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W Guido

Publications and source records attributed to W Guido.

At least 19 recordsLinked to original sources

Synaptic plasticity in the trigeminal principal nucleus during the period of barrelette formation and consolidation.

We examined whether the postsynaptic responses of cells in the principal sensory nucleus of the trigeminal nerve (PrV) are subject to long-term changes in synaptic strength, and if such changes were correlated the whisker-specific patterning during and just after the critical period for pattern formation. We used an in vitro brainstem preparation in which the trigeminal ganglion (TG) and PrV remained attached. By electrically activating TG afferents, we evoked large-amplitude extracellular field potentials. These responses were postsynaptic in origin and blocked by the glutamate antagonist, DNQX. At P1, a time when barrelettes are consolidating, high frequency stimulation of their afferents led to an immediate (<1 min) and long-lasting (> or =90 min) reduction (35%) in the amplitude of the evoked response. At P3-7, when the pattern of barrelettes have stabilized, the same form of tetanus led to an immediate and long-lasting increase (40%) in the amplitude of the response. Both forms of synaptic plasticity were mediated by the activation of L-type Ca(2+) channels. Application of the L-type channel blocker, nitrendipine, led to a complete blockade of any the tetanus induced changes. These associative processes may regulate the patterning and maintenance of whisker-specific patterns in the brainstem trigeminal nuclei.

2-Amino-5-phosphonovalerate↗

Burst and tonic response modes in thalamic neurons during sleep and wakefulness.

Thalamic neurons can exhibit two distinct firing modes: tonic and burst. In the lateral geniculate nucleus (LGN), the tonic mode appears as a relatively faithful relay of visual information from retina to cortex. The function of the burst mode is less understood. Its prevalence during slow-wave sleep (SWS) and linkage to synchronous cortical electroencephalogram (EEG) suggest that it has an important role during this form of sleep. Although not nearly as common, bursting can also occur during wakefulness. The goal of this study was to identify conditions that affect burst probability, and to compare burst incidence during sleeping and waking. LGN neurons are extraordinarily heterogenous in the degree to which they burst, during both sleeping and waking. Some LGN neurons never burst under any conditions during wakefulness, and several never burst during slow-wave sleep. During wakefulness, <1% of action potentials were associated with bursting, whereas during sleep this fraction jumps to 18%. Although bursting was most common during slow-wave sleep, more than 50% of the bursting originated from 14% of the LGN cells. Bursting during sleep was largely restricted to episodes lasting 1-5 s, with approximately 47% of these episodes being rhythmic and in the delta frequency range (0.5-4 Hz). In wakefulness, although visual stimulation accounted for the greatest number of bursts, it was still a small fraction of the total response (4%, 742 bursts/17,744 cycles in 93 cells). We identified two variables that appeared to influence burst probability: size of the visual stimuli used to elicit responses and behavioral state. Increased stimulus size increased burst probability. We attribute this to the increased influence large stimuli have on a cell's inhibitory mechanisms. As with sleep, a large fraction of bursting originated from a small number of cells. During visual stimulation, 50% of bursting was generated by 9% of neurons. Increased vigilance was negatively correlated with burst probability. Visual stimuli presented during active fixation (i.e., when the animal must fixate on an overt fixation point) were less likely to produce bursting, than when the same visual stimuli were presented but no fixation point present ("passive" fixation). Such observations suggest that even brief departures from attentive states can hyperpolarize neurons sufficiently to de-inactivate the burst mechanism. Our results provide a new view of the temporal structure of bursting during slow-wave sleep; one that supports episodic rhythmic activity in the intact animal. In addition, because bursting could be tied to specific conditions within wakefulness, we suggest that bursting has a specific function within that state.

Action Potentials↗

A novel means of Y cell identification in the developing lateral geniculate nucleus of the cat.

