Small Clusters of Electrically Coupled Neurons Generate Synchronous Rhythms in the Thalamic Reticular Nucleus

Long, Michael A.; Landisman, Carole E.; Connors, Barry W.

doi:10.1523/jneurosci.3358-03.2004

Cited by 175 publications

(184 citation statements)

References 61 publications

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“…This suggests that while not being overt under normal conditions, a 10 Hz oscillation is still present in cat NRT neurons and might influence firing rate during the slow oscillation up state. The 10 Hz oscillation described by Long et al (2004) was synchronized between closely situated cells via electrical synapses (Landisman et al, 2002). Because evidence for electrical synapses is present in recordings from NRT neurons in the adult cat in vivo (Fuentealba et al, 2004), the possibility exists that electrical synapses might play a role in synchronizing the slow oscillation.…”

Section: Discussionmentioning

confidence: 99%

“…Because evidence for electrical synapses is present in recordings from NRT neurons in the adult cat in vivo (Fuentealba et al, 2004), the possibility exists that electrical synapses might play a role in synchronizing the slow oscillation. Indeed, the particular effectiveness of electrical synapses at transmitting lowfrequency events (Landisman et al, 2002;Long et al, 2004) makes them ideally suited to this role. A similar scenario might also exist for TC neurons (Hughes et al, 2004), where electrical synapses are also present (Hughes et al, 2002b), raising the prospect that a certain degree of slow (Ͻ1 Hz) wave synchronization can occur locally in the thalamus.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study using slices from young rats has also examined the effects of mGluR activation on NRT neurons (Long et al, 2004). In this investigation, the authors describe the appearance of subthreshold membrane potential oscillations at ϳ10 Hz.…”

Section: The Ionic Basis Of the Slow (<1 Hz) Oscillation In Nrt Neuronsmentioning

confidence: 99%

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Neuronal Basis of the Slow (<1 Hz) Oscillation in Neurons of the Nucleus Reticularis ThalamiIn Vitro

et al. 2006

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During deep sleep and anesthesia, the EEG of humans and animals exhibits a distinctive slow (Ͻ1 Hz) rhythm. In inhibitory neurons of the nucleus reticularis thalami (NRT), this rhythm is reflected as a slow (Ͻ1 Hz) oscillation of the membrane potential comprising stereotypical, recurring "up" and "down" states. Here we show that reducing the leak current through the activation of group I metabotropic glutamate receptors (mGluRs) with either trans-ACPD [(ϩ/Ϫ)-1-aminocyclopentane-trans-1,3-dicarboxylic acid] (50 -100 M) or DHPG [(S)-3,5-dihydroxyphenylglycine] (100 M) instates an intrinsic slow oscillation in NRT neurons in vitro that is qualitatively equivalent to that observed in vivo. A slow oscillation could also be evoked by synaptically activating mGluRs on NRT neurons via the tetanic stimulation of corticothalamic fibers. Through a combination of experiments and computational modeling we show that the up state of the slow oscillation is predominantly generated by the "window" component of the T-type Ca 2ϩ current, with an additional supportive role for a Ca 2ϩ -activated nonselective cation current. The slow oscillation is also fundamentally reliant on an I h current and is extensively shaped by both Ca 2ϩ -and Na ϩ -activated K ϩ currents. In combination with previous work in thalamocortical neurons, this study suggests that the thalamus plays an important and active role in shaping the slow (Ͻ1 Hz) rhythm during deep sleep.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Neuronal Basis of the Slow (<1 Hz) Oscillation in Neurons of the Nucleus Reticularis ThalamiIn Vitro

et al. 2006

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“…Having said that, if the capacitance of coupled cells is large, gap junctions could actually inhibit neuronal activity (Kepler et al, 1990). Furthermore, gap junctions play a particularly prominent role coordinating GABAergic inhibitory networks (Long et al, 2004). Thus, even though gap junctions coordinate or amplify the output of a set of neurons, the net effect may still be inhibitory.…”

