scholarly journals MSAP NAT Relay Cell for Combat Networks

2012 ◽  
Vol 37 (2C) ◽  
pp. 196-205
Author(s):  
Ki-Woon Choi ◽  
Young-June Choi
Keyword(s):  
Relay Cell

Feature-linked synchronization of thalamic relay cell firing induced by feedback from the visual cortex

Nature ◽  
1994 ◽  
Vol 369 (6480) ◽  
pp. 479-482 ◽  
Author(s):  
Adam M. Sillito ◽  
Helen E. Jones ◽  
George L. Gerstein ◽  
David C. West
Keyword(s):  
Visual Cortex ◽  
Relay Cell ◽  
Thalamic Relay ◽  
Cell Firing

scholarly journals The Small Subunit Processome Is Required for Cell Cycle Progression at G1

2004 ◽  
Vol 15 (11) ◽  
pp. 5038-5046 ◽  
Author(s):  
Kara A. Bernstein ◽  
Susan J. Baserga
Keyword(s):  
Cell Cycle ◽  
Ribosome Biogenesis ◽  
Cell Cycle Progression ◽  
Small Subunit ◽  
Cellular Growth ◽  
Yeast Cells ◽  
G1 Phase ◽  
Relay Cell ◽  
Ssu Processome ◽  
Nucleolar Rna

Without ribosome biogenesis, translation of mRNA into protein ceases and cellular growth stops. We asked whether ribosome biogenesis is cell cycle regulated in the yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe, and we determined that it is not regulated in the same manner as in metazoan cells. We therefore turned our attention to cellular sensors that relay cell size information via ribosome biogenesis. Our results indicate that the small subunit (SSU) processome, a complex consisting of 40 proteins and the U3 small nucleolar RNA necessary for ribosome biogenesis, is not mitotically regulated. Furthermore, Nan1/Utp17, an SSU processome protein, does not provide a link between ribosome biogenesis and cell growth. However, when individual SSU processome proteins are depleted, cells arrest in the G1 phase of the cell cycle. This arrest was further supported by the lack of staining for proteins expressed in post-G1. Similarly, synchronized cells depleted of SSU processome proteins did not enter G2. This suggests that when ribosomes are no longer made, the cells stall in the G1. Therefore, yeast cells must grow to a critical size, which is dependent upon having a sufficient number of ribosomes during the G1 phase of the cell cycle, before cell division can occur.

Metabotropic glutamate receptors switch visual response mode of lateral geniculate nucleus cells from burst to tonic

1996 ◽  
Vol 76 (3) ◽  
pp. 1800-1816 ◽  
Author(s):  
D. W. Godwin ◽  
J. W. Vaughan ◽  
S. M. Sherman
Keyword(s):  
Glutamate Receptors ◽  
Lateral Geniculate Nucleus ◽  
Metabotropic Glutamate Receptors ◽  
Cell Activity ◽  
Response Mode ◽  
Visual Response ◽  
Relay Cell ◽  
Metabotropic Glutamate ◽  
Lateral Geniculate

1. Metabotropic glutamate receptors (mGluRs) on relay cells of the lateral geniculate nucleus appear to be activated exclusively by cortical inputs. We thus sought to manipulate these receptors in an effort to gain insight into the possible role of the corticogeniculate pathway. We used in vivo recording and pharmacological techniques in cats to activate or inactivate these receptors on geniculate neurons while analyzing their response properties. 2. Iontophoretic application of the mGluR agonist 1-amino-cyclopentane-1,3-dicarboxylic acid (ACPD) to X and Y cells in the geniculate A laminae diminished or abolished burst activity characteristic of low-threshold Ca2+ spikes. This was accompanied by pronounced changes in the visual response, including a decrease in signal detectability as measured with receiver operating characteristic curves. 3. ACPD effects appear specific to mGluRs, because a specific antagonist of ionotropic glutamate receptors (iGluRs) failed to affect the ACPD-evoked responses, and antagonists of ACPD failed to affect iGluR-mediated responses. We found that 3,5-dihydroxyphenylglycine, an agonist reported to be specific for phosphatidylinositol (PI)-linked mGluRs, had effects similar to those of ACPD, implying that these effects are mediated by PI-coupled mGluRs. Furthermore, antagonists reported to be effective against PI-linked mGluRs were effective in antagonizing the ACPD-mediated effects, and substances reported to be agonists to mGluRs coupled to the adenosine 3',5'-cyclic monophosphate cascade did not affect neuronal responses on their own. These data, when added to our preliminary anatomic data, indicate that the receptor responsible for the observed effects may be mGluR1, or a functionally equivalent mGluR. 4. Activation of mGluRs produces changes in geniculate relay cell activity consistent with depolarization of these cells seen during in vitro studies. Such membrane depolarization has been shown to control the activation state of a voltage-dependent Ca2+ conductance, and this, in turn, determines whether the relay cell fires in tonic or burst mode. Our data show that application of ACPD produces a shift in response mode from burst to tonic. Because response mode is an important characteristic of the geniculate relay and because the activation state of certain mGluRs, which helps determine response mode may be controlled by corticogeniculate input, we conclude that an important function of this input is to provide a visuotopically discrete transition from burst to tonic response mode.