We examined the postnatal development of putative Y cells in the dorsal lateral geniculate nucleus (dLGN) using the SMI-32 antibody, which has been demonstrated in the adult cat to stain cells with Y cell morphology. At birth, SMI-32 stained cells were concentrated in the interlaminar zones. During postnatal development, the SMI-32 staining gradually becomes more disperse and by P21 stained cells are found throughout the A and magnocellular C laminae. By the end of the first postnatal week, and in all later ages examined, the SMI-32 stained cells were significantly larger than the overall population of Nissl stained cells and interneurons (stained with an antibody against glutamic acid decarboxylase). Postnatal SMI-32 staining revealed a dramatic increase in soma sizes and the expansion of putative geniculate Y cell dendritic arbors that continued past the second postnatal month. In contrast, the growth of interneurons appeared to be complete by 3-4 postnatal weeks, at which time cell somas stained with SMI-32 have only reached a little over one half of their adult size. Similar to the adult cat, SMI-32 appears to selectively stain the Y cell population during development and may provide a useful morphological marker to examine the participation of Y cells in the developing postnatal circuitry of the dLGN. This further establishes the cat dLGN as a novel model system to study the normal function and pathological reorganization of neurofilaments.

Animals↗

Development of the cholinergic, nitrergic, and GABAergic innervation of the cat dorsal lateral geniculate nucleus.

Cholinergic projections from the brainstem have been shown to be important modulators of visual activity in the dorsal lateral geniculate nucleus (dLGN) of the adult, but little is known about the role of these modulatory inputs during development. We examined the postnatal development of the cholinergic innervation of the dLGN by using an monoclonal antibody against choline acetyl transferase (ChAT). We also investigated the development of GABAergic interneurons in the dLGN by using an antibody against glutamic acid decarboxylase (GAD), and the developmental expression of brain nitric oxide synthase (BNOS) by using an antibody against this enzyme. We found that brainstem cells surrounding the brachium conjunctivum express ChAT at birth, although axons in the dLGN do not express ChAT until the end of the first postnatal week. Cholinergic synaptic contacts were observed as early as the second postnatal week. The number of axons stained with the ChAT antibody increased slowly during the subsequent weeks in the dLGN and reached adult levels by the eighth postnatal week. GABAergic interneurons were present at birth and reached their adult soma size by the third postnatal week. GABAergic fibers are dense at birth but change during development from a diffuse pattern to clustered arrangements that can be recognized as distinct rings of GAD staining by P35. Cellular expression of BNOS was seen within all dLGN laminae during development. The BNOS-stained cells are tentatively identified as interneurons because their soma sizes were similar to those of GAD-stained cells. Although cellular BNOS staining remained robust in the C1-3 laminae through adulthood, cellular expression of BNOS in the A laminae declined during the first five postnatal weeks and remains sparse in the adult. As cellular BNOS staining declined, there was a steady increase in BNOS-stained fibers, which paralleled the increase of ChAT-stained fibers that are known to colocalize BNOS in the adult. Our results emphasize the continued transformations of intrinsic as well as extrinsic innervation patterns that occur during the development, of the dLGN.

Acetylcholine↗

Nitric oxide synthase distribution in the cat superior colliculus and co-localization with choline acetyltransferase.

Nitric oxide and acetylcholine are important neuromodulators implicated in brain plasticity and disease. We have examined the cellular and fiber localization of nitric oxide in the cat superior colliculus (SC) and its degree of co-localization with ACh using nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry and an antibody to neuronal nitric oxide synthase. ACh was localized using an antibody against choline acetyltransferase. We also made injections of biocytin into the region of the parabrachial brainstem to confirm that this region is a source of nitric oxide containing fibers in SC. NADPHd labeled neurons within the superficial layers of the superior colliculus included pyriform, vertical fusiform, and horizontal morphologies. Labeled neurons in the intermediate gray layer were small to medium in size, and mostly of stellate morphology. Neurons in the deepest layers had mostly vertical or stellate morphologies. NADPHd labeled fibers formed dense patches of terminal boutons within the intermediate gray layer and streams of fibers within the deepest layers of SC. Choline acetyltransferase antibody labeling in adjacent sections indicated that many fibers must contain both labels. Over 94% of neurons in the pedunculopontine tegmental and lateral dorsal tegmental nuclei were also labeled by both NADPHd and choline acetyltransferase. In addition, biocytin labeled fibers from this region were localized in the NADPHd labeled patches. We conclude that nitric oxide is contained in a variety of cell types in SC and that both nitric oxide and ACh likely serve as co-modulators in this midbrain structure.

