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Kopell, N.

Publications and source records attributed to Kopell, N..

9 recordsLinked to original sources

Awake alpha bursting emerges as the dynamic working state in a lateral geniculate thalamocortical cell model

The awake thalamus is known to be able to filter primary sensory input with and without external modulation. Through the construction and analysis of a novel computational model of a lateral geniculate thalamocortical neuron, we demonstrate how the processing of sensory retinal input is influenced by the underlying thalamic dynamic state. Our model, using only currents verified against expression data from publicly available datasets, is the first to produce five experimentally established distinct dynamic firing regimes. We demonstrate that the thalamocortical cell transitions between these dynamic states in response to glutamatergic signals from the cortex or cholinergic arousal signals coming from the brainstem. We focus on signal processing in the model dynamic states associated with the awake thalamic alpha rhythm where we find that the ability of retinal inputs to generate thalamic spikes is a balance between the timing of retinal spikes, the excitability break imposed by the M-current, and the decay time of the L-type calcium current. Finally, we explore how these two currents help the thalamus process extra-retinal rhythmic inputs, showing the model produces entrainment to slower inhibitory and excitatory rhythms, as well as detailing the importance of nesting faster frequency rhythms within slow cycles for successful thalamic transmission. Our results suggest that the awake alpha rhythm is indirectly causal by acting as a marker for the interaction of these two currents. This biophysically-constrained lateral geniculate thalamocortical cell model generates predictions regarding rhythmic dynamics under different arousal states, thalamic control of retinogeniculate transmission, and the possible impacts neurological disorders, like schizophrenia, have on thalamic processing. Variations of this model could be used to explore the functions of higher order thalamic nuclei, thereby extending its use to investigating more complex cognitive processes. Author summaryThe thalamus generates multiple distinct brain rhythms, processes primary sensory inputs, and modulates its output using feedback signals. Previous computational models of the thalamus have typically focused on a subset of these three thalamic functions without drawing relationships among them. Here we present a novel computational thalamic cell model that unites these thalamic processes. We focus on the awake alpha rhythm, a well known thalamic oscillation, and show that it is a signature of a critical working state that enables the experimentally observed thalamic filtering of retinal signals. Additionally, we find this state is optimal for processing and passing non-sensory rhythmic signals. Our model generates testable predictions about which ionic currents control the transmission of external signals. It highlights the roles of two currents from our model that do not have specified functions in the awake thalamus in previous computational models. The work concludes with hypotheses about why neurological disorders that perturb the thalamus from this alpha rhythm working state lead to significant processing errors locally within the thalamus and globally within the brain.

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Ketamine can produce oscillatory dynamics by engaging mechanisms dependent on the kinetics of NMDA receptors

Ketamine is an NMDA-receptor antagonist that produces sedation, analgesia and dissociation at low doses and profound unconsciousness with antinociception at high doses. At high and low doses, ketamine can generate gamma oscillations (>25 Hz) in the electroencephalogram (EEG). The gamma oscillations are interrupted by slow-delta oscillations (0.1-4 Hz) at high doses. Ketamines primary molecular targets and its oscillatory dynamics have been characterized. However, how the actions of ketamine at the subcellular level give rise to the oscillatory dynamics observed at the network level remains unknown. By developing a biophysical model of cortical circuits, we demonstrate how NMDA-receptor antagonism by ketamine can produce the oscillatory dynamics observed in human EEG recordings and non-human primate local field potential recordings. We have discovered how impaired NMDA-receptor kinetics can cause disinhibition in neuronal circuits and how a disinhibited interaction between NMDA-receptor-mediated excitation and GABA-receptor-mediated inhibition can produce gamma oscillations at high and low doses, and slow-delta oscillations at high doses. Our work uncovers general mechanisms for generating oscillatory brain dynamics that differs from ones previously reported, and provides important insights into ketamines mechanisms of action as an anesthetic and as a therapy for treatment-resistant depression.

