et al., 1999; Carden and Bickford, 2002). Although striking similarities have been found in the overall organization of dorsal thalamic nuclei (Jones, 1985; Sherman and Guillery, 2001), relatively little is known concerning the GABAergic circuitry of the auditory thalamus. The presence of interneurons in the medial geniculate nucleus (MGN) has been known since Ramo ´n y Cajal’s time (1909). Immunocytochemical studies have supported the idea that interneurons are GABAergic (Winer and Larue, 1988; Winer, 1991; Huang et al., 1999). Electron microscopic studies have examined presumptive interneurons (Majorossy and Re ´thelyi, 1968; Jones and Rockel, 1971; Morest, 1971, 1975; Majorossy and Kiss, 1976a,b), but these studies were limited by a lack of GABA labeling. Together, the electron microscopic and immuno- cytochemical studies clearly identify interneurons as a source of GABA inputs to MGN cells. A second source of GABA in the auditory thalamus originates from GABAergic neurons of the thalamic retic- ular nucleus (TRN; Shosaku and Sumitomo, 1983). In the visual and somatosensory thalamus, TRN projections con- tact primarily thalamocortical cells (Liu et al., 1995; Wang et al., 2001). In these nuclei, collaterals of the relay cells activate the TRN, thus providing a circuit for feedback Grant sponsor: National Institute of Health; Grant number: DC04391; Grant number: DC05277; Grant sponsor: NINDS; Grant number: 35377. *Correspondence to: Brett R. Schofield, Department of Anatomical Sci- ences and Neurobiology, University of Louisville, 500 S. Preston St., Lou- isville, KY 40202. E-mail: brscho01@gwise.louisville.edu Received 3 April 2002; Revised 16 May 2002; Accepted 27 June 2002 DOI 10.1002/cne.10387 Published online the week of September 16, 2002 in Wiley InterScience (www.interscience.wiley.com). THE JOURNAL OF COMPARATIVE NEUROLOGY 453:45–56 (2002) © 2002 WILEY-LISS, INC.