Pacemaker Oscillations Research Articles

Chimera Patterns of Synchrony in a Frustrated Array of Hebb Synapses.

The union of the Kuramoto–Sakaguchi model and the Hebb dynamics reproduces the Lisman switch through a bistability in synchronized states. Here, we show that, within certain ranges of the frustration parameter, the chimera pattern can emerge, causing a different, time-evolving, distribution in the Hebbian synaptic strengths. We study the stability range of the chimera as a function of the frustration (phase-lag) parameter. Depending on the range of the frustration, two different types of chimeras can appear spontaneously, i.e., from randomized initial conditions. In the first type, the oscillators in the coherent region rotate, on average, slower than those in the incoherent region; while in the second type, the average rotational frequencies of the two regions are reversed, i.e., the coherent region runs, on average, faster than the incoherent region. We also show that non-stationary behavior at finite N can be controlled by adjusting the natural frequency of a single pacemaker oscillator. By slowly cycling the frequency of the pacemaker, we observe hysteresis in the system. Finally, we discuss how we can have a model for learning and memory.

Remote pacemaker control of chimera states in multilayer networks of neurons.

Networks of coupled nonlinear oscillators allow for the formation of nontrivial partially synchronized spatiotemporal patterns, such as chimera states, in which there are coexisting coherent (synchronized) and incoherent (desynchronized) domains. These complementary domains form spontaneously, and it is impossible to predict where the synchronized group will be positioned within the network. Therefore, possible ways to control the spatial position of the coherent and incoherent groups forming the chimera states are of high current interest. In this work we investigate how to control chimera patterns in multiplex networks of FitzHugh-Nagumo neurons, and in particular we want to prove that it is possible to remotely control chimera states exploiting the multiplex structure. We introduce a pacemaker oscillator within the network: this is an oscillator that does not receive input from the rest of the network but is sending out information to its neighbors. The pacemakers can be positioned in one or both layers. Their presence breaks the spatial symmetry of the layer in which they are introduced and allows us to control the position of the incoherent domain. We demonstrate how the remote control is possible for both uni- and bidirectional coupling between the layers. Furthermore we show which are the limitations of our control mechanisms when it is generalized from single-layer to multilayer networks.

Controlling chimera states via minimal coupling modification.

We propose a method to control chimera states in a ring-shaped network of nonlocally coupled phase oscillators. This method acts exclusively on the network's connectivity. Using the idea of a pacemaker oscillator, we investigate which is the minimal action needed to control chimeras. We implement the pacemaker choosing one oscillator and making its links unidirectional. Our results show that a pacemaker induces chimeras for parameters and initial conditions for which they do not form spontaneously. Furthermore, the pacemaker attracts the incoherent part of the chimera state, thus controlling its position. Beyond that, we find that these control effects can be achieved with modifications of the network's connectivity that are less invasive than a pacemaker, namely, the minimal action of just modifying the strength of one connection allows one to control chimeras.

Genetic and epigeneticregulations of mammalian circadian rhythms.

The circadian clocks are vital to many organisms for their survival and adaption to the surrounding environment. More and more people are interested in the circadian clock and related researches. One of the key characteristics of this endogenous clock is its periodicity. Mechanisms underlying the mammalian circadian rhythms with ~24 h periodicity involve interlocked transcriptional and translational feedback loops. The circadian clock system in mammals consists of hierarchical structures, with the suprachiasmatic nucleus (SCN) as the central pacemaker and peripheral oscillators in other organs. In spite of the central and peripheral oscillators, the molecular mechanisms are the same within the SCN and peripheral organs. In the past decades, major achievements are accomplished by using forward and reverse genetics, as well as epigenetic approaches. In this review, we recapitulate the history of how clock-related genes were identified, and summarize the main achievements in genetics and epigenetics to understand the molecular underpinnings. We hope it can offer basic knowledge for further researches, a reference for experimental designs aiming to adjust organisms' homeostasis by modulating the clock, and provide a foundation to build interdisciplinary research networks.

