Active Dendritic Integration of Inhibitory Synaptic Inputs In Vivo

• Published in: Journal of neurophysiology 2003-12, Vol.90 (6), p.3617-3624
• Main Authors: Kuo, Jason J, Lee, Robert H, Johnson, Michael D, Heckman, Heather M, Heckman, C. J
• Format: Article
• Language: English
• Subjects: Animals; Biogenic Monoamines - physiology; Cats; Dendrites - physiology; Electric Stimulation; Electrophysiology; Ion Channels - physiology; Motor Neurons - physiology; Patch-Clamp Techniques; Spinal Cord - physiology; Synapses - physiology
• ISSN: 0022-3077; 1522-1598
• DOI: 10.1152/jn.00521.2003

1 Department of Physiology, 2 Department of Physical Medicine and Rehabilitation, and 3 Institute for Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611; and 4 Department of Biomedical Engineering, Emory University, Atlanta, Georgia 30322 Submitted 30 May 2003; accepted in final form 18 August 2003 Synaptic integration in vivo often involves activation of many afferent inputs whose firing patterns modulate over time. In spinal motoneurons, sustained excitatory inputs undergo enormous enhancement due to persistent inward currents (PICs) that are generated primarily in the dendrites and are dependent on monoaminergic neuromodulatory input from the brain stem to the spinal cord. We measured the interaction between dendritic PICs and inhibition generated by tonic electrical stimulation of nerves to antagonist muscles during voltage clamp in motoneurons in the lumbar spinal cord of the cat. Separate samples of cells were obtained for two different states of monoaminergic input: standard (provided by the decerebrate preparation, which has tonic activity in monoaminergic axons) and minimal (the chloralose anesthetized preparation, which lacks tonic monoaminergic input). In the standard state, steady inhibition that increased the input conductance of the motoneurons by an average of 38% reduced the PIC by 69%. The range of this reduction, from 100%, was proportional to the magnitude of the applied inhibition. Thus nearly linear integration of synaptic inhibition may occur in these highly active dendrites. In the minimal state, PICs were much smaller, being approximately equal to inhibition-suppressed PICs in the standard state. Inhibition did not further reduce these already small PICs. Overall, these results demonstrate that inhibition from local spinal circuits can oppose the facilitation of dendritic PICs by descending monoaminergic inputs. As a result, local inhibition may also suppress active dendritic integration of excitatory inputs. Address for reprint requests and other correspondence: C. J. Heckman, Physiology, M211, Northwestern Univ. School of Medicine, 303 E. Chicago Ave., Chicago, IL 60611 (E-mail: c-heckman{at}northwestern.edu ).