Animals↗

Electrophysiological properties and synaptic responses of cells in the trigeminal principal sensory nucleus of postnatal rats.

In the rodent brain stem trigeminal complex, select sets of neurons form modular arrays or "barrelettes," that replicate the patterned distribution of whiskers and sinus hairs on the ipsilateral snout. These cells detect the patterned input from the trigeminal axons that innervate the whiskers and sinus hairs. Other brain stem trigeminal cells, interbarrelette neurons, do not form patterns and respond to multiple whiskers. We examined the membrane properties and synaptic responses of morphologically identified barrelette and interbarrelette neurons in the principal sensory nucleus (PrV) of the trigeminal nerve in early postnatal rats shortly after whisker-related patterns are established. Barrelette cell dendritic trees are confined to a single barrelette, whereas the dendrites of interbarrelette cells span wider territories. These two cell types are distinct from smaller GABAergic interneurons. Barrelette cells can be distinguished by a prominent transient A-type K(+) current (I(A)) and higher input resistance. On the other hand, interbarrelette cells display a prominent low-threshold T-type Ca(2+) current (I(T)) and lower input resistance. Both classes of neurons respond differently to electrical stimulation of the trigeminal tract. Barrelette cells show either a monosynaptic excitatory postsynaptic potential (EPSP) followed by a large disynaptic inhibitory postsynaptic potential (IPSP) or just simply a disynaptic IPSP. Increasing stimulus intensity produces little change in EPSP amplitude but leads to a stepwise increase in IPSP amplitude, suggesting that barrelette cells receive more inhibitory input than excitatory input. This pattern of excitation and inhibition indicates that barrelette cells receive both feed-forward and lateral inhibition. Interbarrelette cells show a large monosynaptic EPSP followed by a small disynaptic IPSP. Increasing stimulus intensity leads to a stepwise increase in EPSP amplitude and the appearance of polysynaptic EPSPs, suggesting that interbarrelette cells receive excitatory inputs from multiple sources. Taken together, these results indicate that barrelette and interbarrelette neurons can be identified by their morphological and functional attributes soon after whisker-related pattern formation in the PrV.

4-Aminopyridine↗

Neurofilament proteins in Y-cells of the cat lateral geniculate nucleus: normal expression and alteration with visual deprivation.

We examined neurofilament staining in the normal and visually deprived lateral geniculate nucleus (LGN), using the SMI-32 antibody. This antibody preferentially stains LGN cells that display the morphological characteristics of Y-cells. The soma sizes of SMI-32-stained cells were consistent with those of the overall population of Y-cells, and the Golgi-like staining of their dendrites revealed a radial distribution that often crossed laminar boundaries. Labeled cells were distributed within the A laminae (primarily near laminar borders), the magnocellular portion of the C laminae, and the medial intralaminar nucleus, but they were absent in the parvocellular C laminae. Electron microscopic examination of SMI-32-stained tissue revealed that staining was confined to somata, dendrites, and large myelinated axons. Retinal synapses on SMI-32-labeled dendrites were primarily simple axodendritic contacts; few triadic arrangements were observed. In the LGN of cats reared with monocular lid suture, SMI-32 staining was decreased significantly in the A laminae that received input from the deprived eye. Dephosphorylation of the tissue did not alter the cellular SMI-32 staining patterns. Analysis of staining patterns in the C laminae and monocular zone of the A laminae suggests that changes in the cytoskeleton after lid suture reflect cell class and not binocular competition. Taken together, the results from normal and lid-sutured animals suggest that the cat LGN offers a unique model system in which the cytoskeleton of one class of cells can be manipulated by altering neuronal activity.