Mapping of the Functional Interconnections Between Thalamic Reticular Neurons Using Photostimulation

2006 ◽  
Vol 96 (5) ◽  
pp. 2593-2600 ◽  
Author(s):  
Ying-Wan Lam ◽  
Christopher S. Nelson ◽  
S. Murray Sherman
Keyword(s):  
Laser Scanning ◽  
Spatial Extent ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Reticular Cell ◽  
Relay Cell ◽  
Dominant Form ◽  
Electrical Synapses ◽  
Reticular Neurons ◽  
Reticular Cells

The thalamic reticular nucleus is strategically located in the axonal pathways between thalamus and cortex, and reticular cells exert strong, topographic inhibition on thalamic relay cells. Although evidence exists that reticular neurons are interconnected through conventional and electrical synapses, the spatial extent and relative strength of these synapses are unclear. To address these issues, we used uncaging of glutamate by laser-scanning photostimulation to provide precisely localized and consistent activation of reticular cell bodies and dendrites in an in vitro slice preparation from the rat as a means to study reticulo-reticular connections. Among the 47 recorded reticular neurons, 29 (62%) received GABAergic axodendritic input from an area immediately surrounding each of the recorded cell bodies, and 8 (17%) responded with depolarizing spikelets, suggesting inputs through electrical synapses. We also found that TTX completely blocked all evoked IPSCs, implying that any dendrodendritic synapses between reticular cells either are relatively weak, have no nearby glutamatergic receptors, or are dependent on back-propagation of action potentials. Finally, we showed that the GABAergic connections between reticular cells are weaker than those from reticular cells to relay cells. Our results suggest that the GABAergic axodendritic synapse is the dominant form of reticulo-reticular connectivity, and because they are much weaker than the reticulo-relay cell synapses, their functional purpose may be to regulate the spatial extent of the reticular inhibition on relay cells.

Dynamics of neurons in the cat lateral geniculate nucleus: in vivo electrophysiology and computational modeling

1995 ◽  
Vol 74 (3) ◽  
pp. 1222-1243 ◽  
Author(s):  
P. Mukherjee ◽  
E. Kaplan
Keyword(s):  
Computational Modeling ◽  
Spike Train ◽  
Lateral Geniculate Nucleus ◽  
Transfer Functions ◽  
Temporal Frequency ◽  
Relay Cell ◽  
Lateral Geniculate ◽  
Low Pass ◽  
Band Pass

1. We investigated the time domain transformation that thalamocortical relay cells of the cat lateral geniculate nucleus (LGN) perform on their retinal input, and used computational modeling to explore the biophysical properties that determine the dynamics of the LGN relay cells in vivo. 2. We recorded simultaneously the input (S potentials) and output (action potentials) of 50 cat LGN relay cells stimulated by drifting sinusoidal gratings of varying temporal frequency. The temporal modulation transfer functions (TMTFs) of the neurons were derived from these data. The burstiness of the LGN spike trains was also assessed using objective criteria. 3. We found that the form of the TMTF was quite variable among cells, ranging from low-pass to strongly band-pass. The optimal temporal frequency of band-pass neurons was between 2 and 8 Hz. In addition, the TMTF of some cells was nonstationary: their temporal tuning changed with time. 4. The temporal tuning of a cell was directly related to the degree of burstiness of its spike train. Tonically firing relay cells had low-pass TMTFs, whereas the most bursty neurons exhibited the most sharply band-pass transfer functions. This was also true for single cells that altered their temporal tuning: a shift to more band-pass tuning was associated with increased burstiness of the spike train, and vice versa. 5. We constructed a computer simulation of the LGN relay cell. The model was a simplified five-channel version of the thalamocortical neuron model of McCormick and Huguenard. It incorporated the quantitative kinetics of the Ca2+ T channel, as well as the Hodgkin-Huxley Na+ and K+ channels, as the only active membrane currents. To simulate the in vivo dynamics of the relay cell, the input to the model consisted of trains of synaptic potentials, recorded as S potentials in our physiological experiments. 6. When the resting membrane potential of the model neuron was relatively depolarized, the model's TMTF was low-pass, with no bursting evident in the simulated spike train. At hyperpolarized resting membrane potentials, however, the modeled TMTF was band-pass, with frequent burst discharges. Thus the biophysical model reproduced not only the range of dynamics seen in real LGN relay cells, but also the dependence of the overall dynamics on the burstiness of the spike train. However, neither of these phenomena could be simulated without the T channel. Thus the simulations demonstrated that the T-type Ca2+ channel was necessary and sufficient to explain the LGN dynamics observed in physiological experiments.(ABSTRACT TRUNCATED AT 400 WORDS)

