We have recorded intracellularly from pairs of neurons less than 500 microm distant from one another in V1 of anesthetized cats. Cross-correlation of spontaneous fluctuations in membrane potential revealed significant correlations between the cells in each pair. This synchronization was not dependent on the occurrence of action potentials, indicating that it was not caused by mutual interconnections. The cells were synchronized continuously rather than for brief epochs. Much weaker correlations were found between the EEG and intracellular potentials, suggesting local, rather than global, synchrony. The highest correlation occurred among cells with similar connectivity from the LGN and similar receptive fields. During visual stimulation, correlations increased when both cells responded to the stimulus and decreased when neither cell responded.

. We used a juvenile mouse thalamocortical slice preparation with whole cell recording to investigate synaptic properties of corticothalamic inputs from somatosensory cortex to the ventral posterior medial and posterior medial nuclei (98 cells). We compared these data to those obtained from activating retinal and cortical inputs to the lateral geniculate nucleus (8 cells), the former representing a prototypical driver input and the latter, a typical modulator. Retinogeniculate activation evoked large, all-or-none excitatory postsynaptic potentials (EPSPs) that showed paired-pulse depression antagonized by N-methyl-D-aspartate (NMDA) and AMPA receptor blockers but with no sign of a metabotropic glutamate receptor (mGluR) component. Corticogeniculate activation evoked small, graded EPSPs showing paired-pulse facilitation, and the EPSPs showed both NMDA and AMPA receptor component plus an mGluR1 component. In the somatosensory thalamic relays, cortical stimulation elicited glutamatergic EPSPs in all thalamic cells, and these EPSPs fell into two groups. One, elicited from cortical layer 6 to cells of both nuclei, involved small, graded EPSPs with paired-pulse facilitation, and most also showed an mGluR1 component. The other, elicited from layer 5 to cells only of the posterior medial nucleus, involved large, all-ornone EPSPs with paired-pulse depression, and none showed an mGluR component. By analogy with results from the lateral geniculate nucleus, we conclude that the input from layer 6 to both nuclei acts as a modulator but that the layer 5 input to the posterior medial nucleus serves as a driver. Our data extend a common organizing principle from first-order nuclei to higher-order thalamic relays and further implicate the latter in corticocortical communication. I N T R O D U C T I O NGuillery and Sherman have recently proposed that thalamic relays can be divided into two types: first order and higher order Sherman and Guillery 2001, 2002). First-order relays represent the first transmission to cortex of particular type of information from the periphery, and higher-order relays serve to transmit information between cortical areas via a cortico-thalamo-cortical route. Examples of the former are the lateral geniculate nucleus for vision (relaying retinal input) and the ventral posterior nucleus for somesthesis (relaying medial lemniscal input); examples of the latter are most or all of pulvinar for vision and the posterior medial nucleus for somesthesis.A key to this hypothesis is identifying the information actually relayed through thalamus. To do so, Guillery and Sherman have divided inputs to relay cells into drivers, which bring the information to be relayed, and modulators, which serve to modulate thalamic transmission of the driver input (Sherman and Guillery 1998, 2001). Examples of the former are the retinal and medial lemniscal input to the lateral geniculate nucleus and ventral posterior nucleus, respectively. Examples of the latter are brain stem cholinergic inputs from the parabrachial region and feed...

Membrane potentials of cortical neurons fluctuate between a hyperpolarized ('down') state and a depolarized ('up') state which may be separated by up to 30 mV, reflecting rapid but infrequent transitions between two patterns of synaptic input. Here we show that such fluctuations may contribute to representation of visual stimuli by cortical cells. In complex cells of anesthetized cats, where such fluctuations are most prominent, prolonged visual stimulation increased the probability of the up state. This probability increase was related to stimulus strength: its dependence on stimulus orientation and contrast matched each cell's averaged membrane potential. Thus large fluctuations in membrane potential are not simply noise on which visual responses are superimposed, but may provide a substrate for encoding sensory information.

Relay neurons of the lateral geniculate nucleus innervate visual cortex, but they also provide axonal collaterals to neurons in the thalamic reticular nucleus, and these thalamic reticular neurons provide feedback inhibition to relay cells. An alternative source of inhibitory inputs onto geniculate relay neurons arises from intralaminar interneurons that provide feedforward inhibition via retinogeniculate innervation, and perhaps feedback inhibition via the corticothalamic pathway, analogous to that involving thalamic reticular neurons. Several reports indicate that relay neurons may also give rise to axonal collaterals within the lateral geniculate nucleus, constituting another route for feedback or local integration. We now provide new data indicating that collaterals from geniculate relay neurons provide excitatory input to local intralaminar interneurons and that this pathway may serve as a previously unknown means of local feedback inhibition. This circuitry could prove important in such activities as surround inhibition of receptive fields or increasing signal gain over noise.