Alkaline Phosphatase↗

Developmental changes in the electrophysiological properties of brain stem trigeminal neurons during pattern (barrelette) formation.

In the brain stem trigeminal nuclei of rodents there is a patterned representation of whiskers and sinus hairs. The subnucleus interpolaris (SPI) contains the largest and the most conspicuous whisker patterns (barrelettes). Although neural activity plays a role in pattern formation, little is known about the electrophysiological properties of developing barrelette neurons. Here we examined the functional state of early postnatal SPI neurons during and after the consolidation of patterns by using in vitro intracellular recording techniques. After the consolidation of barrelettes [>/= postnatal day (P)4], responses to intracellular current injection consistently reflected the activation of a number voltage-dependent conductances. Most notable was a mixed cation conductance (IH) that prevented strong hyperpolarization and a large low-threshold Ca2+ conductance, which led to Ca2+ spikes and burst firing. At the oldest ages tested (P11-P14) some cells also exhibited an outward K+ conductance (IA), which led to significant delays in action-potential firing. Between P0-3, a time when the formation of barrelettes in the brain stem is still susceptible to damage of the sensory periphery, cells responded linearly to intracellular current injection, indicating they either lacked such voltage-gated properties or weakly expressed them. At all ages tested (P0-14), SPI cells were capable of generating trains of action potentials in response to intracellular injection of depolarizing current pulses. However, during the first few days of postnatal life, spikes were shorter and longer. Additionally, spike trains rose more linearly with stimulus intensity and showed frequency accommodation at early ages. Taken together, these results indicate that the electrophysiological properties of SPI neurons change markedly during the period of barrelette consolidation. Moreover, the properties of developing SPI neurons may play a significant role in pattern formation by minimizing signal distortion and ensuring that excitatory responses from sensory periphery are accurately received and transmitted according to stimulus strength.

Afferent Pathways↗

Functional connectivity in the rodent trigeminal pathway grown in vitro.

In explant cocultures of the rat trigeminal pathway, embryonic trigeminal ganglion cells grow their axons into peripheral cutaneous and central nervous system targets (R.S. Erzurumlu, S. Jhaveri, Target influences on the morphology of trigeminal axons, Exp. Neurol, 135 (1995) 1-16; R.S. Erzurumlu, S. Jhaveri, H. Takahashi, R.D.G. McKay, Target-derived influences on axon growth modes in explant cocultures of trigeminal neurons, Proc. Natl. Acad. Sci. USA 90 (1993) 7235-7239). In heterochronic cocultures, composed of embryonic trigeminal ganglion, embryonic whisker pad and postnatal brainstem slice, trigeminal axons develop arbors and terminal boutons in the brainstem trigeminal nuclei. To determine whether these terminal arbors establish functional connections with the brainstem neurons, we examined the electrophysiological properties of brainstem neurons and their responsiveness to trigeminal ganglion stimulation. Intracellular recordings were done in vitro on cells of the trigeminal subnucleus interpolaris (SPI) in trigeminal pathway cocultures (E15 whisker pad, E15 trigeminal ganglion, and postnatal day (PND) 0-2 brainstem slice) or in the SPI of acutely prepared brainstem slices. Electrophysiological properties of SPI cells in both preparations were virtually identical. The voltage responses of SPI neurons to intracellular current injection were highly linear suggesting they lacked a number of voltage-dependent conductances. Depolarizing current injection produced trains of action potentials with a frequency that varied with stimulus intensity. In explant cocultures, electrical activation of the trigeminal ganglion evoked EPSPs, and EPSPs coupled with IPSPs in SPI cells. Bicuculline blockade of IPSP activity resulted in long lasting EPSPs whose duration increased with membrane depolarization. These results show that brainstem trigeminal neurons can retain their functional properties in culture and establish functional connections with primary sensory afferents.

