Latency variability of responses to visual stimuli in cells of the cat's lateral geniculate nucleus

1995 ◽  
Vol 105 (1) ◽  
Author(s):  
S.-M. Lu ◽  
W. Guido ◽  
J.W. Vaughan ◽  
S.M. Sherman
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Visual Stimuli ◽  
Lateral Geniculate ◽  
Latency Variability ◽  
In Cells

Functional aspects of plasticity in the visual system of adult cats after early monocular deprivation

1977 ◽  
Vol 278 (961) ◽  
pp. 411-424 ◽  
Keyword(s):  
Visual Cortex ◽  
Superior Colliculus ◽  
Lateral Geniculate Nucleus ◽  
Visual Stimuli ◽  
Monocular Deprivation ◽  
Early Deprivation ◽  
Optic Chiasma ◽  
Lateral Geniculate ◽  
Eyes Open ◽  
Y Cells

Responses to visual stimuli and to electrical stimulation of the optic chiasma were analysed in neurons of the lateral geniculate nucleus, visual cortex and superior colliculus in monocularly deprived cats with different post-deprivation periods. If the cats had both eyes open in their post-deprivation period (1 year) no recovery from the effects of early deprivation was found in the responses of neurones in all 3 visual structures. In cats with a post-deprivation reverse closure we found an increase in the proportion of Y-cells recorded in the early deprived layer of LGN when compared to the Y-cell proportion found in the same layers immediately after the deprived eye was opened. In neurons of the visual cortex and superior colliculus the functional abnormalities remained unaltered. The late closure of the non-deprived eye for up to 3 years did not effect neurons normally activated through that eye. Removal of the non-deprived eye unmasked connections of the deprived eye’s pathway onto neurons in the visual cortex and the superior colliculus. The neurons showed no specificity for the direction of movement or the orientation of visual stimuli. This recovery from deprivation was greater after enucleating the cats at the age of 6 months than at 18 months after birth. In the lateral geniculate nucleus of these cats the proportion of Y-cells in the recorded sample driven by the deprived eye had recovered to the value of normal cats. The difficulties in relating these physiological findings to results from morphological or behavioural studies are discussed.

Response latencies of cells in the cat's lateral geniculate nucleus are less variable during burst than tonic firing

1998 ◽  
Vol 15 (2) ◽  
pp. 231-237 ◽  
Author(s):  
W. GUIDO ◽  
S. MURRAY SHERMAN
Keyword(s):  
Signal Detection ◽  
Lateral Geniculate Nucleus ◽  
Visual Stimulus ◽  
Burst Firing ◽  
Signal To Noise ◽  
Response Latencies ◽  
Tonic Firing ◽  
Lateral Geniculate ◽  
In Cells

We measured the variability in latency of the first spike seen in cells of the cat's lateral geniculate nucleus following the onset of a visual stimulus. We found that, in each of the 11 cells tested, this variability was significantly lower during burst than during tonic firing. We suggest that this difference confers an advantage in signal detection during burst compared to tonic firing. This complements other reported advantages of burst firing for signal detection seen in signal-to-noise ratios and in the ability to efficiently drive postsynaptic cells.

Properties of cells responding to visual stimuli in the rat ventral lateral geniculate nucleus

1979 ◽  
Vol 66 (3) ◽  
pp. 721-736 ◽  
Author(s):  
I. Sumitomo ◽  
M. Sugitani ◽  
Y. Fukuda ◽  
K. Iwama
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Visual Stimuli ◽  
Lateral Geniculate

Effects of brain stem parabrachial activation on receptive field properties of cells in the cat's lateral geniculate nucleus

1995 ◽  
Vol 73 (6) ◽  
pp. 2428-2447 ◽  
Author(s):  
D. J. Uhlrich ◽  
N. Tamamaki ◽  
P. C. Murphy ◽  
S. M. Sherman
Keyword(s):  
Receptive Field ◽  
Brain Stem ◽  
Spontaneous Activity ◽  
Lateral Geniculate Nucleus ◽  
Visual Stimuli ◽  
Visual Responses ◽  
Burst Stimulation ◽  
Lateral Geniculate ◽  
Almost All ◽  
The Brain

