A multivariate population density model of the dLGN/PGN relay

Using a population density approach we study the dynamics of two interacting collections of integrate-and-fire-or-burst (IFB) neurons representing thalamocortical (TC) cells from the dorsal lateral geniculate nucleus (dLGN) and thalamic reticular (RE) cells from the perigeniculate nucleus (PGN). Each population of neurons is described by a multivariate probability density function that satisfies a conservation equation with appropriately defined probability fluxes and boundary conditions. The state variables of each neuron are the membrane potential and the inactivation gating variable of the low-threshold Ca²⁺ current I_T. The synaptic coupling of the populations and external excitatory drive are modeled by instantaneous jumps in the membrane potential of postsynaptic neurons. The population density model is validated by comparing its response to time-varying retinal input to Monte Carlo simulations of the corresponding IFB network composed of 100 to 1000 cells per population. In the absence of retinal input, the population density model exhibits rhythmic bursting similar to the 7 to 14 Hz oscillations associated with slow wave sleep that require feedback inhibition from RE to TC cells. When the TC and RE cell potassium leakage conductances are adjusted to represent cholingergic neuromodulation and arousal of the network, rhythmic bursting of the probability density model may either persists or be eliminated depending on the number of excitatory (TC to RE) or inhibitory (RE to TC) connections made by each presynaptic cell. When the probability density model is stimulated with constant retinal input (10–100 spikes/sec), a wide range of responses are observed depending on cellular parameters and network connectivity. These include asynchronous burst and tonic spikes, sleep spindle-like rhythmic bursting, and oscillations in population firing rate that are distinguishable from sleep spindles due to their amplitude, frequency, or the presence of tonic spikes. In this context of dLGN/PGN network modeling, we find the population density approach using 2,500 mesh points and resolving membrane voltage to 0.7 mV is over 30 times more efficient than 1000-cell Monte Carlo simulations. Action Editor: David Golomb     

Bursting as an Effective Relay Mode in a Minimal Thalamic Model

In recent years, accumulating evidence indicates that thalamic bursts are present during wakefulness and participate in information transmission as an effective relay mode with distinctive properties from the tonic activity. Thalamic bursts originate from activation of the low threshold calcium cannels via a local feedback inhibition, exerted by the thalamic reticular neurons upon the relay neurons. This article, examines if this simple mechanism is sufficient to explain the distinctive properties of thalamic bursting as an effective relay mode. A minimal model of thalamic circuit composed of a retinal spike train, a relay neuron and a reticular neuron is simulated to generate the tonic and burst firing modes. The integrate-and-fire-or-burst model is used to simulate the neurons. After discriminating the burst events with criteria based on inter-spike-intervals, statistical indices show that the bursts of the minimal model are stereotypic events. The relation between the rate of bursts and the parameters of the input spike train demonstrates marked nonlinearities. Burst response is shown to be selective to spike-silence-spike sequences in the input spike train. Moreover, burst events represent the input more reliably than the tonic spike in a considerable range of the parameters of the model. In conclusion, many of the distinctive properties of thalamic bursts such as stereotypy, nonlinear dependence on the sensory stimulus, feature selectivity and reliability are reproducible in the minimal model. Furthermore, the minimal model predicts that while the bursts are more frequent in the spike train of the off-center X relay neurons (corresponding to off-center X retinal ganglion cells), they are more reliable when generated by the on-center ones (corresponding to on-center X ganglion cells).     

Patterns of correlated spontaneous bursting activity in the developing mammalian retina

The adult visual system is highly organized in its patterns of connectivity. Connections between the retina and its central target, the dorsal lateral geniculate nucleus (dLGN), are remodeled during development as inappropriate synaptic inputs are eliminated by a process that requires retinal activity. Multineuronal recordings of the neonatal ferret retina reveal that during the refinement period, retinal ganglion cells spontaneously display rhythmic bursting activity in which the bursts of neighboring cells are correlated by propagating excitatory waves. These spontaneous retinal waves have temporal and spatial properties that appear instructive for the refinement of the early patterns of retinogeniculate connections prior to visual stimulation.     