Animals↗

An in vitro model of the kitten retinogeniculate pathway.

An organotypic explant coculture method is described for the developing retinogeniculate pathway of the cat. Retinal explants and thalamic slices containing the dorsal lateral geniculate nucleus (LGN), derived from early postnatal kittens, can be grown in serum-free culture medium for several days. In such cultures, retinal ganglion cells (RGCs) and LGN neurons retained their age-specific morphological features and developed functional connections. Labeling of RGCs and their processes with DiI showed that all three major classes of RGCs (alpha/Y, beta/X, gamma/W) were present in cocultured retinal explants. Retinal axons readily regenerated into thalamic slices and, over time, developed arbors within the LGN. Retrograde labeling from the LGN traced the origin of these axons almost exclusively to alpha-cells in the retina. In vitro intracellular recordings indicated that LGN cells maintained their basic electrophysiological properties in coculture. Current injection generated action potentials, and, at hyperpolarized levels, it led to low-threshold Ca2+ spiking. Regenerated retinal axons also formed functional connections with LGN neurons. Electrical stimulation of the retinal explant elicited excitatory postsynaptic responses (EPSPs) in LGN cells. Drop application of specific glutamate antagonists indicated that EPSPs had both N-methyl-D-aspartate (NMDA) and non-NMDA receptor components. The morphology of the LGN neurons was examined after intracellular injections of biocytin during recording. Labeled cells were very similar to those of early postnatal kittens. Although, in general, they had relatively small soma and simple dendritic branching patterns, a few could be recognized as X- or Y-cells. Thus the coculture model can be used to assay the regenerative propensity of different types of RGCs during development.

Action Potentials↗

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

We constructed average histograms from responses evoked by flashing stimuli and noted previously described variations in the shape of the response profile, particularly with respect to sharpness of the peak. To express this variable, we measured the half-rise latency, which is the latency from stimulus onset required to reach half the maximum response. A short half-rise latency, which is characteristic of nonlagged cells, is associated with a brisk response and sharp peak; a long half-rise latency, characteristic of lagged cells, is associated with a sluggish response and broad peak. Nonlagged cells were readily seen; we attempted to identify cells with long latencies as lagged, but we were unable to do so unambiguously due to failure to observe lagged properties other than latency. We thus refer to these latter cells as having "lagged-like" responses to indicate that we are not certain whether these are indeed lagged cells. In addition to the histograms, we analyzed the individual response trials that were summed to create each histogram, and we used spike density analysis to estimate the initial response latency to the flashing spot for each trial. We found that lagged-like responses were associated with more variability in initial response latency than were nonlagged responses. We then employed an alignment procedure to eliminate latency variation from individual trials; that is, responses during individual trials were shifted in time as needed so that each had a latency equal to the average latency of all trials. We used these "aligned" trials to create a second, "aligned" response histogram for each cell. The alignment procedure had little effect on nonlagged responses, because these were already well aligned due to consistent response latencies amongst trials. For lagged-like responses, however, the alignment made a dramatic difference. The aligned histograms looked very much like those for nonlagged responses: the responses appeared brisk, with a sharply rising peak that was fairly high in amplitude. We thus conclude that the slow build up to a relatively low peak of firing of the lagged-like response histogram is not an accurate reflection of responses on single trials. Instead, the sluggishness of lagged-like responses inferred from average response histograms results from temporal smearing due to latency variability amongst trials. We thus conclude that there is relatively little difference in briskness between nonlagged and lagged-like responses to single stimuli.

Animals↗

Burst responses in thalamic relay cells of the awake behaving cat.

