Nucleus Of Cat Research Articles

Bladder contractility‐related neurons in barrington's nucleus: Axonal projections to the spinal cord in the cat

Barrington's nucleus projects directly to the sacral parasympathetic nucleus. The purpose of this study was to clarify whether neurons in Barrington's nucleus that increase their firing during bladder contractions project to the spinal cord and, if so, to which level(s) the axon reaches. Single units were recorded in Barrington's nucleus of cat with glass microelectrodes, and the termination level of descending axons was determined by antidromic stimulation of the spinal cord. Thirty-nine neurons projecting to the spinal cord were located in rostral parts of the dorsolateral pontine tegmentum, medial and ventral to the mesencephalic trigeminal tract. This finding is consistent with previous neuronal tracing studies. All neurons increased their firing rates during contraction associated with micturition. In 19 examined neurons, the most caudal level of the descending axon distributed between the L7 and the S3 level. Stimulation of the axon at this most caudal level resulted in antidromic spike latencies ranging between 19.5 msec and 45.0 msec. These antidromic latencies were much smaller than previously reported orthodromic conduction times between neurons in Barrington's nucleus and sacral preganglionic neurons innervating the bladder. The mean conduction velocity of the descending axon from the cell body to the border between Th13 and the L1 ranged between 7.2 m/sec and 27.7 m/sec. The decrease of the mean conduction velocity was observed at the lumbar as well as at the sacral segments, suggesting that axons issue collaterals to the lumbar level as well as to the sacral level.

Postnatal refinement of auditory nerve projections to the cochlear nucleus in cats.

Studies of visual system development have suggested that competition driven by activity is essential for refinement of initial topographically diffuse neuronal projections into their precise adult patterns. This has led to the assertion that this process may shape development of topographic connections throughout the nervous system. Because the cat auditory system is very immature at birth, with auditory nerve neurons initially exhibiting very low or no spontaneous activity, we hypothesized that the auditory nerve fibers might initially form topographically broad projections within the cochlear nuclei (CN), which later would become topographically precise at the time when adult-like frequency selectivity develops. In this study, we made restricted injections of Neurobiotin, which labeled small sectors (300-500 microm) of the cochlear spiral ganglion, to study the projections of auditory nerve fibers representing a narrow band of frequencies. Results showed that projections from the basal cochlea to the CN are tonotopically organized in neonates, many days before the onset of functional hearing and even prior to the development of spontaneous activity in the auditory nerve. However, results also demonstrated that significant refinement of the topographic specificity of the primary afferent axons of the auditory nerve occurs in late gestation or early postnatal development. Projections to all three subdivisions of the CN exhibit clear tonotopic organization at or before birth, but the topographic restriction of fibers into frequency band laminae is significantly less precise in perinatal kittens than in adult cats. Two injections spaced > or = 2 mm apart in the cochlea resulted in labeled bands of projecting axons in the anteroventral CN that were 53% broader than would be expected if they were proportional to those in adults, and the two projections were incompletely segregated in the youngest animals studied. Posteroventral CN (PVCN) projections (normalized for CN size) were 36% broader in neonates than in adults, and projections from double injections in the youngest subjects were nearly fused in the PVCN. Projections to the dorsal division of the CN were 32% broader in neonates than in adults when normalized, but the dorsal CN projections were always discrete, even at the earliest ages studied.

The effects of congenital deafness on auditory nerve synapses: Type I and Type II multipolar cells in the anteroventral cochlear nucleus of cats.

Sensory deprivation has been shown to exert detrimental effects on the structure and function of central sensory systems. Congenital deafness represents an extreme form of auditory deprivation, and in the adult white cat, synapses between auditory nerve endings and resident cells of the anteroventral cochlear nucleus exhibited abnormal structure. Endbulbs of Held were reduced in branching and displayed striking hypertrophy of their postsynaptic densities. So-called modified endbulbs showed no change in branching complexity but did exhibit hypertrophy of their postsynaptic densities. These differential pre- and postsynaptic effects prompted the question of how deafness might affect other primary endings and synapses. Thus, we studied type I and type II multipolar cells that receive bouton endings from auditory nerve fibers. Type I multipolar cells project to the contralateral inferior colliculus and have relatively few axosomatic endings; type II multipolar cells project to the contralateral cochlear nucleus and have many axosomatic endings. Compared with normal-hearing cats, bouton endings of congenitally deaf cats were smaller but there was no difference in synaptic vesicle density or size of postsynaptic densities. These data reveal that different classes of primary endings and second-order neurons exhibit different degrees of synaptic anomalies to deafness.