Optogenetic Stimulation of the Corticothalamic Pathway Affects Relay Cells and GABAergic Neurons Differently in the Mouse Visual Thalamus

The dorsal lateral geniculate nucleus (dLGN) serves as the primary conduit of retinal information to visual cortex. In addition to retinal input, dLGN receives a large feedback projection from layer VI of visual cortex. Such input modulates thalamic signal transmission in different ways that range from gain control to synchronizing network activity in a stimulus-specific manner. However, the mechanisms underlying such modulation have been difficult to study, in part because of the complex circuitry and diverse cell types this pathway innervates. To address this and overcome some of the technical limitations inherent in studying the corticothalamic (CT) pathway, we adopted a slice preparation in which we were able to stimulate CT terminal arbors in the visual thalamus of the mouse with blue light by using an adeno-associated virus to express the light-gated ion channel, ChIEF, in layer VI neurons. To examine the postsynaptic responses evoked by repetitive CT stimulation, we recorded from identified relay cells in dLGN, as well as GFP expressing GABAergic neurons in the thalamic reticular nucleus (TRN) and intrinsic interneurons of dLGN. Relay neurons exhibited large glutamatergic responses that continued to increase in amplitude with each successive stimulus pulse. While excitatory responses were apparent at postnatal day 10, the strong facilitation noted in adult was not observed until postnatal day 21. GABAergic neurons in TRN exhibited large initial excitatory responses that quickly plateaued during repetitive stimulation, indicating that the degree of facilitation was much larger for relay cells than for TRN neurons. The responses of intrinsic interneurons were smaller and took the form of a slow depolarization. These differences in the pattern of excitation for different thalamic cell types should help provide a framework for understanding how CT feedback alters the activity of visual thalamic circuitry during sensory processing as well as different behavioral or pathophysiological states.     

猫外侧膝状体周核神经元对正弦光栅刺激的反应特性

以正弦光栅研究了猫外侧膝状体周核(Perigeniculate Nuclells,PGN)神经元的空间频率和朝向调谐特性,以及空间总和性质.通常,PGN神经元空间频率调谐可分带通和低通二类.朝向特性可分为较宽范围朝向选择、无朝向选择和不规则朝向选择三类.用对比度翻转(ContrastReversal Grating(的光栅刺激时,少部分细胞存在零相位位置(Null Phase Positions),大多数呈现“二倍频”反应(Frequency Doubling Response).实验说明PGN神经元可能存在-X类型和-Y类型.     

High-frequency (300-800 Hz) components in cat geniculate (dLGN) early visual responses.

We analysed the early visual responses of relay cells of the dorsal part of cat lateral geniculate nucleus (dLGN) for the occurrence and characteristics of high-frequency (>300 Hz) spike patterns comparable to the high-frequency oscillations (HFO) found in the human somatosensory system. By using a special algorithm for correcting response latency, we can show that the vast majority of dLGN visual responses which were elicited by a sudden change in contrast show HFOs in the range of 300 to more than 800 Hz. After response time correction these HFOs are clearly visible in summed responses, indicating that these patterns are highly reproducible by identical stimuli. On this basis we analysed the HFOs in more detail. We found the oscillation frequency to increase with stimulus contrast and the area of the receptive field centre covered by an excitatory stimulus. Inhibition reduces the oscillation frequency as demonstrated with additional stimulation of the antagonistic surround of the receptive field and by blocking inhibition with micro-iontophoretical application of bicuculline methiodide. The HFO was almost independent of the state of the system as estimated from the EEG pattern. Based on these findings we discuss whether bursts of action potentials triggered by the low-threshold calcium spike (LTS) can contribute to this pattern of visual thalamic activity.     

Reciprocal inhibition and slow calcium decay in perigeniculate interneurons explain changes of spontaneous firing of thalamic cells caused by cortical inactivation

The role of cortical feedback in the thalamocortical processing loop has been extensively investigated over the last decades. With an exception of several cases, these searches focused on the cortical feedback exerted onto thalamo-cortical relay (TC) cells of the dorsal lateral geniculate nucleus (LGN). In a previous, physiological study, we showed in the cat visual system that cessation of cortical input, despite decrease of spontaneous activity of TC cells, increased spontaneous firing of their recurrent inhibitory interneurons located in the perigeniculate nucleus (PGN). To identify mechanisms underlying such functional changes we conducted a modeling study in NEURON on several networks of point neurons with varied model parameters, such as membrane properties, synaptic weights and axonal delays. We considered six network topologies of the retino-geniculo-cortical system. All models were robust against changes of axonal delays except for the delay between the LGN feed-forward interneuron and the TC cell. The best representation of physiological results was obtained with models containing reciprocally connected PGN cells driven by the cortex and with relatively slow decay of intracellular calcium. This strongly indicates that the thalamic reticular nucleus plays an essential role in the cortical influence over thalamo-cortical relay cells while the thalamic feed-forward interneurons are not essential in this process. Further, we suggest that the dependence of the activity of PGN cells on the rate of calcium removal can be one of the key factors determining individual cell response to elimination of cortical input.     