1. Relay cells of the dorsal lateral geniculate nucleus (LGN) respond in one of two modes: tonic or burst. The purpose of this study was to determine whether, and under what conditions, burst responses occur in LGN cells of an awake, behaving animal. 2. We recorded the extracellular responses of cells located in the A layers of LGN in two cats trained to perform a simple fixation task. In our paradigm, head position was fixed and gaze monitored with the use of the scleral search coil technique. They were trained to fixate on a small target light while we probed the receptive field of an isolated LGN cell with drifting gratings. 3. Many LGN cells (37/48; 77%) recorded in the awake cat showed some form of burst firing. However, the degree of burstiness a given cell displayed was relatively low. The probability of recording a burst response during any second within the fixation task was 0.09. This reflects the fact that during wakefulness, LGN cells are generally in a state of relative depolarization and the low-threshold Ca2+ conductance underlying burst firing is inactivated. 4. The majority of bursts occurred (262/377; 71%) during visual stimulation. These comprised the initial response to the grating and were confined to the early phase of fixation. As the cat continued to hold fixation and as subsequent cycles of the grating passed through the cell's receptive field, the response shifted from a burst to a tonic firing pattern. Some bursts (67/377, 18%) were related to eye movements. All of these were postsaccadic, and most occurred > 150 ms from the onset of the eye movement. Finally, some bursts were neither visually driven nor related to eye movements. However, these spontaneous bursts were infrequent (41/377; 11%) and never rhythmic. 5. Burst firing in LGN cells has a dual purpose. During quiescent states such as slow-wave sleep, they support the decoupling of retinal signals from LGN. During the waking state, bursts can facilitate signal transmission during target acquisition and early phases of fixation.

Animals↗

Cellular bases for the control of retinogeniculate signal transmission.

The dorsal lateral geniculate nucleus (LGN) is the major thalamic relay for retinal signals en route to cortex. However, LGN cells operate as more than just a simple relay of their retinal inputs. Rather, they function as a variable gate, determining what, when, and how much retinal information gets passed to visual cortex. Two factors that are key to this control are the innervation patterns and electrophysiological membrane properties of geniculate cells. This paper discusses three active membrane properties and the manner in which they modulate the transfer of retinal signals to cortex. They are the low threshold calcium (Ca2+) conductance, a transient potassium (K+) conductance, and NMDA receptor-mediated excitatory postsynaptic potentials (EPSPs). The low-threshold Ca2+ conductance transforms a geniculate cell from a state of single spike activity to one of bursting discharge, the potassium current leads to a delay in membrane depolarization to reach spike threshold, and NMDA receptor activity modulates EPSP amplitude and duration near spike threshold. Additionally, we consider how nonretinal inputs, such as the ascending cholinergic pathway from the brainstem parabrachial region and the descending pathway from layer VI of visual cortex, influence the expression of these membrane properties through their control of membrane potential.

Acetylcholine↗

Evidence that cholinergic axons from the parabrachial region of the brainstem are the exclusive source of nitric oxide in the lateral geniculate nucleus of the cat.