Fourier Analysis of Sinusoidally Driven Thalamocortical Relay Neurons and a Minimal Integrate-and-Fire-or-Burst Model

2000 ◽  
Vol 83 (1) ◽  
pp. 588-610 ◽  
Author(s):  
Gregory D. Smith ◽  
Charles L. Cox ◽  
S. Murray Sherman ◽  
John Rinzel
Keyword(s):  
Fourier Analysis ◽  
Large Scale ◽  
Relay Cell ◽  
Low Frequencies ◽  
Integrate And Fire ◽  
Large Scale Network ◽  
Relay Neuron ◽  
Low Pass ◽  
Network Simulations ◽  
Relay Neurons

We performed intracellular recordings of relay neurons from the lateral geniculate nucleus of a cat thalamic slice preparation. We measured responses during both tonic and burst firing modes to sinusoidal current injection and performed Fourier analysis on these responses. For comparison, we constructed a minimal “integrate-and-fire-or-burst” (IFB) neuron model that reproduces salient features of the relay cell responses. The IFB model is constrained to quantitatively fit our Fourier analysis of experimental relay neuron responses, including: the temporal tuning of the response in both tonic and burst modes, including a finding of low-pass and sometimes broadband behavior of tonic firing and band-pass characteristics during bursting, and the generally greater linearity of tonic compared with burst responses at low frequencies. In tonic mode, both experimental and theoretical responses display a frequency-dependent transition from massively superharmonic spiking to phase-locked superharmonic spiking near 3 Hz, followed by phase-locked subharmonic spiking at higher frequencies. Subharmonic and superharmonic burst responses also were observed experimentally. Characterizing the response properties of the “tuned” IFB model leads to insights regarding the observed stimulus dependence of burst versus tonic response mode in relay neurons. Furthermore the simplicity of the IFB model makes it a candidate for large scale network simulations of thalamic functioning.

Action potential backpropagation in a model thalamocortical relay cell

2004 ◽  
Vol 58-60 ◽  
pp. 393-400
Author(s):  
Nada A.B. Yousif ◽  
Mike Denham
Keyword(s):  
Action Potential ◽  
Relay Cell

Precision of the Pacemaker Nucleus in a Weakly Electric Fish: Network Versus Cellular Influences

2000 ◽  
Vol 83 (2) ◽  
pp. 971-983 ◽  
Author(s):  
Katherine T. Moortgat ◽  
Theodore H. Bullock ◽  
Terrence J. Sejnowski
Keyword(s):  
Electric Fish ◽  
Electric Organ Discharge ◽  
Electric Organ ◽  
Spike Timing ◽  
Weakly Electric Fish ◽  
Pacemaker Cells ◽  
Relay Cell ◽  
Spike Timing Precision ◽  
Pacemaker Nucleus ◽  
Weakly Electric

We investigated the relative influence of cellular and network properties on the extreme spike timing precision observed in the medullary pacemaker nucleus (Pn) of the weakly electric fish Apteronotus leptorhynchus. Of all known biological rhythms, the electric organ discharge of this and related species is the most temporally precise, with a coefficient of variation (CV = standard deviation/mean period) of 2 × 10−4 and standard deviation (SD) of 0.12–1.0 μs. The timing of the electric organ discharge is commanded by neurons of the Pn, individual cells of which we show in an in vitro preparation to have only a slightly lesser degree of precision. Among the 100–150 Pn neurons, dye injection into a pacemaker cell resulted in dye coupling in one to five other pacemaker cells and one to three relay cells, consistent with previous results. Relay cell fills, however, showed profuse dendrites and contacts never seen before: relay cell dendrites dye-coupled to one to seven pacemaker and one to seven relay cells. Moderate (0.1–10 nA) intracellular current injection had no effect on a neuron's spiking period, and only slightly modulated its spike amplitude, but could reset the spike phase. In contrast, massive hyperpolarizing current injections (15–25 nA) could force the cell to skip spikes. The relative timing of subthreshold and full spikes suggested that at least some pacemaker cells are likely to be intrinsic oscillators. The relative amplitudes of the subthreshold and full spikes gave a lower bound to the gap junctional coupling coefficient of 0.01–0.08. Three drugs, called gap junction blockers for their mode of action in other preparations, caused immediate and substantial reduction in frequency, altered the phase lag between pairs of neurons, and later caused the spike amplitude to drop, without altering the spike timing precision. Thus we conclude that the high precision of the normal Pn rhythm does not require maximal gap junction conductances between neurons that have ordinary cellular precision. Rather, the spiking precision can be explained as an intrinsic cellular property while the gap junctions act to frequency- and phase-lock the network oscillations.

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