A computational model of how an interaction between the thalamocortical and thalamic reticular neurons transforms the low-frequency oscillations of the globus pallidus

In Parkinson’s disease, neurons of the internal segment of the globus pallidus (GPi) display the low-frequency tremor-related oscillations. These oscillatory activities are transmitted to the thalamic relay nuclei. Computer models of the interacting thalamocortical (TC) and thalamic reticular (RE) neurons were used to explore how the TC-RE network processes the low-frequency oscillations of the GPi neurons. The simulation results show that, by an interaction between the TC and RE neurons, the TC-RE network transforms a low-frequency oscillatory activity of the GPi neurons to a higher frequency of oscillatory activity of the TC neurons (the superharmonic frequency transformation). In addition to the interaction between the TC and RE neurons, the low-threshold calcium current in the RE and TC neurons and the hyperpolarization-activated cation current (I _h) in the TC neurons have significant roles in the superharmonic frequency transformation property of the TC-RE network. The external globus pallidus (GPe) oscillatory activity, which is directly transmitted to the RE nucleus also displays a significant modulatory effect on the superharmonic frequency transformation property of the TC-RE network. Action Editor: John Rinzel     

High Frequency Stimulation of the Subthalamic Nucleus Eliminates Pathological Thalamic Rhythmicity in a Computational Model

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) or the internal segment of the globus pallidus (GPi) has recently been recognized as an important form of intervention for alleviating motor symptoms associated with Parkinson's disease, but the mechanism underlying its effectiveness remains unknown. Using a computational model, this paper considers the hypothesis that DBS works by replacing pathologically rhythmic basal ganglia output with tonic, high frequency firing. In our simulations of parkinsonian conditions, rhythmic inhibition from GPi to the thalamus compromises the ability of thalamocortical relay (TC) cells to respond to depolarizing inputs, such as sensorimotor signals. High frequency stimulation of STN regularizes GPi firing, and this restores TC responsiveness, despite the increased frequency and amplitude of GPi inhibition to thalamus that result. We provide a mathematical phase plane analysis of the mechanisms that determine TC relay capabilities in normal, parkinsonian, and DBS states in a reduced model. This analysis highlights the differences in deinactivation of the low-threshold calcium T -current that we observe in TC cells in these different conditions. Alternative scenarios involving convergence of thalamic signals in the cortex are also discussed, and predictions associated with these results, including the occurrence of rhythmic rebound bursts in certain TC cells in parkinsonian states and their drastic reduction by DBS, are stated. These results demonstrate how DBS could work by increasing firing rates of target cells, rather than shutting them down.     

视皮层反馈对猫外膝体神经元方位调制特性的影响

以扫描正弦光栅作为刺激,用冰冻法毁损皮层17、18、19区和外侧上雪氏回(LS区)来阻断皮层对外膝体的反馈投射,记录并描绘了猫外膝体597个细胞的方位调制特性.去视皮层猫外膝体神经元的平均方位选择性强度(Bias)为0.154,与正常猫(0.155)几乎相同,其最优方位偏向于水平方位.与正常猫外膝体不同的是,去视皮层猫外膝体失去了最优方位的切向分布规律,用GABA或KCl压抑皮层活动得到了相近的实验结果.结果说明正常外膝体的最优方位切向分布规律来自皮层反馈投射.     

Effect of destruction of basolateral nuclei of the amygdala on the character of electrical activity of the dorsomedial thalamic nucleus in rats

Characteristics of slow global and of unit activity in the dorsomedial thalamic nucleus were studied at various times after destruction of nuclei of the basolateral amygdala in semichronic experiments on anesthetized rats. Destruction of this kind was found to cause periodic transformation of the neuronal discharge into rhythmic bursts of spikes, and into the development of bursts of paroxysmal activity in the form of groups of four to six pointed waves with a mean duration of 60.5±20.6 msec, appearing with a frequency of 1.5±0.3 Hz. A change in the coefficient of correlation was found between the duration of bursts and their frequency during the 20–22-sec period of their generation. Interference was demonstrated between bursts and orthodromic focal potentials, evoked by stimulation of the anterior periamygdalar cortex and anterior amygdalar region. Neurons were described with long (up to 1 sec) responses to stimulation of the periamygdalar cortex and amygdalar region, in the form of regular bursts of spikes or tonic activation, correlating with the appearance of a rhythmic after-discharge. Bursts of this kind, which were most marked during the first 3 or 4 days after destruction of the basolateral amygdala, were observed to begin to disappear toward the end of the first postoperative week. It is suggested that one mechanism of the change in the adaptive behavior of animals with destruction of the amygdala is a disturbance, linked with the bursts, of the relay and integrative functions of the dorsomedial thalamic nucleus.     

