Different temporal processing of sensory inputs in the rat thalamus during quiescent and information processing states in vivo

Sensory inputs from the whiskers reach the primary somatosensory thalamus through the medial lemniscus tract. The main role of the thalamus is to relay these sensory inputs to the neocortex according to the regulations dictated by behavioural state. Intracellular recordings in urethane-anaesthetized rats show that whisker stimulation evokes EPSP-IPSP sequences in thalamic neurons. Both EPSPs and IPSPs depress with repetitive whisker stimulation at frequencies above 2 Hz. Single-unit recordings reveal that during quiescent states thalamic responses to repetitive whisker stimulation are suppressed at frequencies above 2 Hz, so that only low-frequency sensory stimulation is relayed to the neocortex. In contrast, during activated states, induced by stimulation of the brainstem reticular formation or application of acetylcholine in the thalamus, high-frequency whisker stimulation at up to 40 Hz is relayed to the neocortex. Sensory suppression is caused by the depression of lemniscal EPSPs in relatively hyperpolarized thalamocortical neurons. Sensory suppression is abolished during activated states because thalamocortical neurons depolarize and the depressed lemniscal EPSPs are able to reach firing threshold. Strong IPSPs may also contribute to sensory suppression by hyperpolarizing thalamocortical neurons, but during activated states IPSPs are strongly reduced altogether. The results indicate that the synaptic depression of lemniscal EPSPs and the level of depolarization of thalamocortical neurons work together in thalamic primary sensory pathways to suppress high-frequency sensory inputs during non-activated (quiescent) states while permitting the faithful relay of high-frequency sensory information during activated (processing) states.     

Synaptic properties of thalamic and intracortical inputs to layer 4 of the first- and higher-order cortical areas in the auditory and somatosensory systems

The thalamus is an essential structure in the mammalian forebrain conveying information topographically from the sensory periphery to primary neocortical areas. Beyond this initial processing stage, "higher-order" thalamocortical connections have been presumed to serve only a modulatory role, or are otherwise functionally disregarded. Here we demonstrate that these "higher-order" thalamic nuclei share similar synaptic properties with the "first-order" thalamic nuclei. Using whole cell recordings from layer 4 neurons in thalamocortical slice preparations in the mouse somatosensory and auditory systems, we found that electrical stimulation in all thalamic nuclei elicited large, glutamatergic excitatory postsynaptic potentials (EPSPs) that depress in response to repetitive stimulation and that fail to activate a metabotropic glutamate response. In contrast, the intracortical inputs from layer 6 to layer 4 exhibit facilitating EPSPs. These data suggest that higher-order thalamocortical projections may serve a functional role similar to the first-order nuclei, whereas both are physiologically distinct from the intracortical layer 6 inputs. These results suggest an alternate route for information transfer between cortical areas via a corticothalamocortical pathway.     

High-pass filtering of corticothalamic activity by neuromodulators released in the thalamus during arousal: in vitro and in vivo

The thalamus is the principal relay station of sensory information to the neocortex. In return, the neocortex sends a massive feedback projection back to the thalamus. The thalamus also receives neuromodulatory inputs from the brain stem reticular formation, which is vigorously activated during arousal. We investigated the effects of two neuromodulators, acetylcholine and norepinephrine, on corticothalamic responses in vitro and in vivo. Results from rodent slices in vitro showed that acetylcholine and norepinephrine depress the efficacy of corticothalamic synapses while enhancing their frequency-dependent facilitation. This produces a stronger depression of low-frequency responses than of high-frequency responses. The effects of acetylcholine and norepinephrine were mimicked by muscarinic and alpha(2)-adrenergic receptor agonists and blocked by muscarinic and alpha-adrenergic antagonists, respectively. Stimulation of the brain stem reticular formation in vivo also strongly depressed corticothalamic responses. The suppression was very strong for low-frequency responses, which do not produce synaptic facilitation, but absent for high-frequency corticothalamic responses. As in vitro, application of muscarinic and alpha-adrenergic antagonists into the thalamus in vivo abolished the suppression of corticothalamic responses induced by stimulating the reticular formation. In conclusion, cholinergic and noradrenergic activation during arousal high-pass filters corticothalamic activity. Thus, during arousal only high-frequency inputs from the neocortex are allowed to reach the thalamus. Neuromodulators acting on corticothalamic synapses gate the flow of cortical activity to the thalamus as dictated by behavioral state.     