La cronodisrupción como causa de envejecimiento

Modern life leads to a more active nocturnal lifestyle, reduced sleep hours and sometimes abrupt shifts across time zones (such as jet lag and shift work) that generate chronodisruption (CD) which can result in premature ageing. CD is defined as a significant disturbance of the internal temporal order of biochemical, physiological and behavioural circadian rhythms. Epidemiological studies show that CD induced by shift work, chronic jet lag, social jet lag and excessive exposure of bright light at night is associated with an increased incidence of metabolic syndrome, cardiovascular disease, cognitive and affective impairment, sleep disorders, some cancers and premature ageing. CD may be the result of disturbances in different components of the circadian system (central pacemaker and peripheral oscillators, inputs to central clock, mainly due to visual deficiencies, and output signals from the pacemaker and oscillators). Exposure to different synchronizers (light, meal times, physical and social activities) with a regular pattern results in a chronoenhacement that can prevent age-related CD.

Effect of nifedipine on electrophysiological properties of rat ureter spontaneous activity

The work studied effect of various concentrations of nifedipine on the slow and fast spontaneous activities evoked in the perivesical and perirenal areas of the rat ureter. Whereas in the proximal zone of the organ at the low dose of nifedipine (0.06 and 0.12 mg/kg), inhibition is revealed both of slow waves and of their corresponding spikes, in the perivesical part the opposite effect is observed. Besides, with further increase of the nifedipine dose to 0.15 and 0.2 mg/kg, in the ureter area adjacent to the urinary bladder, alongside with acceleration of slow pacemaker oscillations, the appearance of the antiperistaltically directed action potentials is also possible.

Delay-aided stochastic multiresonances on scale-free FitzHugh–Nagumo neuronal networks

The stochastic resonance in paced time-delayed scale-free FitzHugh–Nagumo (FHN) neuronal networks is investigated. We show that an intermediate intensity of additive noise is able to optimally assist the pacemaker in imposing its rhythm on the whole ensemble. Furthermore, we reveal that appropriately tuned delays can induce stochastic multiresonances, appearing at every integer multiple of the pacemaker's oscillation period. We conclude that fine-tuned delay lengths and locally acting pacemakers are vital for ensuring optimal conditions for stochastic resonance on complex neuronal networks.

Generation of scale-free topology in complex networks by phase entrainment

A collection of connected phase oscillators, initially unsynchronised, are subjected to a growing process. In such a process, pacemaker oscillators attach to the original network following an exclusively dynamical criterion oriented to entrain the network. Under these conditions, we show that successful entrainment always corresponds to the generation of a scale-free topology in the original graph.

Real-time imaging of calcium dynamics in rhythmically active neurons of thespinal network for locomotion

Event Abstract Back to Event Real-time imaging of calcium dynamics in rhythmically active neurons of thespinal network for locomotion Di Wang1*, Sten Grillner1 and Peter Wallén1 1 Karolinska Institutet, Sweden The neuronal network underlying locomotion in vertebrates has been investigated in considerable detail in the lamprey spinal cord in vitro model. The isolated spinal cord preparation can be made to produce well-coordinated rhythmic activity, with left-right alternation and intersegmental phase-coupling, corresponding to locomotion (swimming). The rhythm-generating capacity of the network is the result of an interplay between network connectivity properties and the dynamic membrane properties of the individual network neurons. These different kinds of membrane properties typically rely on localized influx of calcium, leading to, for instance, the activation of calcium-dependent potassium channels (KCa-channels). Among the key calcium-dependent membrane properties are the NMDA-receptor-dependent membrane potential pacemaker oscillations, the slow afterhyperpolarization (sAHP) following the action potential, and the postinhibitory rebound depolarization following a period of hyperpolarization. Although much is known about the detailed operation of the network, specific information on the calcium dynamics – both in the temporal and the spatial domain – is still to a large degree lacking. We are therefore investigating different membrane properties of lamprey spinal neurons by utilizing confocal calcium imaging in combination with intracellular membrane potential recordings. During rhythmic network operation (fictive locomotion), calcium fluctuations can be detected in dendrites of individual neurons, even during subthreshold membrane potential oscillations (cf. Bacskai et al., Neuron 14:19-28, 1995). Furthermore, during NMDA-dependent pacemaker oscillations in the presence of TTX, dendritic calcium fluctuations are also seen, timed to the membrane potential oscillations (Fig. 1). During burst firing, the sAHP´s following each spike will add and produce a pronounced summed sAHP, which contributes to the termination of the burst. Calcium imaging during spike trains has revealed a distinct influx of calcium in conjunction with the sAHP. This calcium enters via N (CaV 2.2)- and P/Q (CaV 2.1) types of HVA calcium channels, while L-type channels (CaV 1) are not involved. Correspondingly, blockade of N- and P/Q-type channels reduced the calcium influx in the soma and proximal dendrites, while blockade of L-type channels did not. This indicates that the calcium channels responsible for activating the KCa channels involved in the sAHP are primarily located in the soma and proximal dendrites of the cell. In contrast, L-type calcium channels appear to be mainly localized to distal dendrites in lamprey spinal neurons. Confocal fluorescence imaging of calcium influx, and other dynamic events, with high spatial and temporal resolution, in combination with electrophysiological recordings from the same neuron in the functional network, holds promise to reveal important insights into the cellular and subcellular mechanisms governing network operation. tn_image2 conference image2 conference Conference: Neuroinformatics 2008, Stockholm, Sweden, 7 Sep - 9 Sep, 2008. Presentation Type: Poster and Short Oral Presentation Topic: Neuroimaging Citation: Wang D, Grillner S and Wallén P (2008). Real-time imaging of calcium dynamics in rhythmically active neurons of thespinal network for locomotion. Front. Neuroinform. Conference Abstract: Neuroinformatics 2008. doi: 10.3389/conf.neuro.11.2008.01.060 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 25 Jul 2008; Published Online: 25 Jul 2008. * Correspondence: Di Wang, Karolinska Institutet, Stockholm, Sweden, di.wang@ki.se Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract Supplemental Data The Authors in Frontiers Di Wang Sten Grillner Peter Wallén Google Di Wang Sten Grillner Peter Wallén Google Scholar Di Wang Sten Grillner Peter Wallén PubMed Di Wang Sten Grillner Peter Wallén Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.