We investigated the source of axons and terminals in the cat's lateral geniculate nucleus that stain positively for NADPH-diaphorase. The functional significance of such staining is that NADPH-diaphorase is identical to the enzyme nitric oxide synthetase, and thus it is thought to reveal cells and axons that use nitric oxide as a neuromodulator. Within the lateral geniculate and adjacent perigeniculate nuclei, a dense network of axons and terminals is labeled for NADPH-diaphorase. The pattern of NADPH-diaphorase staining here is remarkably similar to that of choline acetyltransferase (ChAT) staining, suggesting that the source of these axons and terminals might be the parabrachial region of the brainstem because this provides the major cholinergic input to the lateral geniculate nucleus. In other areas of the brain to which parabrachial axons project, there is also a similar staining pattern for NADPH-diaphorase and ChAT. Furthermore, the patterns of cell staining within the parabrachial region for NADPH-diaphorase and ChAT are virtually identical. However, the relationship between ChAT and NADPH-diaphorase staining for the parabrachial region is not a general property of cholinergic neurons. Other cholinergic cells and axons, such as the trochlear nerve, the oculomotor nerve and nucleus, and the parabigeminal nucleus, which all label densely for ChAT, stain poorly or not at all for NADPH-diaphorase. It is significant that the parabigeminal nucleus, which provides a cholinergic input to the lateral geniculate nucleus, has no cells that label for NADPH-diaphorase. We used double labeling methods to identify further the source of NADPH-diaphorase staining in the lateral geniculate nucleus. We found that parabrachial cells co-localize NADPH-diaphorase and ChAT. Noradrenergic and serotoninergic cells in the brainstem also innervate the lateral geniculate nucleus, but we found that none of these co-localize NADPH-diaphorase. Finally, by combining NADPH-diaphorase histochemistry with retrograde labeling of cells that project to the lateral geniculate nucleus, we found that the cholinergic cells of the parabrachial region are essentially the sole source of NADPH-diaphorase in the lateral geniculate nucleus. We thus conclude that cells from the parabrachial region that innervate the lateral geniculate nucleus use both acetylcholine and nitric oxide for neurotransmission, and that this is virtually the only afferent input to this region that uses nitric oxide.

Animals↗

How complete is physiological compensation in extrastriate cortex after visual cortex damage in kittens?

Previous studies indicate that neurons in the cat's posteromedial lateral suprasylvian (PMLS) visual area of cortex show physiological compensation after neonatal but not adult damage to areas 17, 18, and 19 of the visual cortex (collectively, VC). Thus, VC damage in adults produces a loss of direction selectivity and a decrease in response to the ipsilateral eye among PMLS cells, but these changes are not seen in adult cats that received VC damage as kittens. This represents compensation for early VC damage in the sense that PMLS neurons develop properties they would have had if there had been no brain damage. However, this is only a partial compensation for the effects of VC damage. A full compensation would involve development of properties of the VC cells that were removed in the damage. The present study investigated whether this type of compensation occurs for detailed spatial- and temporal-frequency processing. Single-cell recordings were made in PMLS cortex of adult cats that had received a VC lesion on the day of birth or at 8 weeks of age. Responses to sine-wave gratings that varied in spatial frequency, contrast, and temporal frequency were assessed quantitatively. We found that the spatial- and temporal-frequency processing of PMLS cells in adult cats that had neonatal VC damage were not significantly different from PMLS cells in normal cats. Therefore, there was no evidence that PMLS cells can compensate for VC damage by developing properties that are better than normal and like those of the striate cortex cells that were damaged. We also assessed the effects of long-term VC damage in adult cats to determine whether the normal properties seen in cats with neonatal VC damage represent a compensation for abnormalities in PMLS cortex present after adult damage. In a previous study, we found that acute VC damage in adult cats has small but reliable effects on maximal response amplitude, maximal contrast sensitivity, and spatial resolution (Guido et al. 1990b). In the present study, we found that long-term VC damage in adult cats does not increase these abnormalities as a result of secondary degenerative changes. In fact, the minor abnormalities that were present after an acute VC lesion were virtually absent following a long-term adult lesion, perhaps because they were due to transient traumatic effects. Therefore, there was little evidence for abnormalities in spatial- or temporal-frequency processing following long-term adult VC damage for which PMLS cells might show compensation following long-term neonatal damage.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗

Binocular interactions in the cat's dorsal lateral geniculate nucleus, II: Effects on dominant-eye spatial-frequency and contrast processing.