Synapse- and subtype-specific modulation of synaptic transmission by nicotinic acetylcholine receptors in the ventrobasal thalamus

The rodent thalamic ventrobasal complex (VB) which is a subdivision of somatosensory thalamus receives two excitatory inputs through the medial lemniscal synapse, which is a sensory afferent synapse, and the corticothalamic synapse from layer VI of the somatosensory cortex. In addition, the VB also receives cholinergic inputs from the brain stem, and nicotinic acetylcholine receptors (nAChRs) are highly expressed in the VB. Little is known, however, how acetylcholine (ACh) modulates synaptic transmission at the medial lemniscal and corticothalamic synapses in the VB. Furthermore, it remains unclear which subtype of nAChRs contributes to VB synaptic transmission. We report here that the activation of nAChRs presynaptically depressed corticothalamic synaptic transmission, whereas it did not affect medial lemniscal synaptic transmission in juvenile mice. This presynaptic modulation was mediated by the activation of nAChRs that contained α4 and β2 subunit, but not by α7 nAChRs. Moreover, galanthamine, an allosteric modulator of α4β2α5 nAChR, enhanced the ACh-induced depression of corticothalamic excitatory postsynaptic currents (EPSCs), indicating that α4β2α5 nAChRs at corticothalamic axon terminals specifically contribute to the depression of corticothalamic synaptic transmission.     

Contrary roles of kainate receptors in transmitter release at corticothalamic synapses onto thalamic relay and reticular neurons

Corticothalamic fibres, which originate from layer VI pyramidal neurons in the cerebral cortex, provide excitatory synaptic inputs to both thalamic relay neurons and reticular neurons; reticular neurons in turn supply inhibitory inputs to thalamic relay neurons. Pyramidal cells in layer VI in the mouse somatosensory cortex highly express mRNA encoding kainate receptors, which facilitate or depress transmitter release at several synapses in the central nervous system. We report here that contrary modulation of transmitter release from corticothalamic fibres onto thalamic relay and reticular neurons is mediated by activation of kainate receptors in mouse thalamic ventrobasal complex and thalamic reticular nucleus. Exogenous kainate presynaptically depresses the synaptic transmission at corticothalamic synapses onto thalamic relay neurons, but facilitates it at corticothalamic synapses onto reticular neurons. Meanwhile, the lemniscal synaptic transmission, which sends primary somatosensory inputs to relay neurons, is not affected by kainate. In addition, GluR5-containing kainate receptors are involved in the depression of corticothalamic synaptic transmission onto relay neurons, but not onto reticular neurons. Furthermore, synaptically activated kainate receptors mimic these effects; high-frequency stimulation of corticothalamic fibres depresses synaptic transmission onto relay neurons, but facilitates it onto reticular neurons. Our results suggest that the opposite sensitivity of kainate receptors at the two corticothalamic synapses is governed by cortical activity and regulates the balance of excitatory and inhibitory inputs to thalamic relay neurons and therefore their excitability.     

Synaptic properties of thalamic input to layers 2/3 and 4 of primary somatosensory and auditory cortices

We studied the synaptic profile of thalamic inputs to cells in layers 2/3 and 4 of primary somatosensory (S1) and auditory (A1) cortices using thalamocortical slices from mice age postnatal days 10-18. Stimulation of the ventral posterior medial nucleus (VPM) or ventral division of the medial geniculate body (MGBv) resulted in two distinct classes of responses. The response of all layer 4 cells and a minority of layers 2/3 cells to thalamic stimulation was Class 1, including paired-pulse depression, all-or-none responses, and the absence of a metabotropic component. On the other hand, the majority of neurons in layers 2/3 showed a markedly different, Class 2 response to thalamic stimulation: paired-pulse facilitation, graded responses, and a metabotropic component. The Class 1 and Class 2 response characteristics have been previously seen in inputs to thalamus and have been described as drivers and modulators, respectively. Driver input constitutes a main information bearing pathway and determines the receptive field properties of the postsynaptic neuron, whereas modulator input influences the response properties of the postsynaptic neuron but is not a primary information bearing input. Because these thalamocortical projections have comparable properties to the drivers and modulators in thalamus, we suggest that a driver/modulator distinction may also apply to thalamocortical projections. In addition, our data suggest that thalamus is likely to be more than just a simple relay of information and may be directly modulating cortex.     