Stochastic Aspects of Cardiac Arrhythmias

Abnormal cardiac rhythms (cardiac arrhythmias) often display complex changes over time that can have a random or haphazard appearance. Mathematically, these changes can on occasion be identified with bifurcations in difference or differential equation models of the arrhythmias. One source for the variability of these rhythms is the fluctuating environment. However, in the neighborhood of bifurcation points, the fluctuations induced by the stochastic opening and closing of individual ion channels in the cell membrane, which results in membrane noise, may lead to randomness in the observed dynamics. To illustrate this, we consider the effects of stochastic properties of ion channels on the resetting of pacemaker oscillations and on the generation of early afterdepolarizations. The comparison of the statistical properties of long records showing arrhythmias with the predictions from theoretical models should help in the identification of different mechanisms underlying cardiac arrhythmias.

In search of the pathways for light-induced pacemaker resetting in the suprachiasmatic nucleus.

Within the suprachiasmatic nucleus (SCN) of the mammalian hypothalamus is a circadian pacemaker that functions as a clock. Its endogenous period is adjusted to the external 24-h light-dark cycle, primarily by light-induced phase shifts that reset the pacemaker's oscillation. Evidence using a wide variety of neurobiological and molecular genetic tools has elucidated key elements that comprise the visual input pathway for SCN photoentrainment in rodents. Important questions remain regarding the intracellular signals that reset the autoregulatory molecular loop within photoresponsive cells in the SCN's retino-recipient subdivision, as well as the intercellular coupling mechanisms that enable SCN tissue to generate phase shifts of overt behavioral and physiological circadian rhythms such as locomotion and SCN neuronal firing rate. Multiple neurotransmitters, protein kinases, and photoinducible genes add to system complexity, and we still do not fully understand how dawn and dusk light pulses ultimately produce bidirectional, advancing and delaying phase shifts for pacemaker entrainment.

Pacemaker calcium oscillations in thalamic astrocytes in situ.

During development, astrocytes in the ventrobasal thalamus display spontaneous intracellular calcium [Ca(2+)](i) oscillations, that can lead to the excitation of adjacent thalamocortical neurons via an NMDA receptor-mediated mechanism. In this study, we show that while astrocytes usually exhibit oscillations of irregular amplitude and frequency, a subset of spontaneously active thalamic astrocytes exhibits rhythmic, i.e. pacemaker, [Ca(2+)](i) oscillations with an average frequency of 0.019 Hz. This frequency of the pacemaker oscillations is close to the modal frequency of the irregularly oscillating astrocytes, suggesting that there is a preferred frequency for astrocytic [Ca(2+)](i) oscillations. If pacemaker [Ca(2+)](i) oscillations underlie excitatory signaling to neurons, the result would be rhythmic activation of thalamocortical neurons and astrocyte-driven synchronized oscillations within neurons of the thalamocortical loop.