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Basolateral amygdala oscillations enable fear learning in a biophysical model

The basolateral amygdala (BLA) is a key site where fear learning takes place through synaptic plasticity. Rodent research shows prominent low theta ([~]3-6 Hz), high theta ([~]6-12 Hz), and gamma (>30 Hz) rhythms in the BLA local field potential recordings. However, it is not understood what role these rhythms play in supporting the plasticity. Here, we create a biophysically detailed model of the BLA circuit to show that several classes of interneurons (PV, SOM, and VIP) in the BLA can be critically involved in producing the rhythms; these rhythms promote the formation of a dedicated fear circuit shaped through spike-timing-dependent plasticity. Each class of interneurons is necessary for the plasticity. We find that the low theta rhythm is a biomarker of successful fear conditioning. The model makes use of interneurons commonly found in the cortex and, hence, may apply to a wide variety of associative learning situations. SignificanceOur paper accounts for the experimental evidence showing that amygdalar rhythms exist, suggests network origins for these rhythms, and points to their central role in the mechanisms of plasticity involved in associative learning. It is one of the few papers to address high-order cognition with biophysically detailed models, which are sometimes thought to be too detailed to be adequately constrained. Our paper provides a template for how to use information about brain rhythms to constrain biophysical models. It shows in detail, for the first time, how multiple interneurons help to provide time scales necessary for some kinds of spike-timing-dependent plasticity (STDP). It spells out the conditions under which such interactions between interneurons are needed for STDP and why. Finally, our work helps to provide a framework by which some of the discrepancies in the fear learning literature might be reevaluated. In particular, we discuss issues about Hebbian plasticity in fear learning; we show in the context of our model how neuromodulation might resolve some of those issues. The model addresses issues more general than that of fear learning since it is based on interactions of interneurons that are prominent in the cortex, as well as the amygdala.

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Neuromodulation due to propofol affects anesthetic oscillatory coupling

Propofol-mediated unconsciousness elicits strong alpha/low-beta and slow oscillations in the electroencephalogram (EEG) of patients. As anesthetic dose increases, the EEG signal changes in ways that give clues to the level of unconsciousness; the network mechanisms of these changes are only partially understood. Here, we construct a biophysical thalamocortical network involving brainstem influences that reproduces transitions in dynamics seen in the EEG involving the evolution of the power and frequency of alpha/low beta and slow rhythm, as well as their interactions. Our model suggests propofol engages thalamic spindle and cortical sleep mechanisms to elicit persistent alpha/low-beta and slow rhythms, respectively. The thalamocortical network fluctuates between two mutually exclusive states on the timescale of seconds. One state is characterized by continuous alpha/low-beta frequency spiking in thalamus (C-state), while in the other, thalamic alpha spiking is interrupted by periods of co-occurring thalamic and cortical silence (I-state). In the I-state, alpha co-localizes to the peak of the slow; in the C-state, there is a variable relationship between an alpha/beta rhythm and the slow oscillation. The C-state predominates near loss of consciousness; with increasing dose, the proportion of time spent in the I-state increases, recapitulating EEG phenomenology. Cortical synchrony drives the switch to the I-state by changing the nature of the thalamocortical feedback. Brainstem influence on the strength of thalamocortical feedback mediates the amount of cortical synchrony. Our model implicates loss of low-beta, cortical synchrony, and coordinated thalamocortical silent periods as contributing to the unconscious state. New & NoteworthyGABAergic anesthetics induce alpha/low-beta and slow oscillations in the EEG, which interact in dose-dependent ways. We construct a thalamocortical model to investigate how these interdependent oscillations change with propofol dose. We find two dynamic states of thalamocortical coordination, which change on the timescale of seconds and dose-dependently mirror known changes in EEG. Thalamocortical feedback determines the oscillatory coupling and power seen in each state, and this is primarily driven by cortical synchrony and brainstem neuromodulation.

