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This Article Full Text Full Text (PDF) All Versions of this Article: 98/2/681    most recent 00235.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Smith, P. H. Articles by Kowalkowski, A. Search for Related Content PubMed PubMed Citation Articles by Smith, P. H. Articles by Kowalkowski, A.

Cortical and Collicular Inputs to Cells in the Rat Paralaminar Thalamic Nuclei Adjacent to the Medial Geniculate Body

¹Department of Anatomy, University of Wisconsin Medical School–Madison, Madison, Wisconsin; and ²Departments of Biological Sciences and Biomedical Engineering, Purdue University, West Lafayette, Indiana

Submitted 4 March 2007; accepted in final form 25 May 2007

The paralaminar nuclei, including the medial division of the medial geniculate nucleus, surround the auditory thalamus medially and ventrally. This multimodal area receives convergent inputs from auditory, visual, and somatosensory structures and sends divergent outputs to cortical layer 1, amygdala, basal ganglia, and elsewhere. Studies implicate this region in the modulation of cortical 40-Hz oscillations, cortical information binding, and the conditioned fear response. We recently showed that the basic anatomy and intrinsic physiology of paralaminar cells are unlike that of neurons elsewhere in sensory thalamus. Here we evaluate the synaptic inputs to paralaminar cells from the inferior and superior colliculi and the cortex. Combined physiological and anatomical evidence indicates that paralaminar cells receive both excitatory and inhibitory inputs from both colliculi and excitatory cortical inputs. Excitatory inputs from all three sources typically generate small summating EPSPs composed of AMPA and NMDA components and terminate primarily on smaller dendrites and occasionally on dendritic spines. The cortical input shows strong paired-pulse facilitation (PPF), whereas both collicular inputs show weak PPF or paired-pulse depression (PPD). EPSPs of cells with no low-threshold calcium conductance do not evoke a burst response when the cell is hyperpolarized. Longer-latency EPSPs were seen and our evidence indicates that these arise from axon collateral inputs of other synaptically activated paralaminar cells. The inhibitory collicular inputs are GABAergic, activate GABA_A receptors, and terminate on dendrites. Their activation can greatly alter EPSP-generated spike number and timing.