Auditory thalamocortical transmission is reliable and temporally precise

We have used the auditory thalamocortical slice to characterize thalamocortical transmission in primary auditory cortex (ACx) of the juvenile mouse. "Minimal" stimulation was used to activate medial geniculate neurons during whole cell recordings from regular-spiking (RS cells; mostly pyramidal) and fast-spiking (FS, putative inhibitory) neurons in ACx layers 3 and 4. Excitatory postsynaptic potentials (EPSPs) were considered monosynaptic (thalamocortical) if they met three criteria: low onset latency variability (jitter), little change in latency with increased stimulus intensity, and little change in latency during a high-frequency tetanus. Thalamocortical EPSPs were reliable (probability of postsynaptic responses to stimulation was approximately 1.0) as well as temporally precise (low jitter). Both RS and FS neurons received thalamocortical input, but EPSPs in FS cells had faster rise times, shorter latencies to peak amplitude, and shorter durations than EPSPs in RS cells. Thalamocortical EPSPs depressed during repetitive stimulation at rates (2-300 Hz) consistent with thalamic spike rates in vivo, but at stimulation rates > or = 40 Hz, EPSPs also summed to activate N-methyl-D-aspartate receptors and trigger long-lasting polysynaptic activity. We conclude that thalamic inputs to excitatory and inhibitory neurons in ACx activate reliable and temporally precise monosynaptic EPSPs that in vivo may contribute to the precise timing of acoustic-evoked responses.     

Different composition of glutamate receptors in corticothalamic and lemniscal synaptic responses and their roles in the firing responses of ventrobasal thalamic neurons in juvenile mice

Thalamic ventrobasal (VB) relay neurons receive information via two major types of glutamatergic synapses, that is, from the medial lemniscus (lemniscal synapses) and primary somatosensory cortex (corticothalamic synapses). These two synapses influence and coordinate firing responses of VB neurons, but their precise operational mechanisms are not yet well understood. In this study, we compared the composition of glutamate receptors and synaptic properties of corticothalamic and lemniscal synapses. We found that the relative contribution of NMDA receptor-mediated excitatory postsynaptic currents (EPSCs) to non-NMDA receptor-mediated EPSCs was significantly greater in corticothalamic synapses than in lemniscal synapses. Furthermore, NMDA receptor 2B-containing NMDA receptor- and kainate receptor-mediated currents were observed only in corticothalamic synapses, but not in lemniscal synapses. EPSCs in corticothalamic synapses displayed the postsynaptic summation in a frequency-dependent manner, in which the summation of the NMDA receptor-mediated component was largely involved. The summation of kainate receptor-mediated currents also partially contributed to the postsynaptic summation in corticothalamic synapses. In contrast, the contribution of NMDA receptor-mediated currents to the postsynaptic summation of lemniscal EPSCs was relatively minor. Furthermore, our results indicated that the prominent NMDA receptor-mediated component in corticothalamic synapses was the key determinant for the late-persistent firing of VB neurons in response to corticothalamic stimuli. In lemniscal synapses, in contrast, the onset-transient firing in response to lemniscal stimuli was regulated mainly by AMPA receptors.     

Long-term potentiation of thalamic input to the motor cortex induced by coactivation of thalamocortical and corticocortical afferents

1. Intracellular recordings were obtained from neurons in the motor cortex (MCx), in which excitatory postsynaptic potentials (EPSPs) were evoked by microstimulation of the somatosensory cortex (SCx) and the ventrolateral nucleus (VL) of the thalamus. The effects of combined tetanic stimulation of SCx and VL on the amplitudes of these EPSPs were studied. 2. Amplitudes of both corticocortical (CC) and thalamocortical (TC) EPSPs were potentiated after combined tetanic stimulation. This potentiation occurred exclusively in neurons that were located in the superficial layers (II/III) and that received direct input from both the SCx and VL, with both inputs synapsing in close proximity to each other. In all cases, the potentiation lasted until the electrode went out of the cell (21 +/- 25 min, mean +/- SD) the longest being 90 min. We therefore refer to this potentiation as long-term potentiation (LTP). 3. Tetanic stimulation of the thalamus only did not produce LTP in neurons receiving direct input from the VL. 4. LTP was not induced in either CC or TC EPSPs in neurons located in layer V and/or in neurons receiving long-latency CC EPSPs. 5. It is concluded that TC input from the VL to the MCx is potentiated only when coactivated with the CC input from the SCx.     