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Deep brain stimulation in the subthalamic nucleus for Parkinson's disease can restore dynamics of striatal networks

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is highly effective in alleviating movement disability in patients with Parkinsons disease (PD). However, its therapeutic mechanism of action is unknown. The healthy striatum exhibits rich dynamics resulting from an interaction of beta, gamma and theta oscillations. These rhythms are at the heart of selection, initiation and execution of motor programs, and their loss or exaggeration due to dopamine (DA) depletion in PD is a major source of the behavioral deficits observed in PD patients. Interrupting abnormal rhythms and restoring the interaction of rhythms as observed in the healthy striatum may then be instrumental in the therapeutic action of DBS. We develop a biophysical networked model of a BG pathway to study how abnormal beta oscillations can emerge throughout the BG in PD, and how DBS can restore normal beta, gamma and theta striatal rhythms. Our model incorporates STN projections to the striatum, long known but understudied, that were recently shown to preferentially target fast spiking interneurons (FSI) in the striatum. We find that DBS in STN is able to normalize striatal medium spiny neuron (MSN) activity by recruiting FSI dynamics, and restoring the inhibitory potency of FSIs observed in normal condition. We also find that DBS allows the re-expression of gamma and theta rhythms, thought to be dependent on high DA levels and thus lost in PD, through cortical noise control. Our study shows how BG connectivity can amplify beta oscillations, and delineates the role of DBS in disrupting beta oscillations and providing corrective input to STN efferents to restore healthy striatal dynamics. It also suggests how gamma oscillations can be leveraged to enhance or supplement DBS treatment and improve its effectiveness.

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Layer and rhythm specificity for predictive routing

In predictive coding, experience generates predictions that attenuate the feeding forward of predicted stimuli while passing forward unpredicted "errors". Different models have different neural implementations of predictive coding. We recorded spikes and local field potentials from laminar electrodes in five cortical areas (V4, LIP, area 7A, FEF, and PFC) while monkeys performed a task that modulated visual stimulus predictability. Pre-stimulus predictions were associated with increased alpha/beta (8-30 Hz) power/coherence that fed back the cortical hierarchy primarily via deep-layer cortex. Unpredictable stimuli were associated with increases in spiking and in gamma-band (40-90 Hz) power/coherence that fed forward up the cortical hierarchy via superficial-layer cortex. Area 7A uniquely showed increases in high-beta (~22-28 Hz) power/coherence to unpredicted stimuli. These results suggest that predictive coding may be implemented via lower-frequency alpha/beta rhythms that "prepare" pathways processing predicted inputs by inhibiting feedforward gamma rhythms and associated spiking.

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Constraints on Persistent Activity in a Biologically Detailed Network Model of the Prefrontal Cortex with Heterogeneities