Linear mechanistic models for the dorsal lateral geniculate nucleus of cat probed using drifting-grating stimuli

Experiments with sinusoidal visual stimuli in the early visual pathway have traditionally been interpreted in terms of descriptive filter models. We present an alternative mechanistic approach for interpretation of this type of data recorded from X cells in the dorsal lateral geniculate nucleus (dLGN) of cat. A general, linear, rate-based mathematical expression for the geniculate transfer ratio, i.e. the ratio between the first-harmonic components of the output of a geniculate relay cell and its retinal input, is derived. In linear theory this ratio is independent of the signal processing occurring at the retinal level. Further, the ratio is straightforwardly accessible in experiments due to the presence of S-potentials, representing the retinal input, in extracellular recordings from dLGN. The expression accounts for feedforward inputs from retina and intrageniculate interneurons as well as feedback inputs from cortex and the thalamic reticular nucleus and can be used to experimentally test different mechanistic models for the geniculate circuitry. Two examples of this are considered: a purely feedforward model incorporating relay cell inputs from retinal ganglion cells and interneurons, and a model including cortical feedback inhibition of relay cells via intrageniculate interneurons.

Effects of Standardized Extracts of St. John's Wort on the Single-Unit Activity of Serotonergic Dorsal Raphe Neurons in Awake Cats: Comparisons with Fluoxetine and Sertraline

St. John's wort is widely used as an herbal remedy for depression. Although its mechanism of action remains unknown, some evidence suggests that St. John's wort might act via brain serotonin (e.g., as a serotonin reuptake inhibitor). To determine whether St. John's wort affects the central serotonergic system, we monitored the discharge rate of serotonin-containing neurons in the dorsal raphe nucleus of awake cats following systemic administration of two clinical preparations of St. John's wort, Jarsin® 300 (15–600 mg/kg, p.o.) and Hyperforat® (0.5–4.0 ml, i.v.). Both preparations were found to have no effect on neuronal activity. This contrasts sharply with the action of fluoxetine and sertraline (2 mg/kg, p.o.), two selective serotonin reuptake inhibitors (SSRIs), which markedly depressed neuronal activity by increasing the synaptic availability of serotonin at inhibitory somatodendritic 5-HT1A autoreceptors. The failure of St. John's wort to depress neuronal activity cannot be attributed to an impairment of the 5-HT1A autoreceptor mechanism, since pretreatment with Jarsin® 300 (300 mg/kg, p.o.) did not alter the responsiveness of serotonergic neurons to the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (10 μg/kg, i.v.). Overall, these findings indicate that the mode of action of St. John's wort is different from that of conventional antidepressant drugs, which elevate brain serotonin and evoke negative feedback control of serotonergic neurons.

Variability and information in a neural code of the cat lateral geniculate nucleus.

A central theme in neural coding concerns the role of response variability and noise in determining the information transmission of neurons. This issue was investigated in single cells of the lateral geniculate nucleus of barbiturate-anesthetized cats by quantifying the degree of precision in and the information transmission properties of individual spike train responses to full field, binary (bright or dark), flashing stimuli. We found that neuronal responses could be highly reproducible in their spike timing (approximately 1-2 ms standard deviation) and spike count (approximately 0.3 ratio of variance/mean, compared with 1.0 expected for a Poisson process). This degree of precision only became apparent when an adequate length of the stimulus sequence was specified to determine the neural response, emphasizing that the variables relevant to a cell's response must be controlled to observe the cell's intrinsic response precision. Responses could carry as much as 3.5 bits/spike of information about the stimulus, a rate that was within a factor of two of the limit the spike train could transmit. Moreover, there appeared to be little sign of redundancy in coding: on average, longer response sequences carried at least as much information about the stimulus as would be obtained by adding together the information carried by shorter response sequences considered independently. There also was no direct evidence found for synergy between response sequences. These results could largely, but not entirely, be explained by a simple model of the response in which one filters the stimulus by the cell's impulse response kernel, thresholds the result at a fairly high level, and incorporates a postspike refractory period.

Temporal properties of pattern adaptation of relay cells in the lateral geniculate nucleus of cats

The temporal properties of pattern adaptation of relay cells induced by repeated sinusoidal drifting grating were investigated in the dorsal lateral geniculate nucleus (dLGN) of cats. The results showed that the response amplitude declined and the response latency prolonged when relay cells were pattern-adapted in dLGN, like the similar findings in visual cortex. However, in contrast to the result in cortex, the response phase of relay cells advanced. This implies that an inhibition with relatively long latency may participate in the pattern adaptation of dLGN cells and the adaptation in dLGN may be via a mechanism different from that of visual cortex.