Distinct properties of corticothalamic and primary sensory synapses to thalamic neurons

An unique synaptic feature of thalamic relay neurons is that, in addition to receiving primary sensory synapses, they receive massive feedback synapses originating from the cerebral cortex (corticothalamic synapses). These two synapses are both glutamatergic and coordinate the firing responses of thalamic neurons. It has been revealed in the past decade that various glutamate receptors are involved in synaptic responses in the thalamus. However, differences in the compositions of glutamate receptors between corticothalamic and primary sensory synapses have not been fully determined. This update article aims to provide an overview of the differences in the synaptic properties, including the compositions of glutamate receptors, between primary sensory and corticothalamic synapses in the ventrobasal nucleus of the somatosensory thalamus, and then elucidate how these differences in the two synapses influence the firing properties of thalamic neurons.     

Distinct properties of corticothalamic and primary sensory synapses to thalamic neurons

An unique synaptic feature of thalamic relay neurons is that, in addition to receiving primary sensory synapses, they receive massive feedback synapses originating from the cerebral cortex (corticothalamic synapses). These two synapses are both glutamatergic and coordinate the firing responses of thalamic neurons. It has been revealed in the past decade that various glutamate receptors are involved in synaptic responses in the thalamus. However, differences in the compositions of glutamate receptors between corticothalamic and primary sensory synapses have not been fully determined. This update article aims to provide an overview of the differences in the synaptic properties, including the compositions of glutamate receptors, between primary sensory and corticothalamic synapses in the ventrobasal nucleus of the somatosensory thalamus, and then elucidate how these differences in the two synapses influence the firing properties of thalamic neurons.     

Somatostatin inhibits GABAergic transmission in the sensory thalamus via presynaptic receptors

The action of somatostatin on GABA-mediated transmission was investigated in cat and rat thalamocortical neurons of the dorsal lateral geniculate nucleus and ventrobasal thalamus in vitro. In the cat thalamus, somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons and on the postsynaptic response elicited in these cells by bath or iontophoretic application of (+/-)baclofen (5-10 microM) or GABA, respectively. However, somatostatin (1-10 microM) decreased by a similar amount (45-55%) the amplitude of electrically evoked GABA(A) and GABA(B) inhibitory postsynaptic potentials in 71 and 50% of neurons in the lateral geniculate and ventrobasal nucleus, respectively. In addition, the neuropeptide abolished spontaneous bursts of GABA(A) inhibitory postsynaptic potentials in 85% of kitten lateral geniculate neurons, and decreased (40%) the amplitude of single spontaneous GABA(A) inhibitory postsynaptic potentials in 87% of neurons in the cat lateral geniculate nucleus. Similar results were obtained in the rat thalamus. Somatostatin (10 microM) had no effect on the passive membrane properties of thalamocortical neurons in this species, or on the outward current elicited by puff-application of (+/-)baclofen (5-10 microM). However, in 57 and 22% of neurons in the rat lateral geniculate and ventrobasal nuclei, respectively, somatostatin (1 microM) reduced the frequency, but not the amplitude, of miniature GABA(A) inhibitory postsynaptic currents by 31 and 37%, respectively. In addition, the neuropeptide (1 microM) decreased the amplitude of evoked GABA(A) inhibitory postsynaptic currents in 20 and 55% of rat ventrobasal neurons recorded in normal conditions and during enhanced excitability, respectively: this effect was stronger on bursts of inhibitory postsynaptic currents(100% decrease) than on single inhibitory postsynaptic currents (41% decrease).These results demonstrate that in the sensory thalamus somatostatin inhibits GABA(A)- and GABA(B)-mediated transmission via a presynaptic mechanism, and its action is more prominent on bursts of GABAergic synaptic currents/potentials.     