Probing the circadian pacemaker of a mouse using two light pulses.

In two separate sets of experiments, the phases of the locomotor activity rhythm of the nocturnal field mouse Mus booduga were probed using two light pulses (LPs). In the first set of experiments, the circadian pacemaker underlying the locomotor activity rhythm was perturbed at circadian time 14 (CT 14) using a resetting light pulse LP1 of 1000 lux intensity and 15 min duration. The phases of the resetting pacemaker were then probed at all even CTs between CT 16 and CT 14 using a PRC probing light pulse LP2 of equal strength. The "LP2 PRC" thus obtained was then compared with the single light pulse PRC in terms of the area under delay (D) and advance (A) zones of the PRCs. The time course and waveform of the two LP PRCs suggest that the LP2 PRC resembled the single LP PRC, displaced by 2 h toward the right. The LP1 PRC had smaller D compared to the single LP PRC (p = 0.007), whereas both the PRCs had A of equal magnitude (p = 0.23). This suggests that the pacemaker phase shifts rapidly after LP perturbations. In the second set of experiments, the LP1 was administered at CT 14. The phase of the pacemaker was then perturbed on day 1 (next cycle after LP1) either 2 h after activity onset (at ca. CT 14 of the transient cycle) or 8 h after activity onset (at ca. CT 20 of the transient cycle) using an LP2 of equal strength. It was observed that the steady-state phase shifts evoked by positioning an LP2, 2 h after activity onset, were positively correlated with the phase shifts observed on day 1. The steady-state phase shifts observed, when the LP2 was positioned, 8 h after activity onset, were negatively correlated with the phase shifts observed on day 1. These results suggest that the transient cycles do not mirror the state of the pacemaker oscillator.

Blockade of SK-type Ca2+-activated K+ channels uncovers a Ca2+-dependent slow afterdepolarization in nigral dopamine neurons.

Sharp electrode current-clamp recording techniques were used to characterize the response of nigral dopamine (DA)-containing neurons in rat brain slices to injected current pulses applied in the presence of TTX (2 microM) and under conditions in which apamin-sensitive Ca2+-activated K+ channels were blocked. Addition of apamin (100-300 nM) to perfusion solutions containing TTX blocked the pacemaker oscillation in membrane voltage evoked by depolarizing current pulses and revealed an afterdepolarization (ADP) that appeared as a shoulder on the falling phase of the voltage response. ADP were preceded by a ramp-shaped slow depolarization and followed by an apamin-insensitive hyperpolarizing afterpotential (HAP). Although ADPs were observed in all apamin-treated cells, the duration of the response varied considerably between individual neurons and was strongly potentiated by the addition of TEA (2-3 mM). In the presence of TTX, TEA, and apamin, optimal stimulus parameters (0.1 nA, 200-ms duration at -55 to -68 mV) evoked ADP ranging from 80 to 1,020 ms in duration (355.3 +/- 56.5 ms, n = 16). Both the ramp-shaped slow depolarization and the ensuing ADP were markedly voltage dependent but appeared to be mediated by separate conductance mechanisms. Thus, although bath application of nifedipine (10-30 microM) or low Ca2+, high Mg2+ Ringer blocked the ADP without affecting the ramp potential, equimolar substitution of Co2+ for Ca2+ blocked both components of the voltage response. Nominal Ca2+ Ringer containing Co2+ also blocked the HAP evoked between -55 and -68 mV. We conclude that the ADP elicited in DA neurons after blockade of apamin-sensitive Ca2+-activated K+ channels is mediated by a voltage-dependent, L-type Ca2+ channel and represents a transient form of the regenerative plateau oscillation in membrane potential previously shown to underlie apamin-induced bursting activity. These data provide further support for the notion that modulation of apamin-sensitive Ca2+-activated K+ channels in DA neurons exerts a permissive effect on the conductances that are involved in the expression of phasic activity.

Phenotypic specification of hindbrain rhombomeres and the origins of rhythmic circuits in vertebrates.