Section: Development Of Brainstem Neurons and Synaptogenesismentioning

confidence: 99%

Neonatal maturation of the hypercapnic ventilatory response and central neural CO2 chemosensitivity

Putnam

Conrad

Gdovin

et al. 2005

Respiratory Physiology & Neurobiology

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The ventilatory response to CO 2 changes as a function of neonatal development. In rats, a ventilatory response to CO 2 is present in the first 5 days of life, but this ventilatory response to CO 2 wanes and reaches its lowest point around postnatal day 8. Subsequently, the ventilatory response to CO 2 rises towards adult levels. Similar patterns in the ventilatory response to CO 2 are seen in some other species, although some animals do not exhibit all of these phases. Different developmental patterns of the ventilatory response to CO 2 may be related to the state of development of the animal at birth. The triphasic pattern of responsiveness (early decline, a nadir, and subsequent achievement of adult levels of responsiveness) may arise from the development of several processes, including central neural mechanisms, gas exchange, the neuromuscular junction, respiratory muscles and respiratory mechanics. We only discuss central neural mechanisms here, including altered CO 2 sensitivity of neurons among the various sites of central CO 2 chemosensitivity, changes in astrocytic function during development, the maturation of electrical and chemical synaptic mechanisms (both inhibitory and excitatory mechanisms) or changes in the integration of chemosensory information originating from peripheral and multiple central CO 2 chemosensory sites. Among these central processes, the maturation of synaptic mechanisms seems most important and the relative maturation of synaptic processes may also determine how plastic the response to CO 2 is at any particular age.

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“…Indispensable components for generation of these oscillations are GABA B and AMPA receptors as well as T-type calcium channels [4], however, many other factors modulate oscillatory activity, e.g. HCN channels, neuropeptides and electrical synapses [3,16,17,18,27,34]. Neuropeptide Y (NPY) is an inhibitor of absence seizures [23] and thalamic oscillations [25].…”

Section: Introductionmentioning

confidence: 99%

NPY signaling through Y1 receptors modulates thalamic oscillations

2007

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Neuropeptide Y is the ligand of a family of G-protein coupled receptors (Y 1 to Y 6 ). In the thalamus, exogenous and endogenously released NPY can shorten the duration of thalamic oscillations in brain slices from P13 to P15 rats, an in vitro model of absence seizures. Here, we examine which Y receptors are involved in this modulation. Application of the Y 1 receptor agonist Leu 31 Pro 34 NPY caused a reversible reduction in the duration of thalamic oscillations (−26.6 +/− 7.8%), while the Y 2 receptor agonist peptideYY and the Y 5 receptor agonist BWX-46 did not exert a significant effect. No Y receptor agonist affected oscillation period. Application of antagonists of Y 1 , Y 2 and Y 5 receptors (BIBP3226, BIIE0246 and L152,806, respectively) produced results consistent with those obtained from agonists. BIBP3226 caused a reversible disinhibition, an effect that increases oscillation duration (18.2 +/− 9.7%) while BIIE0246 and L152,806 had no significant effect. Expression of NPY is limited to neurons in the reticular thalamic nucleus (nRt), but Y 1 receptors are expressed in both nRt and adjacent thalamic relay nuclei. Thus, intra-nRt or nRt to relay nucleus NPY release could cause Y 1 receptor mediated inhibition of thalamic oscillations.

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Small Clusters of Electrically Coupled Neurons Generate Synchronous Rhythms in the Thalamic Reticular Nucleus

Cited by 175 publications

References 61 publications

Neuronal Basis of the Slow (<1 Hz) Oscillation in Neurons of the Nucleus Reticularis ThalamiIn Vitro

Neuronal Basis of the Slow (<1 Hz) Oscillation in Neurons of the Nucleus Reticularis ThalamiIn Vitro

Neonatal maturation of the hypercapnic ventilatory response and central neural CO2 chemosensitivity

NPY signaling through Y1 receptors modulates thalamic oscillations

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