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Volume 16, Number 20, Issue of October 15, 1996 pp. 6592-6600
Copyright ©1996 Society for Neuroscience

Trans-Synaptic Stimulation of Cortical Acetylcholine Release after Partial 192 IgG-Saporin-Induced Loss of Cortical Cholinergic Afferents

Received Feb. 14, 1996; revised July 8, 1996; accepted July 29, 1996.

Jim Fadel, Holly Moore, Martin Sarter, and John P. Bruno

Department of Psychology and Neuroscience Program, The Ohio State University, Columbus, Ohio 43210

Environmental and pharmacological stimulation of cortical acetylcholine (ACh) efflux was determined in rats sustaining partial deafferentation of cortical cholinergic inputs. Rats were bilaterally infused with the selective cholinotoxin 192 IgG-saporin (0.005 µg/0.5 µl/site) into the frontoparietal cortex. In the first experiment, animals were pretrained to associate the onset of darkness with presentation of a palatable fruit cereal reward. The ability of this stimulus to enhance frontoparietal ACh efflux alone, and with the benzodiazepine receptor (BZR) weak inverse agonist ZK 93,426 (1.0 or 5.0 mg/kg, i.p.), was determined in lesioned and sham-lesioned rats. Intracortical infusions of 192 IgG-saporin reduced basal cortical ACh efflux by 47% of sham-lesioned values, consistent with reductions in the density of AChE-positive fibers. In spite of this deafferentation, ZK 93,426 produced a transient potentiation of the cortical ACh efflux induced by the darkness/cereal stimulus similar to that observed in control animals. In the second experiment, the ability of the more efficacious BZR partial inverse agonist FG 7142 (8.0 mg/kg, i.p.) to enhance basal cortical ACh efflux was compared in lesioned and sham-lesioned rats. Again, lesioned rats exhibited an increase comparable to control animals after FG 7142. This drug-induced stimulation of cortical ACh efflux was comparably and completely blocked in both groups by co-perfusion with tetrodotoxin (1.0 µM). These results suggest similarities in the modulation of cortical ACh efflux in intact and partially deafferented rats and indicate the potential of BZR inverse agonists for restoring transmission in animals with partial loss of cortical cholinergic inputs.

Key words: acetylcholine; cortex; lesion; microdialysis; 192 IgG-saporin; benzodazepine receptor; inverse agonist; deafferentation

This article has been cited by other articles:

				J. McGaughy, J. W. Dalley, C. H. Morrison, B. J. Everitt, and T. W. Robbins Selective Behavioral and Neurochemical Effects of Cholinergic Lesions Produced by Intrabasalis Infusions of 192 IgG-Saporin on Attentional Performance in a Five-Choice Serial Reaction Time Task J. Neurosci., March 1, 2002; 22(5): 1905 - 1913. [Abstract] [Full Text] [PDF]

				D. J. Bucci, P. C. Holland, and M. Gallagher Removal of Cholinergic Input to Rat Posterior Parietal Cortex Disrupts Incremental Processing of Conditioned Stimuli J. Neurosci., October 1, 1998; 18(19): 8038 - 8046. [Abstract] [Full Text] [PDF]

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