Electrophysiological properties and input-output organization of callosal neurons in cat association cortex

Intracellular recordings from association cortical areas 5 and 7 were performed in cats under barbiturate or ketamine-xylazine anesthesia to investigate the activities of different classes of neurons involved in callosal pathways, which were electrophysiologically characterized by depolarizing current steps. Excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs), and/or antidromic responses were elicited by stimulating homotopic sites in the contralateral cortical areas. Differential features of EPSPs related to latencies, amplitudes, and slopes were detected in closely located (50 microm or less) neurons recorded in succession along the same electrode track. In contrast to synchronous thalamocortical volleys that excited most neurons within a cortical column, stimuli applied to homotopic sites in the contralateral cortex activated neurons at restricted cortical depths. Median latencies of callosally evoked EPSPs were 1.5 to 4 ms in various cortical cell-classes. Fast-rhythmic-bursting neurons displayed EPSPs whose amplitudes were threefold larger, and latencies two- or threefold shorter, than those found in the three other cellular classes. Converging callosal and thalamic inputs were recorded in the same cortical neuron. EPSPs or IPSPs were elicited by stimulating foci spaced by <1 mm in the contralateral cortex. In the overwhelming majority of neurons, latencies of antidromic responses were between 1.2 and 3.1 ms; however, some callosal neurons had much longer latencies, 相似文献   

Nicotinic control of axon excitability regulates thalamocortical transmission

The thalamocortical pathway, a bundle of myelinated axons that arises from thalamic relay neurons, carries sensory information to the neocortex. Because axon excitation is an obligatory step in the relay of information from the thalamus to the cortex, it represents a potential point of control. We now show that, in adult mice, the activation of nicotinic acetylcholine receptors (nAChRs) in the initial portion of the auditory thalamocortical pathway modulates thalamocortical transmission of information by regulating axon excitability. Exogenous nicotine enhanced the probability and synchrony of evoked action potential discharges along thalamocortical axons in vitro, but had little effect on synaptic release mechanisms. In vivo, the blockade of nAChRs in the thalamocortical pathway reduced sound-evoked cortical responses, especially those evoked by sounds near the acoustic threshold. These data indicate that endogenous acetylcholine activates nAChRs in the thalamocortical pathway to lower the threshold for thalamocortical transmission and to increase the magnitude of sensory-evoked cortical responses. Our results show that a neurotransmitter can modulate sensory processing by regulating conduction along myelinated thalamocortical axons.     

Modulation of lemniscal input during conditioned arm movements in the monkey

Summary Modulation of sensory transmission in the lemniscal system was investigated in 2 monkeys trained to perform a simple elbow flexion in response to an auditory cue. Evoked responses to peripheral stimulation were recorded in the medial lemniscus, sensory thalamus (ventral posterior lateral nucleus, caudal division, VPLc) and somatosensory cortex. Simultaneous recordings were made from the cortex and either the medial lemniscus or VPLc. At all recording sites, evoked responses to natural (air puff) or electrical, percutaneous stimulation were depressed prior to and during active movement. The time course of the depression was similar at all three levels; the magnitude of the decrease during movement was most pronounced at the cortical level. Cortical evoked responses to central stimulation of effective sites in either the medial lemniscus or VPLc were decreased during, but not before, the onset of movement. The decrease was less than that seen for peripheral evoked potentials. Passive movement of the forearm significantly decreased all but the lemniscal evoked potential. The results indicate that there is a centrally mediated suppression of somatosensory transmission prior to, and during movement, occurring at the level of the first relay, the dorsal column nuclei. During movement, reafferent signals from the moving arm decrease transmission at the thalamocortical level.     

Thalamocortical conduction times and stimulus-evoked responses in the rat whisker-to-barrel system

Studies of the rodent whisker system indicate that somatosensory cortical circuitry operates at a millisecond timescale to transform sensory afferent signals from the thalamus. We measured axon conduction times and whisker-evoked responses of 48 thalamocortical (TC) neurons in the rat whisker-to-barrel pathway. Conduction times were derived from spike-triggered averages of local field potentials evoked in layer 4 cortical whisker-related barrels by the spontaneous firing of individual topographically aligned neurons in the ventral posterior medial thalamus. Conduction times varied fourfold, from 0.31 to 1.34 ms, and faster conducting TC neurons responded earlier and more robustly to controlled whisker deflections. Early arrival of highly responsive TC inputs, thought to contact inhibitory barrel neurons preferentially, could prime the cortical network, rendering it more selective for later-arriving signals.     