Retinal and cortical nonlinearities combine to produce masking in V1 responses to plaids

The visual response of a cell in the primary visual cortex (V1) to a drifting grating stimulus at the cell’s preferred orientation decreases when a second, perpendicular, grating is superimposed. This effect is called masking. To understand the nonlinear masking effect, we model the response of Macaque V1 simple cells in layer 4Cα to input from magnocellular Lateral Geniculate Nucleus (LGN) cells. The cortical model network is a coarse-grained reduction of an integrate-and-fire network with excitation from LGN input and inhibition from other cortical neurons. The input is modeled as a sum of LGN cell responses. Each LGN cell is modeled as the convolution of a spatio-temporal filter with the visual stimulus, normalized by a retinal contrast gain control, and followed by rectification representing the LGN spike threshold. In our model, the experimentally observed masking arises at the level of LGN input to the cortex. The cortical network effectively induces a dynamic threshold that forces the test grating to have high contrast before it can overcome the masking provided by the perpendicular grating. The subcortical nonlinearities and the cortical network together account for the masking effect. Melinda Koelling is formerly from Center for Neural Science and Courant Institute, New York University.     

Synchronization of Isolated Downstates (K-Complexes) May Be Caused by Cortically-Induced Disruption of Thalamic Spindling

Sleep spindles and K-complexes (KCs) define stage 2 NREM sleep (N2) in humans. We recently showed that KCs are isolated downstates characterized by widespread cortical silence. We demonstrate here that KCs can be quasi-synchronous across scalp EEG and across much of the cortex using electrocorticography (ECOG) and localized transcortical recordings (bipolar SEEG). We examine the mechanism of synchronous KC production by creating the first conductance based thalamocortical network model of N2 sleep to generate both spontaneous spindles and KCs. Spontaneous KCs are only observed when the model includes diffuse projections from restricted prefrontal areas to the thalamic reticular nucleus (RE), consistent with recent anatomical findings in rhesus monkeys. Modeled KCs begin with a spontaneous focal depolarization of the prefrontal neurons, followed by depolarization of the RE. Surprisingly, the RE depolarization leads to decreased firing due to disrupted spindling, which in turn is due to depolarization-induced inactivation of the low-threshold Ca²⁺ current (I_T). Further, although the RE inhibits thalamocortical (TC) neurons, decreased RE firing causes decreased TC cell firing, again because of disrupted spindling. The resulting abrupt removal of excitatory input to cortical pyramidal neurons then leads to the downstate. Empirically, KCs may also be evoked by sensory stimuli while maintaining sleep. We reproduce this phenomenon in the model by depolarization of either the RE or the widely-projecting prefrontal neurons. Again, disruption of thalamic spindling plays a key role. Higher levels of RE stimulation also cause downstates, but by directly inhibiting the TC neurons. SEEG recordings from the thalamus and cortex in a single patient demonstrated the model prediction that thalamic spindling significantly decreases before KC onset. In conclusion, we show empirically that KCs can be widespread quasi-synchronous cortical downstates, and demonstrate with the first model of stage 2 NREM sleep a possible mechanism whereby this widespread synchrony may arise.     

Network Oscillations Drive Correlated Spiking of ON and OFF Ganglion Cells in the rd1 Mouse Model of Retinal Degeneration

