Mechanisms underlying a thalamocortical transformation during active tactile sensation

During active somatosensation, neural signals expected from movement of the sensors are suppressed in the cortex, whereas information related to touch is enhanced. This tactile suppression underlies low-noise encoding of relevant tactile features and the brain’s ability to make fine tactile discriminations. Layer (L) 4 excitatory neurons in the barrel cortex, the major target of the somatosensory thalamus (VPM), respond to touch, but have low spike rates and low sensitivity to the movement of whiskers. Most neurons in VPM respond to touch and also show an increase in spike rate with whisker movement. Therefore, signals related to self-movement are suppressed in L4. Fast-spiking (FS) interneurons in L4 show similar dynamics to VPM neurons. Stimulation of halorhodopsin in FS interneurons causes a reduction in FS neuron activity and an increase in L4 excitatory neuron activity. This decrease of activity of L4 FS neurons contradicts the "paradoxical effect" predicted in networks stabilized by inhibition and in strongly-coupled networks. To explain these observations, we constructed a model of the L4 circuit, with connectivity constrained by in vitro measurements. The model explores the various synaptic conductance strengths for which L4 FS neurons actively suppress baseline and movement-related activity in layer 4 excitatory neurons. Feedforward inhibition, in concert with recurrent intracortical circuitry, produces tactile suppression. Synaptic delays in feedforward inhibition allow transmission of temporally brief volleys of activity associated with touch. Our model provides a mechanistic explanation of a behavior-related computation implemented by the thalamocortical circuit

Electro-oculographic abnormalities in amblyopia.

BACKGROUND--Electrodiagnostic tests have been used to investigate retinal function in amblyopia but previous results have been conflicting. METHODS--It was decided to investigate whether the electro-oculogram (EOG) showed any abnormalities in 12 adult amblyopes and 12 age and sex matched controls with normal vision. The mean amplitudes of the EOG recordings from each eye during 12 minutes of darkness and 18 minutes of light were compared. RESULTS--The mean values from the amblyopic eyes were lower than those from the fellow non-amblyopic eyes. At most time points the difference was significant (p < 0.05). After normalisation of the data to minimise intersubject variation, the reduction in EOG amplitudes of the amblyopic eyes at all time points was significant (p < 0.05). There was no significant difference between the mean values obtained from the right and left control eyes at any time point, either before or after normalisation. CONCLUSIONS--These results provide evidence for a retinal abnormality in amblyopia and implicate the retinal pigment epithelium as being involved. A deficiency in retinal dopaminergic function in amblyopia is proposed as a possible mechanism causing these results