This essay considers the ontogeny and phylogeny of the cranial neural circuitry producing rhythmic behaviors in vertebrates. These behaviors are characterized by predictable temporal patterns established by a neuronal network variously referred to as either a pacemaker, neural oscillator or central pattern generator. Comparative vertebrate studies have demonstrated that the embryonic hindbrain is divided into segmented compartments called rhombomeres, each of which gives rise to a distinct complement of cranial motoneurons and, as yet, unidentified populations of interneurons. We now propose that novel rhythmic circuits were innovations associated with the adoption of cardiac and respiratory pumps during the protochordate-vertebrate transition. We further suggest that the pattern-generating circuits of more recent innovations, such as the vocal, electromotor and extraocular systems, have originated from the same Hox gene-specified compartments of the embryonic hindbrain (rhombomeres 7-8) that gave rise to rhythmically active cardiac and respiratory circuits. Lastly, we propose that the capability for pattern generation by neurons originating from rhombomeres 7 and 8 is due to their electroresponsive properties producing pacemaker oscillations, as best typified by the inferior olive which also has origins from these same hindbrain compartments and has been suggested to establish rhythmic oscillations coupled to sensorimotor function throughout the neuraxis of vertebrates.

Apamin-sensitive Ca(2+)-activated K+ channels regulate pacemaker activity in nigral dopamine neurons.

Mesencephalic dopamine-containing neurons exhibit a Ca(2+)-dependent oscillation in membrane potential believed to underlie the ability of these cells to maintain spontaneous activity in the absence of afferent synaptic drive. In the present series of experiments, sharp electrode intracellular recording techniques were used in conjunction with an in vitro brain slice preparation to explore the ionic mechanisms underlying rhythmogenesis in nigral dopamine neurons in the rat. Our results indicate that the K+ channel producing the prolonged post-spike afterhyperpolarization exhibited by these neurons is also principally responsible for generating the falling phase of the autogenous pacemaker oscillation. Alterations in the expression of this conductance are associated with marked changes in neuronal firing pattern, indicating that modulation of ligand-gated Ca(2+)-activated K+ channels may constitute a functional means of altering temporal coding among the major mesotelencephalic dopamine systems.

Effects of dihydropyridine calcium antagonists on rat midbrain dopaminergic neurones.

1. The effects of the dihydropyridine calcium channel antagonists, nifedepine and nimodipine (300 nM-30 microM) were tested in vitro on intracellularly recorded dopaminergic neurones in the rat ventral mesencephalon. 2. Bath applied nifedipine and nimodipine inhibited in a concentration-dependent manner the spontaneous firing discharge of the action potentials, whereas, the dihydropyridine calcium channel agonist, Bay K 8644 increased the firing rate. 3. Pacemaker oscillations and bursts of action potentials were produced by loading the cells with caesium. Nifedipine and nimodipine reduced the rate and the duration of the caesium-induced membrane oscillations and decreased the number of action potentials in a burst. During the blockade of potassium currents the dopaminergic neurones often developed a prolonged (100-800 ms) afterdepolarization that was also inhibited by dihydropyridines. 4. The spontaneous discharge of calcium spikes was also inhibited by both dihydropyridine calcium antagonists. The apparent input resistance and the level of membrane potential were not affected by the dihydropyridine calcium antagonists. 5. If the action potential duration was less than 150 ms the shape of the spike was not clearly influenced by both calcium antagonists. However, when the duration of the action potential was longer than 150-200 ms due to the intracellular injection of caesium ions plus the extracellular application of tetraethylammonium (10-50 mM), both nifedipine and nimodipine reversibly shortened the plateau potential. 6. It is suggested that nifedipine and nimodipine depress the rhythmic and bursting activity of the dopaminergic cells and shorten the calcium action potential by blocking dihydropyridine-sensitive high-threshold calcium currents.

Conservation of photoperiod-responsive mechanisms in humans.

In animals, circadian pacemakers respond to seasonal changes in day length by making corresponding adjustments in the durations of diurnal and nocturnal periods of circadian rhythms; these adjustments mediate effects of photoperiod on breeding and other seasonally recurring phenomena. Little is known about photoperiod responses of human circadian pacemakers. To investigate this question, we recorded and compared circadian rhythm profiles of 15 individuals after chronic exposures to short (8 h) and long (14 h) nights. As occurs in animals, durations of nocturnal periods of active melatonin secretion (11.9 +/- 1.6 vs. 10.3 +/- 1.3 h, df = 14, t = 4.583, P < 0.0005, paired t test), high prolactin secretion (12.9 +/- 2.1 vs. 9.9 +/- 2.2 h, df = 11, t = 2.917, P < 0.01), and sleep (10.6 +/- 0.8 vs. 7.6 +/- 0.4 h, df = 14, t = 17.122, P < 0.0005) were longer after exposure to long nights than after short ones. Durations of nocturnal periods of low rectal temperature (11.6 +/- 2.3 vs. 9.5 +/- 1.6 h, df = 12, t = 3.912, P < 0.001) and rising cortisol secretion (10.8 +/- 1.6 vs. 9.3 +/- 1.9 h, df = 14, t = 3.130, P < 0.005) were also longer. Some of these differences persisted during 24-h periods of enforced wakefulness in constant dim light, indicating that prior exposure to the two regimes induced abiding changes in the timing of internal processes, such as circadian pacemaker oscillations, that control the durations of nocturnal and diurnal periods of the rhythms.