Following photoreceptor degeneration, ON and OFF retinal ganglion cells (RGCs) in the rd-1/rd-1 mouse receive rhythmic synaptic input that elicits bursts of action potentials at ∼10 Hz. To characterize the properties of this activity, RGCs were targeted for paired recording and morphological classification as either ON alpha, OFF alpha or non-alpha RGCs using two-photon imaging. Identified cell types exhibited rhythmic spike activity. Cross-correlation of spike trains recorded simultaneously from pairs of RGCs revealed that activity was correlated more strongly between alpha RGCs than between alpha and non-alpha cell pairs. Bursts of action potentials in alpha RGC pairs of the same type, i.e. two ON or two OFF cells, were in phase, while bursts in dissimilar alpha cell types, i.e. an ON and an OFF RGC, were 180 degrees out of phase. This result is consistent with RGC activity being driven by an input that provides correlated excitation to ON cells and inhibition to OFF cells. A2 amacrine cells were investigated as a candidate cellular mechanism and found to display 10 Hz oscillations in membrane voltage and current that persisted in the presence of antagonists of fast synaptic transmission and were eliminated by tetrodotoxin. Results support the conclusion that the rhythmic RGC activity originates in a presynaptic network of electrically coupled cells including A2s via a Na⁺-channel dependent mechanism. Network activity drives out of phase oscillations in ON and OFF cone bipolar cells, entraining similar frequency fluctuations in RGC spike activity over an area of retina that migrates with changes in the spatial locus of the cellular oscillator.     

The influence of the corticothalamic projection on responses in thalamus and cortex

We review results on the in vivo properties of neurons in the dorsal lateral geniculate nucleus (dLGN) that receives its afferent input from the retina and projects to the visual cortex. In addition, the dLGN receives input from the brain stem and from a rather strong corticothalamic back-projection, which originates in layer 6 of the visual cortex. We compare the behaviour of dLGN cells during spontaneous changes of the frequency contents of the electroencephalograph (EEG) (which are mainly related to a changing brain stem influence), with those that are obtained when experimentally silencing the corticothalamic feedback. The spatial and temporal response properties of dLGN cells are compared during these two conditions, and we report that the neurons behave similarly during a synchronized EEG state and during inactive corticothalamic feedback. In both situations, dLGN cells are rather phasic and their remaining tonic activity is temporally dispersed, indicating a hyperpolarizing effect. By means of a novel method, we were able to chronically eliminate a large proportion of the corticothalamic projection neurons from the otherwise intact cortex. In this condition, we found that cortical cells also lose their EEG specific response differences but, in this instance, probably due to a facilitatory (depolarizing) plasticity reaction of the remaining network.     

Active dendritic conductances dynamically regulate GABA release from thalamic interneurons

Inhibitory interneurons in the dorsal lateral geniculate nucleus (dLGN) process visual information by precisely controlling spike timing and by refining the receptive fields of thalamocortical (TC) neurons. Previous studies indicate that dLGN interneurons inhibit TC neurons by releasing GABA from both axons and dendrites. However, the mechanisms controlling GABA release are poorly understood. Here, using simultaneous whole-cell recordings from interneurons and TC neurons and two-photon calcium imaging, we find that synchronous activation of multiple retinal ganglion cells (RGCs) triggers sodium spikes that propagate throughout interneuron axons and dendrites, and calcium spikes that invade dendrites but not axons. These distinct modes of interneuron firing can trigger both a rapid and a sustained component of inhibition onto TC neurons. Our studies suggest that active conductances make LGN interneurons flexible circuit-elements that can shift their spatial and temporal properties of GABA release in response to coincident activation of functionally related subsets of RGCs.     

A multi-compartment model for interneurons in the dorsal lateral geniculate nucleus

GABAergic interneurons (INs) in the dorsal lateral geniculate nucleus (dLGN) shape the information flow from retina to cortex, presumably by controlling the number of visually evoked spikes in geniculate thalamocortical (TC) neurons, and refining their receptive field. The INs exhibit a rich variety of firing patterns: Depolarizing current injections to the soma may induce tonic firing, periodic bursting or an initial burst followed by tonic spiking, sometimes with prominent spike-time adaptation. When released from hyperpolarization, some INs elicit rebound bursts, while others return more passively to the resting potential. A full mechanistic understanding that explains the function of the dLGN on the basis of neuronal morphology, physiology and circuitry is currently lacking. One way to approach such an understanding is by developing a detailed mathematical model of the involved cells and their interactions. Limitations of the previous models for the INs of the dLGN region prevent an accurate representation of the conceptual framework needed to understand the computational properties of this region. We here present a detailed compartmental model of INs using, for the first time, a morphological reconstruction and a set of active dendritic conductances constrained by experimental somatic recordings from INs under several different current-clamp conditions. The model makes a number of experimentally testable predictions about the role of specific mechanisms for the firing properties observed in these neurons. In addition to accounting for the significant features of all experimental traces, it quantitatively reproduces the experimental recordings of the action-potential- firing frequency as a function of injected current. We show how and why relative differences in conductance values, rather than differences in ion channel composition, could account for the distinct differences between the responses observed in two different neurons, suggesting that INs may be individually tuned to optimize network operation under different input conditions.     

