The Cellular Mechanisms Underlying Olfaction Deficit Induced Cross-modal Plasticity In Whisker Tactile

Objective: This study is to investigate the cellular mechanisms underlying the cross-modal plasticity of barrel cortex induced by olfactory input deficit, in which we mainlyfocus on comparing the functional changes of pyramidal neurons in barrel cortex A5-E1and C9-E4corresponding to long and short whiskers.Methods：1. The animal model of cross-modal plasticity: The mice were devided intotwo groups, control and olfactory dysfunction. The olfactory tactile inputs were blockedby damaging olfactory epithelia with chloroform (10ul/g) that was dropped on the topsurface of left nasal cavity in postnatal days (PND)12mice. Seven days after the injuryof olfactory epithelia, the presence of the cross-modal plasticity in whisker tactile wastested by monitoring the behavior of whiskers under a digital video camera, in whichthe whisking frequency was analyzed to identify the functional status of whisker tactile.2. Patch-clamp experiments: Mice after the injury of olfactory epithelia for a week wereanesthetized by isoflurane. The cerebral cortex was quickly isolated, and the corticalslices (400m) were cut. The barrel cortex in our studies was divided into areas A5-E1and C9-E4that receive tactile inputs from long and short whiskers, respectively. Theslices were then held in oxygenated artificial cerebrospinal fluid (ACSF) at25C for1~2hours. A slice was transferred to a submersion chamber and perfused with theoxygenated ACSF at31C. By an Axoclamp-200B amplifier, we recorded the intrinsicproperties of sequential spikes, such as inter-spike intervals and threshold potentials, atbarrel pyramidal neurons under DIC microscopy (Nikon E600FN). Electrical signalswere acquired with Clampex10.2and analyzed with Clampfit10.2.Results:1. Compared with controls, the whisking frequency in the mice with olfactoryinjury was significantly increased, especially longer whiskers (P<0.05).2. The ability offiring spikes at barrel pyramidal neurons is significantly higher in mice with olfactorydysfunction than those in control (P<0.05), especially the upregulation of the neurons inarea A5-E1of barrel cortex that receives tactile inputs from longer whiskers (P<0.05).There is no stastistical difference between control C9-E4and control A5-E1.Conclusion:1.The functional upregulation of pyramidal neurons in barrel cortex is associated with the cross-modal plasticity of whiker tactile induced by olfaction deficit.2. The cross-modal plasticity of whisker tactile and barrel pyramidal neurons mainlyoccurs in longer whiskers and their inputted area A5-E1.