A role for low-frequency, rhythmic synaptic potentials in the synchronization of cat thalamocortical cells.

1. Low-frequency, rhythmic synaptic potentials and their ability to evoke and modulate membrane potential oscillations in thalamocortical (TC) cells of the cat dorsal lateral geniculate nucleus (dLGN) were investigated using intracellular recordings in a brain slice preparation. Three types of rhythmic synaptic potentials were distinguished: EPSPs, IPSPs and 'complex synaptic potentials' consisting of an IPSP followed by an EPSP. 2. The frequency of all three types of synaptic potentials was insensitive to changes in the membrane potential. At potentials positive to -50 mV, the EPSPs and the complex potentials gave rise to action potentials, while between -65 and -80 mV all three types of synaptic potential evoked low-threshold Ca2+ potentials. TC cells which displayed rhythmic synaptic potentials were either cells that showed spontaneous pacemaker oscillation or cells that were brought to oscillate by the rhythmic EPSPs or depolarizing (i.e. reversed IPSPs. 3. The low-frequency (1.9 +/- 0.2 Hz), rhythmic EPSPs were observed in 23 (out of 192) cells, were abolished by tetrodotoxin (TTX; n = 4) and by the combined application of DL-2-amino-5-phosphonovaleric acid and 6-cyano-7-nitroquinoxaline-2,3-dione (n = 3), and were insensitive to bicuculline (n = 4). Paired intracellular recordings (n = 32) demonstrated the presence of simultaneously occurring EPSPs in a pair of cells situated 75 microns apart. 4. The low-frequency (2.2 +/- 0.3 Hz), rhythmic IPSPs were observed in 5 (out of 192) cells, were blocked by bicuculline (n = 3), and reversed in polarity at -65 mV. The low-frequency (1.3 +/- 0.3 Hz), rhythmic 'complex potentials' were observed in 5 (out of 192) cells and were abolished by TTX (n = 2). 5. Intracellular depolarizing current pulses delivered at different phases of the pacemaker oscillations revealed the existence of two different types of phase resetting. Furthermore, a current pulse of critical amplitude and duration applied at a specific phase of the cycle abolished the pacemaker oscillations. 6. These results indicate that the low-frequency, rhythmic synaptic potentials recorded in TC cells of the dLGN (i) originate from other TC cells that are in the pacemaker oscillating mode, (ii) are capable of driving other TC cells to oscillate rhythmically, or of modulating the frequency of pacemaker oscillations, and (iii) provide a means by which oscillatory activities of TC cells can be synchronized in the absence of sensory, cortical and reticular thalamic inputs.

A coupled pacemaker-slave model for the insect photoperiodic clock: interpretation of ovarian diapause data in Drosophila melanogaster.

A coupled circadian oscillator model for the insect photoperiodic clock is described which consists of a hierarchically arranged pacemaker and slave. The pacemaker is self-sustained, temperature compensated, and entrainable by the light cycle; the slave is a damping oscillation receiving entrainment from two sources, from the pacemaker via a coupling factor, and also directly from the light. The damping slave oscillation is seen as the "photoperiodic oscillator", equivalent to that proposed earlier by Lewis and Saunders (1987). The present simulations describe the effect of the strength of the coupling factor between hypothetical short- and long-period pacemaker oscillations (modelled on the "clock" mutants perS and perL2 in Drosophila melanogaster) and a slave oscillation with a period of about 24 hours. The output is presented in terms of photoperiodic response curves and Nanda-Hamner, or resonance, plots. With a high coupling strength, the pacemakers strongly entrain the slave, but with a low coupling strength the slave's properties are more evident. The model is presented as a possible explanation for recent ovarian diapause data in D. melanogaster "clock" mutants (Saunders 1990), but also as a more general model for the role of the insect circadian system in seasonal time measurement.