Auditory Long Term Potentiation (LTP) with Users of Cochlear Implants

Abstract

Introduction: Long Term Potentiation (LTP) has been documented in hippocampal tissues, both through ex-vivo and non-invasive studies in animals and humans. LTP is accepted as a neural mechanism underlying memory involving hippocampus (Lomo and Bliss, 1973). Clapp, Hamm, Shephard & Taylor (2005) showed rapid pure tone auditory stimulation induces LTP-like effects on N1 of the obligatory cortical auditory evoked potential. Wilson, J. (2011) demonstrated this effect occurs only at a 13 Hz stimulation rate; LTP did not occur at 9 or 15 Hz. Zaehle, Clapp, Hamm, Meyer, and Kirk (2007) presented fMRI evidence supporting induction of auditory LTP; rapid repeated stimulation (tetanus) resulted in increased BOLD (blood-oxygen-level dependent) signal. All three studies suggest auditory LTP could have implications for rehabilitation and objective measurement of auditory plasticity. Aims: Replicate Clapp et al.’s (2005) findings independently using clinical EEG equipment, and investigate if binaural stimulation is necessary for auditory LTP induction. Investigate if tetanic stimulation could be used as a passive auditory rehabilitation therapy for cochlear implant (CI) recipients. Method: Twenty-eight right handed participants with normal hearing (NH) were tested; 12 using binaural stimulation and 16 using monaural (right ear) stimulation. Eight recipients of a right-sided cochlear implant were also assessed behaviourally on divided auditory attention (Brief Test of Attention) and sentence recognition in noise (50% SRT), as well as EEG. Ageand sex-controlled comparisons are presented. Results: Auditory LTP was not evident in either the NH or CI groups, when investigating the N1 obligatory cortical response. A baseline shift for N1 amplitude was evident. The Brief Test of Attention scores for CI are not comparable to standardized scores due to hearing loss; with a wide range of performance. The percentage correct scores are correlated with length of time using a CI (r=0.708, p=0.049). Speech recognition in noise was similarly varied in performance. There was a correlation between speech recognition in noise and N1 amplitude recorded at frontal electrodes. Conclusions: The findings of Clapp et al. (2005) were not replicated, nor was LTP observed with monaural stimulation. Passive exposure to tetanizing auditory stimuli may not induce LTP for N1 in people who use cochlear implants. Attending to the tetanizing stimulus or more lengthy exposure to the tetanising stimulus may be required to reliably induce auditory LTP in human participants with and without hearing loss.