Enhanced cholinergic suppression of previously strengthened synapses enables the formation of self-organized representations in olfactory cortex.
Computational modeling assists in analyzing the specific functional role of the cellular effects of acetylcholine within cortical structures. In particular, acetylcholine may regulate the dynamics of encoding and retrieval of information by regulating the magnitude of synaptic transmission at excitatory recurrent connections. Many abstract models of associative memory function ignore the influence of changes in synaptic strength during the storage process and apply the effect of these changes only during a so-called recall-phase. Efforts to ensure stable activity with more realistic, continuous updating of the synaptic strength during the storage process have shown that the memory capacity of a realistic cortical network can be greatly enhanced if cholinergic modulation blocks transmission at synaptic connections of the association fibers during the learning process. We here present experimental data from an olfactory cortex brain slice preparation showing that previously potentiated fibers show significantly greater suppression (presynaptic inhibition) by the cholinergic agonist carbachol than unpotentiated fibers. We conclude that low suppression of non-potentiated fibers during the learning process ensures the formation of self-organized representations in the neural network while the higher suppression of previously potentiated fibers minimizes interference between overlapping patterns. We show in a computational model of olfactory cortex, that, together, these two phenomena reduce the overlap between patterns that are stored within the same neural network structure. These results further demonstrate the contribution of acetylcholine to mechanisms of cortical plasticity. The results are consistent with the extensive evidence supporting a role for acetylcholine in encoding of new memories and enhancement of response to salient sensory stimuli.
Linster
Christiane
C
Department of Psychology Center for Memory and Brain and Program in Neuroscience, Boston University, 2 Cummington Street, Boston, MA 02215, USA. CL243@cornell.edu
Maloney
Michaella
M
Patil
Madhvi
M
Hasselmo
Michael E
ME
D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000008:administration & dosage / Q000494:pharmacology; D006801:Humans; D016571:Neural Networks, Computer; D009833:Olfactory Pathways / Q000187:drug effects / Q000378:metabolism*; D018091:Receptors, AMPA / Q000378:metabolism; D011950:Receptors, Cholinergic / Q000187:drug effects / Q000378:metabolism*; D018079:Receptors, GABA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D013569:Synapses / Q000187:drug effects / Q000378:metabolism*
D018679:Cholinergic Agonists; D018091:Receptors, AMPA; D011950:Receptors, Cholinergic; D018079:Receptors, GABA; D016194:Receptors, N-Methyl-D-Aspartate; D002217:Carbachol