Dynamics of sensory thalamocortical synaptic networks during information processing states

The thalamocortical network consists of the pathways that interconnect the thalamus and neocortex, including thalamic sensory afferents, corticothalamic and thalamocortical pathways. These pathways are essential to acquire, analyze, store and retrieve sensory information. However, sensory information processing mostly occurs during behavioral arousal, when activity in thalamus and neocortex consists of an electrographic sign of low amplitude fast activity, known as activation, which is caused by several neuromodulator systems that project to the thalamocortical network. Logically, in order to understand how the thalamocortical network processes sensory information it is essential to study its response properties during states of activation. This paper reviews the temporal and spatial response properties of synaptic pathways in the whisker thalamocortical network of rodents during activated states as compared to quiescent (non-activated) states. The evidence shows that these pathways are differentially regulated via the effects of neuromodulators as behavioral contingencies demand. Thus, during activated states, the temporal and spatial response properties of pathways in the thalamocortical network are transformed to allow the processing of sensory information.     

A reanalysis of the ventrolateral input in slow and fast pyramidal tract neurons of the cat motor cortex

In deeply anesthetized cats the temporal characteristics of ventro-lateral (thalamic) excitatory postsynaptic potentials (EPSPs) induced in pyramidal tract cells were studied with an averaging technique. Stimulation of the ventrolateral thalamus induced EPSPs in all pyramidal tract neurons at latencies of 1–5 ms. It was found that there was a positive relationship between the latency and rise time of stimulation-induced EPSPs and the latency of antidromic invasions of pyramidal tract neurons. In response to two closely spaced shocks the second EPSP had the same latency and amplitude as the first one in both slow and fast pyramidal tract neurons. Moreover, the span of antidromic latencies of ventrolateral thalamic relay cells to motor cortex stimulation showed that these thalamic neurons had the necessary conduction velocities to account for the distribution of EPSP latencies recorded in pyramidal tract neurons. From these electrophysiological results, it has been concluded that slow and fast pyramidal tract neurons receive a monosynaptic input from neurons in the ventrolateral thalamus. We also report morphological evidence, obtained at the electron-microscopic level, supporting this conclusion. Terminal degeneration induced by a lesion in the ventrolateral thalamus was found on the apical dendrite of a slow pyramidal tract neuron that had been injected with horseradish peroxidase.It is proposed that the matching between the latencies of EPSPs evoked from the ventrolateral thalamus and the latencies of antidromic invasions of pyramidal tract neurons may reflect a matching between the conduction velocity of thalamocortical and cortico-spinal neurons and/or it may be due to the electrotonic properties of the apical dendrites.     

Developmental refinement in the mammalian thalamus

The sensory relay synapses in the thalamus undergo extensive refinement during early life. Disruptions of spontaneous activity, but not sensory deprivation, can induce large-scale re-organization of neuronal connections in the thalamus. Recent studies also reveal an extended period of synaptic refinement in the visual and somatosensory relay synapses, where sensory deprivation produces some unexpected effects on synaptic remodeling. This article aims to provide a brief overview of recent findings and current ideas about the refinement of relay synapses in the thalamus.     

Synaptic interactions between thalamic and cortical inputs onto cortical neurons in vivo

To study the interactions between thalamic and cortical inputs onto neocortical neurons, we used paired-pulse stimulation (PPS) of thalamic and cortical inputs as well as PPS of two cortical or two thalamic inputs that converged, at different time intervals, onto intracellularly recorded cortical and thalamocortical neurons in anesthetized cats. PPS of homosynaptic cortico-cortical pathways produced facilitation, depression, or no significant effects in cortical pathways, whereas cortical responses to thalamocortical inputs were mostly facilitated at both short and long intervals. By contrast, heterosynaptic interactions between either cortical and thalamic, or thalamic and cortical, inputs generally produced decreases in the peak amplitudes and depolarization area of evoked excitatory postsynaptic potentials (EPSPs), with maximal effect at approximately 10 ms and lasting from 60 to 100 ms. All neurons tested with thalamic followed by cortical stimuli showed a decrease in the apparent input resistance (R(in)), the time course of which paralleled that of decreased responses, suggesting that shunting is the factor accounting for EPSP's decrease. Only half of neurons tested with cortical followed by thalamic stimuli displayed changes in R(in). Spike shunting in the thalamus may account for those cases in which decreased synaptic responsiveness of cortical neurons was not associated with decreased R(in) because thalamocortical neurons showed decreased firing probability during cortical stimulation. These results suggest a short-lasting but strong shunting between thalamocortical and cortical inputs onto cortical neurons.