The present study tested the hypothesis that nondominant-eye influences on lateral geniculate nucleus (LGN) neurons affect the processing of spatial and contrast information from the dominant eye. To do this, we determined the effects of stimulating the nondominant eye at its optimal spatial frequency on the responses of LGN cells to sine-wave gratings of different spatial frequency and contrast presented to the dominant eye. Detailed testing was carried out on 49 cells that had statistically significant responses to stimulation of the nondominant eye alone. Spatial-frequency response functions to nondominant-eye stimulation indicated that the responses were spatially tuned, as reported previously (Guido et al., 1989). Optimal spatial frequencies through the nondominant eye were significantly correlated with the optimal spatial frequencies through the dominant eye (r = 0.54; P less than 0.0001), and the optimal spatial frequencies were fairly similar for the two eyes. Nondominant-eye stimulation changed the maximal amplitude of the fundamental (F1) response to dominant-eye stimulation for only about 45% (22 of 49) of the cells that responded to nondominant-eye stimulation alone. The response vs. contrast function through the dominant eye was altered for 73% of the cells (51% independent of spatial frequency). Three types of effects were observed: a change in the initial slope of the response vs. contrast function (contrast gain), a change in the response amplitude at which saturation occurred, or an overall change in response at all contrasts. The incidence of these changes was similar for X and Y cells in LGN layers A, A1, and C (only four W cells were tested). Nondominant-eye stimulation had little or no effect on the sizes or sensitivities of the receptive-field centers or surrounds for the dominant eye. In addition, nondominant-eye stimulation had little or no effect on optimal spatial frequency, spatial resolution, or the bandwidth of spatial-frequency contrast sensitivity curves for the dominant eye. Possible functions of binocular interactions in the LGN are considered. The present results suggest a role in interocular contrast-gain control. Interocular contrast differences can occur before the acquisition of binocular fusion, when the two eyes are viewing different aspects of a visual stimulus. Psychophysical and physiological studies suggest that an interocular mechanism exists to maintain relatively constant binocular interactions despite differences in interocular contrast. The present results suggest that at least part of this mechanism occurs in the LGN.

Animals↗

Effects of membrane voltage on receptive field properties of lateral geniculate neurons in the cat: contributions of the low-threshold Ca2+ conductance.

1. Thalamic relay cells, including those of the lateral geniculate nucleus, display a low-threshold spike (LT spike), which is a large depolarization due to an increased Ca2+ conductance. Typically riding the crest of each LT spike is a burst of from two to seven action potentials, which we refer to as the LT burst. The LT spike is voltage dependent, because if the cell's resting membrane potential is more depolarized than roughly -60 mV, the LT spike is inactivated, but if more hyperpolarized, the spike is deinactivated and can be activated by a depolarization, such as from an afferent excitatory postsynaptic potential (EPSP). Thalamic relay cells thus display two response modes: a relay or tonic mode, when the cell is depolarized and LT spikes are inactivated, leading to tonic firing of action potentials; and a burst mode, when the cell is hyperpolarized and tends to respond with LT spikes and their associated bursts of action potentials. 2. We were interested in the contribution of the LT spike on the transmission of visually evoked signals through geniculate relay cells to visual cortex. We recorded intracellularly from geniculate cells in an anesthetized, paralyzed, in vivo cat preparation to study the effects of membrane voltage, and thus the presence or absence of LT spikes, on responses to drifting sine-wave gratings. We monitored the visually evoked responses of 14 geniculate neurons (6 X, 7 Y, and 1 unclassified) at different membrane potentials at which LT spikes were inactivated or deinactivated. 3. Changing membrane voltage during visual stimulation switched the response mode of every cell between the relay and burst modes. In the burst mode, LT spikes occurred in phase with the visual stimulus and not at rhythmic intervals uncorrelated to visual stimuli. To any given stimulus cycle, the cell responded usually with an LT burst or a tonic response, and rarely was more than one LT burst evoked by a stimulus cycle. Occasionally a single cycle evoked both an LT burst and tonic response, but always the LT burst occurred first. 4. The spatial tuning characteristics of the cells did not differ dramatically as a function of membrane potential, because the tuning of the LT bursts was quite similar to that of the tonic response component. Although we did not obtain complete temporal tuning properties, we did note that hyperpolarized cells responded reliably with LT bursts at several temporal frequencies. 5. A consistent difference was seen between the LT burst and tonic response components in terms of response linearity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