1. The lateral geniculate nucleus is the primary thalamic relay for the transfer of retinal signals to the visual cortex. Geniculate cells are heavily innervated from nonretinal sources, and these modify retinogeniculate transmission. A major ascending projection to the lateral geniculate nucleus arises from cholinergic cells in the parabrachial region of the brain stem. This is an important pathway in the ascending control of arousal. In an in vivo preparation, we used extracellular recordings to study the effects of electrical activation of the parabrachial region on the spontaneous activity and visual responses of X and Y cells in the lateral geniculate nucleus of the cat. 2. We studied the effects of two patterns of parabrachial activation on the spontaneous activity of geniculate cells. Burst stimulation consisted of a short pulse at high frequency (16 ms at 250 Hz). Train stimulation was of longer duration at lower frequency (e.g., 1 s at 50 Hz). The firing rate of almost all geniculate cells was enhanced by either pattern of stimulation. However, the burst pattern of stimulation elicited a short, modulated response with excitatory and inhibitory epochs. We found that the different epochs could differentially modulate the visual responses to drifting gratings. Thus the temporal alignment of the brain stem and visual stimuli was critical with burst stimulation, and varied alignments could dramatically confound the results. In comparison, the train pattern of stimulation consistently produced a relatively flat plateau of increased firing, after a short initial period of more variable effects. We used the less confounding pattern of train stimuli to study the effects of parabrachial activation on visual responses. 3. Our main emphasis was to examine the parabrachial effects on the visual responses of geniculate cells. For most visual stimuli, we used drifting sine wave gratings that varied in spatial frequency; these evoked modulated responses from the geniculate cells. Parabrachial activation enhanced the visual responses of almost all geniculate cells, and this enhancement included both increased depth of modulation and greater response rates. 4. Our results were incorporated quantitatively into a difference-of-Gaussians model of visual receptive fields in order to study the parabrachial effects on the spatial structure of the receptive field. This model fit our data well and provided measures of the response amplitude and radius of the receptive field center (Kc and Rc, respectively) and the response amplitude and radius of the receptive field surround (Ks and Rs, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

The brain-stem parabrachial region controls mode of response to visual stimulation of neurons in the cat’s lateral geniculate nucleus

1993 ◽  
Vol 10 (4) ◽  
pp. 631-642 ◽  
Author(s):  
Shao-Ming Lu ◽  
William Guido ◽  
S. Murray Sherman
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Visual Stimulation ◽  
Visual Stimuli ◽  
Membrane Potentials ◽  
Total Response ◽  
Response Component ◽  
Tonic Response ◽  
Lateral Geniculate ◽  
Low Threshold ◽  
Stimulation Of

AbstractWe recorded the responses of neurons from the cat’s lateral geniculate nucleus to drifting sine-wave grating stimuli both before and during electrical stimulation of the parabrachial region of the midbrain. The parabrachial region provides a mostly cholinergic input to the lateral geniculate nucleus, and our goal was to study its effect on responses of geniculate cells to visual stimulation. Geniculate neurons respond to visual stimuli in one of two modes. At relatively hyperpolarized membrane potentials, low threshold (LT) Ca2+ spikes are activated, leading to high-frequency burst discharges (burst mode). At more depolarized levels, the low threshold Ca2+ spike is inactivated, permitting a more tonic response (relay or tonic mode). During our intracellular recordings of geniculate cells, we found that, at initially hyperpolarized membrane potentials, LT spiking in response to visual stimulation was pronounced, but that parabrachial activation abolished this LT spiking and associated burst discharges. Coupled with the elimination of LT spiking, parabrachial activation also led to a progressive increase in tonic responsiveness. Parabrachial activation thus effectively switched the responses to visual stimulation of geniculate neurons from the burst to relay mode. Accompanying this switch was a gradual depolarization of resting membrane potential by about 5–10 mV and a reduction in the hyperpolarization that normally occurs in response to the inhibitory phase of the visual stimulus. Presumably, the membrane depolarization was sufficient to inactivate the LT spikes. We were able to extend and confirm our intracellular observations on the effects of parabrachial activation to a sample of cells recorded extracellularly. This was made possible by adopting empirically determined criteria to distinguish LT bursts from tonic responses solely on the basis of the temporal pattern of action potentials. During parabrachial activation, every cell responded only in the relay mode, an effect that corresponds to our intracellular observations. We quantified the effects of parabrachial activation on various response measures. The fundamental Fourier response amplitude (Fl) was calculated separately for the total response, the tonic response component, and the LT burst component. Parabrachial activation resulted in an increased Fl amplitude for the total response. This increase was due to an increase in the tonic response component. For a subset of cells showing epochs of LT bursting, parabrachial activation concurrently reduced LT bursting and increased the amplitude of the tonic response. Parabrachial activation, by eliminating LT bursting, also caused cells to respond with more linearity. By keeping geniculate cells in the relay mode, the parabrachial region serves to maintain a more linear retinogeniculate transfer of information to cortex, and this may be important for detailed analysis of visual targets. However, when a geniculate neuron becomes hyperpolarized, as may occur during states of visual inattention, it would not respond well to visual stimuli without the sort of nonlinear amplification provided by the LT spike. Thus, the LT spike may permit hyperpolarized cells to relay to cortex the presence of a potentially salient or dangerous stimulus, but this is done at the expense of linearity. This may serve as a sort of “wake-up call” that redirects attention to a particular stimulus and eventually enhances activity of appropriate parabrachial inputs to switch the critical geniculate neurons into the relay mode.

