Short-Term Plasticity during Intrathalamic Augmenting Responses in Decorticated Cats

Abstract

The intrathalamic mechanisms of frequency-dependent augmenting responses were investigated in decorticated cats by means of intracellular recordings from thalamocortical ( TC) neurons in ventrolateral (VL) nucleus, including simultaneous impalements from two TC neurons. Pulse trains (10 Hz) applied to VL nucleus elicited two types of augmenting responses: (1) in 68% of cells, the incremental responses occurred on a progressive depolarization associated with the decrease in IPSPs produced by preceding stimuli in the train; (2) in the remaining cells, progressively growing low-threshold (LT ) responses resulted from the enhancement of Cl Ϫ -dependent IPSPs, giving rise to postinhibitory rebound bursts, followed by a selfsustained sequence of spindle waves. Although in some TC cells the augmenting responses developed from LT responses once the latter reached a given level of depolarization, other neurons displayed augmenting responses immediately after the early antidromic spike that depolarized the neuron to the required level, without an intermediate step of LT rebound. Repeated pulse trains led to a progressive and persistent increase in slow depolarizing responses of TC cells, as well as to a persistent and prolonged decrease in the amplitudes of the IPSPs. On the basis of parallel experiments, we propose that the two types of augmentation in TC cells are a result of contrasting responses of thalamic reticular neurons evoked by repetitive thalamic stimuli: decremental responses, which may account for disinhibition leading to depolarizing responses in TC cells, and incremental responses, explaining the progressive hyperpolarization of TC cells. These data demonstrate that frequency-dependent changes in neuronal excitability are present in the thalamus of a decorticated hemisphere and suggest that short-term plasticity processes in the gateway to the cerebral cortex may decisively influence cortical excitability during repetitive responses.

Intracortical Augmenting Responses in Networks of Reduced Compartmental Models of Tufted Layer 5 Cells

“…9) as well as in earlier experiments (Castro-Alamancos et al 1996a). The model shares several properties with augmentation occurring in thalamic and thalamocortical networks (Bazhenov et al 1998a,b;Steriade et al 1997;Timofeev et al 1998). Simulations in the thalamus point to an instrumental role for low-threshold calcium current I T in two interacting populations (RE and TC) cells.…”

Sensorimotor cortical influences on cuneate nucleus rhythmic activity in the anesthetized cat

“…The spike-and-wave paroxysms at 2-4 Hz may develop from 7-to 14-Hz spindle waves that often occur without apparent discontinuity from sleep oscillations, 53 with the cortex having a leading role in their development. 49 The experimental paroxysms obtained by direct cortical stimulation also began within the same range of frequencies, thus constituting a suitable experimental model.…”

Photic-Induced Sensitization: Acquisition of an Augmenting Spike-Wave Response in the Adult Rat Through Repeated Strobe Exposure

“…The progressive build-up in response to successive flashes early in the strobe train resembles the thalamocortical augmenting response, a rapidly growing enhancement in cortical evoked responses to repetitive electrical stimulation of the thalamus first described by Dempsey and Morison (1943); also see Bazhenov et al 1998a,b;CastroAlamancos and Connors 1996a,b,c;Morison and Dempsey 1943;Steriade and Timofeev 1997). The augmenting response is proposed to be involved in the generation of sleep spindles and pathological thalamocortical oscillations.…”

“…In addition, trains of electrical shocks to the thalamus or cortex produce a form of short-term neuroplasticity, the thalamocortical augmenting response (Bazhenov et al 1998a,b;CastroAlamancos and Connors 1996a-c;Dempsey and Morison 1943;Steriade and Timofeev 1997), which in some cases can lead to self-sustaining paroxysmal activity (Steriade et al 1993). Thus we theorized that trains of intense photic stimulation might be efficacious in inducing neuroplastic change leading to photoparoxysmal activity.…”