“…This is not only supported by the abolition of the ISO in a subset of extracellular recordings by putative pharmacological GJ blockade but also by the presence of unambiguous spikelets and burstlets in intracellular recordings that are rhythmically modulated on an infra-slow timescale. The presence of these rhythmically modulated spikelets and burstlets fits well with our finding that ISO-modulated HT bursting neurons appear to drive additional cells during α wave epochs and shows that the ongoing infra-slow modulation of α activity that is commonly observed in vivo
[9], [40]–[47] can also be a feature of these oscillations in the isolated thalamus in vitro
[25], [27], [48]. Whilst we cannot completely discount a possible contribution of GJs between non-neuronal cells in these phenomena, these findings overwhelmingly endorse previous suggestions that GJs between TC neurons are an important determinant of local thalamic network activity [25], [27], [49], [50].…”
An increasing number of EEG and resting state fMRI studies in both humans and animals indicate that spontaneous low frequency fluctuations in cerebral activity at <0.1 Hz (infra-slow oscillations, ISOs) represent a fundamental component of brain functioning, being known to correlate with faster neuronal ensemble oscillations, regulate behavioural performance and influence seizure susceptibility. Although these oscillations have been commonly indicated to involve the thalamus their basic cellular mechanisms remain poorly understood. Here we show that various nuclei in the dorsal thalamus in vitro can express a robust ISO at ∼0.005–0.1 Hz that is greatly facilitated by activating metabotropic glutamate receptors (mGluRs) and/or Ach receptors (AchRs). This ISO is a neuronal population phenomenon which modulates faster gap junction (GJ)-dependent network oscillations, and can underlie epileptic activity when AchRs or mGluRs are stimulated excessively. In individual thalamocortical neurons the ISO is primarily shaped by rhythmic, long-lasting hyperpolarizing potentials which reflect the activation of A1 receptors, by ATP-derived adenosine, and subsequent opening of Ba2+-sensitive K+ channels. We argue that this ISO has a likely non-neuronal origin and may contribute to shaping ISOs in the intact brain.
“…This is not only supported by the abolition of the ISO in a subset of extracellular recordings by putative pharmacological GJ blockade but also by the presence of unambiguous spikelets and burstlets in intracellular recordings that are rhythmically modulated on an infra-slow timescale. The presence of these rhythmically modulated spikelets and burstlets fits well with our finding that ISO-modulated HT bursting neurons appear to drive additional cells during α wave epochs and shows that the ongoing infra-slow modulation of α activity that is commonly observed in vivo
[9], [40]–[47] can also be a feature of these oscillations in the isolated thalamus in vitro
[25], [27], [48]. Whilst we cannot completely discount a possible contribution of GJs between non-neuronal cells in these phenomena, these findings overwhelmingly endorse previous suggestions that GJs between TC neurons are an important determinant of local thalamic network activity [25], [27], [49], [50].…”
An increasing number of EEG and resting state fMRI studies in both humans and animals indicate that spontaneous low frequency fluctuations in cerebral activity at <0.1 Hz (infra-slow oscillations, ISOs) represent a fundamental component of brain functioning, being known to correlate with faster neuronal ensemble oscillations, regulate behavioural performance and influence seizure susceptibility. Although these oscillations have been commonly indicated to involve the thalamus their basic cellular mechanisms remain poorly understood. Here we show that various nuclei in the dorsal thalamus in vitro can express a robust ISO at ∼0.005–0.1 Hz that is greatly facilitated by activating metabotropic glutamate receptors (mGluRs) and/or Ach receptors (AchRs). This ISO is a neuronal population phenomenon which modulates faster gap junction (GJ)-dependent network oscillations, and can underlie epileptic activity when AchRs or mGluRs are stimulated excessively. In individual thalamocortical neurons the ISO is primarily shaped by rhythmic, long-lasting hyperpolarizing potentials which reflect the activation of A1 receptors, by ATP-derived adenosine, and subsequent opening of Ba2+-sensitive K+ channels. We argue that this ISO has a likely non-neuronal origin and may contribute to shaping ISOs in the intact brain.