Current Clamp and Modeling Studies of Low-Threshold Calcium Spikes in Cells of the Cat’s Lateral Geniculate Nucleus

1999 ◽  
Vol 81 (5) ◽  
pp. 2360-2373 ◽  
Author(s):  
X. J. Zhan ◽  
C. L. Cox ◽  
J. Rinzel ◽  
S. Murray Sherman
Keyword(s):  
Membrane Potential ◽  
Lateral Geniculate Nucleus ◽  
Current Clamp ◽  
Calcium Spikes ◽  
Modeling Studies ◽  
Lateral Geniculate ◽  
Voltage Dependent ◽  
Low Threshold ◽  
Variable Latency ◽  
In Cells

Current clamp and modeling studies of low-threshold calcium spikes in cells of the cat’s lateral geniculate nucleus. All thalamic relay cells display a voltage-dependent low-threshold Ca2+ spike that plays an important role in relay of information to cortex. We investigated activation properties of this spike in relay cells of the cat’s lateral geniculate nucleus using the combined approach of current-clamp intracellular recording from thalamic slices and simulations with a reduced model based on voltage-clamp data. Our experimental data from 42 relay cells showed that the actual Ca2+ spike activates in a nearly all-or-none manner and in this regard is similar to the conventional Na+/K+ action potential except that its voltage dependency is more hyperpolarized and its kinetics are slower. When the cell’s membrane potential was hyperpolarized sufficiently to deinactivate much of the low-threshold Ca2+ current ( I T) underlying the Ca2+ spike, depolarizing current injections typically produced a purely ohmic response when subthreshold and a full-blown Ca2+ spike of nearly invariant amplitude when suprathreshold. The transition between the ohmic response and activated Ca2+ spikes was abrupt and reflected a difference in depolarizing inputs of <1 mV. However, activation of a full-blown Ca2+ spike was preceded by a slower period of depolarization that was graded with the amplitude of current injection, and the full-blown Ca2+ spike activated when this slower depolarization reached a sufficient membrane potential, a quasithreshold. As a result, the latency of the evoked Ca2+ spike became less with stronger activating inputs because a stronger input produced a stronger depolarization that reached the critical membrane potential earlier. Although Ca2+ spikes were activated in a nearly all-or-none manner from a given holding potential, their actual amplitudes were related to these holding potentials, which, in turn, determined the level of I T deinactivation. Our simulations could reproduce all of the main experimental observations. They further suggest that the voltage-dependent K+ conductance underlying I A, which is known to delay firing in many cells, does not seem to contribute to the variable latency seen in activation of Ca2+ spikes. Instead the simulations indicate that the activation of I T starts initially with a slow and graded depolarization until enough of the underling transient (or T) Ca2+ channels are recruited to produce a fast, “autocatalytic” depolarization seen as the Ca2+spike. This can produce variable latency dependent on the strength of the initial activation of T channels. The nearly all-or-none nature of Ca2+ spike activation suggests that when a burst of action potentials normally is evoked as a result of a Ca2+ spike and transmitted to cortex, this signal is largely invariant with the amplitude of the input activating the relay cell.

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