Electrical potentials from the eye and optic nerve of Strombus: effects of electrical stimulation of the optic nerve.

1. Photic stimulation of the mature eye of Strombus can evoke in the optic nerve 'on' activity in numerous small afferent fibres and repetitive 'off' bursts of afferent impulses in a smaller number of larger fibres. 2. Synchronous invasion of the eye by electrically evoked impulses in small optic nerve fibres (apparently the 'on' afferents, antidromically activated) can evoke a burst of impulses in the larger 'off' fibres which propagate away from the eye. Invasion of the eye via one branch of optic nerve can evoke an answering burst in another branch. 3. Such electrically evoked bursts are similar to light-evoked 'off' bursts with respect to their impulse composition, their ability to be inhibited by illumination of the eye, and their susceptibility to MgCl2 anaesthesia. 4. Invasion of the eye by a train of repetitive electrically evoked impulses in the absence of photic stimulation can give rise to repetitive 'off' bursts as well as concomitant oscillatory potentials in the eye which are similar to those normally evoked by cessation of a photic stimulus. 5. The electrically evoked 'off' bursts appear to be caused by an excitatory rebound following the cessation of inhibitory synaptic input from photoreceptors which can be antidromically activated by electrical stimulation of the optic nerve. 6. The experimental results suggest that the rhythmic discharge of the 'off' fibres evoked by the cessation of a photic stimulus is mediated by the abrupt decrease of inhibitory synaptic input from the receptors.     

Relative spike timing in stochastic oscillator networks of the Hermissenda eye

The role of relative spike timing on sensory coding and stochastic dynamics of small pulse-coupled oscillator networks is investigated physiologically and mathematically, based on the small biological eye network of the marine invertebrate Hermissenda. Without network interactions, the five inhibitory photoreceptors of the eye network exhibit quasi-regular rhythmic spiking; in contrast, within the active network, they display more irregular spiking but collective network rhythmicity. We investigate the source of this emergent network behavior first analyzing the role of relative input to spike–timing relationships in individual cells. We use a stochastic phase oscillator equation to model photoreceptor spike sequences in response to sequences of inhibitory current pulses. Although spike sequences can be complex and irregular in response to inputs, we show that spike timing is better predicted if relative timing of spikes to inputs is accounted for in the model. Further, we establish that greater noise levels in the model serve to destroy network phase-locked states that induce non-monotonic stimulus rate-coding, as predicted in Butson and Clark (J Neurophysiol 99:146–154, 2008a; J Neurophysiol 99:155–165, 2008b). Hence, rate-coding can function better in noisy spiking cells relative to non-noisy cells. We then study how relative input to spike–timing dynamics of single oscillators contribute to network-level dynamics. Relative timing interactions in the network sharpen the stimulus window that can trigger a spike, affecting stimulus encoding. Also, we derive analytical inter-spike interval distributions of cells in the model network, revealing that irregular Poisson-like spike emission and collective network rhythmicity are emergent properties of network dynamics, consistent with experimental observations. Our theoretical results generate experimental predictions about the nature of spike patterns in the Hermissenda eye.     

Dendritic development in the dorsal lateral geniculate nucleus of ferrets in the postnatal absence of retinal input: A golgi study

In order to determine the ongoing role of retinal fibers in the development of dorsal lateral geniculate nucleus (dLGN) neurons during postnatal development, the development of dLGN neurons in the postnatal absence of retinal input was studied in pigmented ferrets using the Golgi-Hortega technique. The development of four dLGN cell classes, defined on the basis of somatic and dendritic morphology, was described previously in normal ferrets (Sutton and Brunso-Bechtold, 1991, J. Comp. Neurol. 309 : 71–85). The present results indicate that the morphological development of dLGN neurons is strikingly similar in normal and experimental ferrets. The exuberant dendritic appendages that appear after eye opening in normal ferrets are overproduced and eliminated in the postnatal absence of retinal input; however, the final reduction of these transient appendages is delayed. Because exuberant appendages develop in the absence of retinal input, their production cannot depend upon visual experience. Differences in cell body size between normal and experimental ferrets are apparent only after neurons can be classified at the end of the first postnatal month. Cell body size is markedly reduced for class 1 neurons; class 2 cells also are reduced in size but to a far lesser extent. As there is a general trend for class 1 neurons to have the functional properties of Y-cells, it is likely that the dLGN neurons most affected by the absence of retinal input also are Y-cells. © 1993 John Wiley & Sons, Inc.