“…The synaptic structure and connectivity are informed from experimental data based on the dorsal thalamic Lateral Geniculate Nucleus (LGNd) (Horn et al, 2000). The input to the model is assumed to be the ensemble membrane potential of pre-synaptic retinal cells ( V ret ) in a resting state with no sensory input and is simulated using a Gaussian white noise (da Silva et al, 1973). The TCR cells make AMPA receptor mediated glutamatergic synapses on the TRN cells (other types of glutamatergic receptors are ignored in this work for brevity); the TRN cells make GABA-ergic synapses on the TCR cells mediated by both the ligand-gated GABA A and the secondary-messenger-gated GABA B receptors.…”
Section: Methodsmentioning
confidence: 99%
“…The model behavior is observed to be consistent with these studies (von Krosigk et al, 1993; Golomb et al, 1996)—The post synaptic membrane conductance in both the thalamocortical relay (TCR) and thalamic reticular nucleus (TRN) cell population plays a role in effecting a bifurcation in model behavior from spindling mode [oscillations with the characteristic waxing-and-waning pattern seen in early stages of sleep (Steriade et al, 1993; Hughes et al, 2004) as well as in alpha rhythmic oscillations during resting brain state (da Silva et al, 1973)] to a limit-cycle mode (synchronized oscillations as seen in later stages of sleep or during absence seizures). The post-synaptic membrane conductance for both AMPA and GABA in the TRN cell population is responsible for sustaining and modulating spindle oscillations in the model output.…”
A novel direction to existing neural mass modeling technique is proposed where the commonly used “alpha function” for representing synaptic transmission is replaced by a kinetic framework of neurotransmitter and receptor dynamics. The aim is to underpin neuro-transmission dynamics associated with abnormal brain rhythms commonly observed in neurological and psychiatric disorders. An existing thalamocortical neural mass model is modified by using the kinetic framework for modeling synaptic transmission mediated by glutamatergic and GABA (gamma-aminobutyric-acid)-ergic receptors. The model output is compared qualitatively with existing literature on in vitro experimental studies of ferret thalamic slices, as well as on single-neuron-level model based studies of neuro-receptor and transmitter dynamics in the thalamocortical tissue. The results are consistent with these studies: the activation of ligand-gated GABA receptors is essential for generation of spindle waves in the model, while blocking this pathway leads to low-frequency synchronized oscillations such as observed in slow-wave sleep; the frequency of spindle oscillations increase with increased levels of post-synaptic membrane conductance for AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic-acid) receptors, and blocking this pathway effects a quiescent model output. In terms of computational efficiency, the simulation time is improved by a factor of 10 compared to a similar neural mass model based on alpha functions. This implies a dramatic improvement in computational resources for large-scale network simulation using this model. Thus, the model provides a platform for correlating high-level brain oscillatory activity with low-level synaptic attributes, and makes a significant contribution toward advancements in current neural mass modeling paradigm as a potential computational tool to better the understanding of brain oscillations in sickness and in health.
“…Yingling and Skinner (1977) considered the role of the RN essential for the production of spontaneous rhythmic activity. However, the coherence between alpha waves recorded in neighboring cortical areas is larger than the thalamo-cortical coherence (Lopes da Silva, van Lierop, Schrijer & Storm van Leeuwen, 1973). Yet the pulvinar plays an important role in the generation of alpha activity.…”
Anticipatory behavior reveals itself in the perceptual domain and in the motor domain. Expectant attention and motor preparation are characterized by selection, aimed at an amelioration of the signal-to-noise ratio in the information to be processed. The functional similarity of anticipatory attention and motor preparation is re¯ected in the underlying anatomical substrate. The prefrontal cortex, involved in a number of dierent networks, organizes anticipatory behavior in a top-down way by activating cortico-cortical loops and thalamo-cortical loops to sensory and motor areas. The sensory areas are set to receive the impinging stimulus presentation, the motor areas are set to implement and execute the different motor programs. Thalamic nuclei are also activated from the prefrontal cortex, especially the large association nuclei, the dorsomedial nucleus and the pulvinar. In dierent models of selective attention the reticular nucleus of the thalamus has a special role in the distribution of the inhibitory control upon the information processing in the``relay'' nuclei. It is hypothesized that it has the same pivotal position in motor preparation. Although the anatomical relations do not allow a direct test of the proposed hypothesis, the available psychophysiological evidence does not contradict it. Ó
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