Persistent activity, the maintenance of neural activation over short periods of time in cortical networks, is widely thought to underlie the cognitive function of working memory. A large body of modeling studies has reproduced this kind of activity using cell assemblies with strengthened synaptic connections. However, almost all of these studies have considered persistent activity within networks with homogeneous neurons and synapses, making it difficult to judge the validity of such model results for cortical dynamics, which is based on highly heterogeneous neurons. Here, we consider persistent activity in a detailed, strongly data-driven network model of the prefrontal cortex with heterogeneous neuron and synapse parameters. Surprisingly, persistent activity could not be reproduced in this model without incorporating further constraints. We identified three factors that prevent successful persistent activity: heterogeneity in the cell parameters of interneurons, heterogeneity in the parameters of short-term synaptic plasticity and heterogeneity in the synaptic weights. Our model predicts that persistent activity is recovered if the heterogeneity in the activity of individual interneurons is diminished, which could be achieved by a homeostatic plasticity mechanism. Such a plasticity scheme could also compensate the heterogeneities in the synaptic weights and short-term plasticity when applied to the inhibitory synapses. Cell assemblies shaped in this way may be potentially targeted by distinct inputs or become more responsive to specific tuning or spectral properties. Furthermore, the model predicts that a network that exhibits persistent activity is not able to dynamically produce intrinsic in vivo-like irregular activity at the same time, because heterogeneous synaptic connections are required for these dynamics. Thus, the background noise in such a network must either be produced by external input or constitutes an entirely different state of the network, which is brought about, e.g., by neuromodulation.\n\nAuthor summaryTo operate effectively in a constantly changing world, it is crucial to keep relevant information in mind for short periods of time. This ability, called working memory, is commonly assumed to rest on reverberating activity among members of cell assemblies. While effective in reproducing key results of working memory, most cell assembly models rest on major simplifications such as using the same parameters for all neurons and synapses, i.e., assuming homogeneity in these parameters. Here, we show that this homogeneity assumption is necessary for persistent activity to arise, specifically for inhibitory interneurons and synapses. Using a strongly data-driven network model of the prefrontal cortex, we show that the heterogeneities in the above parameters that are implied by in vitro studies prevent persistent activity. When homogeneity is imposed on inhibitory neurons and synapses, persistent activity is recovered. We propose that the homogeneity constraints can be implemented in the brain by means of homeostatic plasticity, a form of learning that keeps the activity of a network in a constant, homeostatic state. The model makes a number of predictions for biological networks, including a structural separation of networks responsible for generating persistent activity and spontaneous, noise-like activity.

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Muscarinic receptors regulate auditory and prefrontal cortical communication during auditory processing

Much of our understanding about how acetylcholine modulates prefrontal cortical (PFC) networks comes from behavioral experiments that examine cortical dynamics during highly attentive states. However, much less is known about how PFC is recruited during passive sensory processing and how acetylcholine may regulate connectivity between cortical areas outside of task performance. To investigate the involvement of PFC and cholinergic neuromodulation in passive auditory processing, we performed simultaneous recordings in the auditory cortex (AC) and PFC in awake head fixed mice presented with a white noise auditory stimulus in the presence or absence of local cholinergic antagonists in AC. We found that a subset of PFC neurons were strongly driven by auditory stimuli even when the stimulus had no associative meaning, suggesting PFC monitors stimuli under passive conditions. We also found that cholinergic signaling in AC shapes the strength of auditory driven response in PFC, by modulating the intra-cortical sensory response through muscarinic interactions in AC. Taken together, these findings provide novel evidence that cholinergic mechanisms have a continuous role in cortical gating through muscarinic receptors during passive processing and expand traditional views of prefrontal cortical function and the contributions of cholinergic modulation in sensory gating.\n\nHighlightsO_LIPrefrontal cortex actively monitors non-associative stimuli under passive conditions\nC_LIO_LIAcetylcholine facilitates cortical signaling even outside of attentional contexts\nC_LIO_LILocal scopolamine infusion reduced intracortical signaling and impaired cortical gating\nC_LIO_LImAChR have an ongoing role in sound processing\nC_LI

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Biased competition in the absence of input bias: predictions from corticostriatal computation

Classical accounts of biased competition (BC) require an input bias to resolve the competition between neuronal ensembles driving downstream processing. However, flexible and reliable selection of behaviorally-relevant ensembles can occur with unbiased stimulation: striatal D1 and D2 spiny projecting neurons (SPNs) receive balanced cortical input, yet their activity determines the choice between GO and NO-GO pathways in the basal ganglia. We present a corticostriatal model identifying three mechanisms that rely on physiological asymmetries to effect rate- and time-coded BC in the presence of balanced inputs. First, tonic input strength determines which SPN phenotype exhibit higher mean firing rate (FR). Second, low strength oscillatory inputs induce higher FR in D2 SPNs but higher coherence between D1 SPNs. Third, high strength inputs oscillating at distinct frequencies preferentially activate D1 or D2 SPN populations. Of these mechanisms, the latter accommodates observed rhythmic activity supporting rule-based decision making in prefrontal cortex.

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