Journal of Neurophysiology

Isayama, Reina; Vesia, Michael; Jegatheeswaran, Gaayathiri; Elahi, Behzad; Gunraj, Carolyn A; Cardinali, Lucilla; Farnè, Alessandro; Chen, Robert

doi: 10.1152/jn.00345.2018pmid: 30625001

The rubber hand illusion (RHI) paradigm experimentally produces an illusion of rubber hand ownership and arm shift by simultaneously stroking a rubber hand in view and a participant's visually occluded hand. It involves visual, tactile and proprioceptive multisensory integration and activates multisensory areas in the brain including the posterior parietal cortex (PPC). Multisensory inputs are transformed into outputs for motor control in association areas such as PPC. A behavioural study reported decreased motor performance after RHI. However, it remains unclear whether RHI modifies the interactions between sensory and motor systems, and between PPC and the primary motor cortex (M1). We used transcranial magnetic stimulation (TMS) and examined the functional connections from the primary somatosensory and association cortices to M1, and from PPC to M1 during RHI. In Experiment 1, short-latency afferent inhibition (SAI) and long-latency afferent inhibition (LAI) were measured before and immediately after a synchronous (RHI) or an asynchronous (control) condition. In Experiment 2, PPC-M1 interaction was measured using two coils. We found that SAI and LAI were reduced in the synchronous condition compared to baseline, suggesting that RHI decreased somatosensory processing in the primary sensory and the association cortices projecting to M1. We also found that greater inhibitory PPC-M1 interaction was associated with stronger RHI assessed by questionnaire. Our findings suggest that RHI modulates both the early and late stages of processing of tactile afferent, which leads to altered M1 excitability by reducing the gain of somatosensory afferents to resolve conflicts among multisensory inputs.

Church, Timothy W.; Brown, Jon T; Marrion, Neil V.

doi: 10.1152/jn.00334.2018pmid: 30625002

Action potential firing in hippocampal pyramidal neurons is regulated by generation of an afterhyperpolarization (AHP). Three phases of AHP are recognised, with the fast AHP regulating action potential firing at the onset of a burst, and the medium and slow AHPs supressing action potential firing over 100s of milliseconds and seconds respectively. Activation of β-adrenergic receptors suppresses the slow AHP by a protein kinase A-dependent pathway. However, little is known regarding modulation of the medium AHP. Application of the selective β-adrenergic receptor agonist isoproterenol suppressed both the medium and slow AHPs evoked in rat CA1 hippocampal pyramidal neurons recorded from slices maintained in organotypic culture. Suppression of the slow AHP was mimicked by intracellular application of cAMP, with the suppression of the medium AHP by isoproterenol still being evident in cAMP-dialysed cells. Suppression of both the medium and slow AHPs was antagonised by the β-adrenergic receptor antagonist propranolol. The effect of isoproterenol to suppress the medium AHP was mimicked by two β3-adrenergic receptor agonists: BRL37344 and SR58611A. The medium AHP was mediated by activation of SK and deactivation of H channels at the resting membrane potential. Suppression of the medium AHP by isoproterenol was reduced by pre-treating cells with the H-channel blocker ZD7288. These data suggest that activation of β3-adrenergic receptors inhibits H-channels, which suppresses the medium AHP in CA1 hippocampal neurons by utilising a pathway that is independent of a rise of intracellular cAMP. This finding highlights a potential new target in modulating H-channel activity, and thereby neuronal excitability.