Soma size of substantia nigra neurons increases after a prenatal neocortical lesion in cats

Seeking an explanation for an increase in volume of the caudate nucleus in adult cats that had sustained a fetal unilateral neocortical lesion, we investigated possible morphological changes in the reciprocally interconnected substantia nigra. In fetal-lesioned cats the cross-sectional area of neuronal somata in substantia nigra, pars reticulata was 33% larger than in control cats ( P<0.05), while in pars compacta there was a marked tendency to an increase (25%, P<0.06). This size increase might have caused the survival of a larger number of caudate nucleus neurons during development, and thus contributed to the reported increase in caudate nucleus volume.

Does exogenous GM1 ganglioside enhance the effects of electrical stimulation in ameliorating degeneration after neonatal deafness?

This study examined the combined effects of administration of exogenous GM1 ganglioside and electrical stimulation on the cochlear nucleus (CN) of cats deafened neonatally by ototoxic drugs. Five normal hearing adult cats served as controls. Another 12 cats were deafened bilaterally by daily injections of neomycin sulfate (60 mg/kg) for 17–21 days after birth until auditory brainstem testing demonstrated profound hearing loss. Six of the deaf animals comprised the GM1 group, which received daily injections of GM1 ganglioside (30 mg/kg) for 28–38 days during the period after profound deafness was confirmed, and prior to receiving a cochlear implant. The non-GM1 group ( n=6) received no treatment during this interim period. All the deafened animals underwent unilateral cochlear implantation at 6–9 weeks postnatal and received several months (mean duration, 32 weeks) of chronic electrical stimulation (4 h/day, 5 days/week). Stimulation was delivered by intracochlear bipolar electrodes, using electrical signals that were designed to be temporally challenging to the central auditory system. Results showed that in the neonatally deafened animals, both the GM1 and non-GM1 groups, the volume of the CN was markedly reduced (to 76% of normal), but there was no difference between the animals that received GM1 and those that did not. The cross sectional areas of spherical cell somata in both GM1 and non-GM1 groups also showed a highly significant reduction in size, to ≤75% of normal after neonatal deafening. Moreover, in both the GM1 and non-GM1 groups, the spherical cells in the CN ipsilateral to the implanted cochlea were significantly larger (6%) than cells in the control, unstimulated CN. Again, however, there was no significant difference between the GM1 group and the non-GM1 group in spherical cell size. These results contrast sharply with previous reports that exogenous GM1 prevents CN degeneration after neonatal conductive hearing loss and partially prevents spiral ganglion cell degeneration when administered immediately after ototoxic drug deafening in adult animals. Taken together, findings to date suggest that GM1 may be effective in preventing degeneration only if the GM1 is administered immediately at the time hearing loss occurs.

Hypocretin (orexin) input to trigeminal and hypoglossal motoneurons in the cat: a double-labeling immunohistochemical study

In trigeminal and hypoglossal motor nuclei of adult cats, hypocretin immunoreactive fiber varicosities were observed in apposition to retrogradely labeled motoneuron somata and dendrites. Among those lateral hypothalamus neurons that project to the hypoglossal nucleus some were determined to be hypocretin immunoreactive and were located amongst the single-labeled hypocretinergic neurons. These data suggest that hypocretin may play a role in the synaptic control of these motoneurons.

Gamma amino butyric acid (GABA) immunoreactivity in the vestibular nuclei of normal and unilateral vestibular neurectomized cats.

Recent neurochemical investigations of the central vestibular pathways have demonstrated that several neurotransmitters are involved in various operations required for stabilizing posture and gaze. Neurons of the vestibular nuclei (VN) receive GABAergic inhibitory afferents, and GABAergic neurons distributed throughout the vestibular complex are implicated in inhibitory vestibulo-ocular and vestibulo-spinal pathways. The aim of this study was to analyse the modifications of GABA immunoreactivity (GABA-ir) in the cat VN after unilateral vestibular neurectomy (UVN). Indeed, compensation of vestibular deficits is a good model for studying adult central nervous system (CNS) plasticity and the GABAergic system is involved in CNS plasticity. We studied GABA-ir by using a purified polyclonal antibody raised against GABA. Light microscopic preparations of thin (20 microm) sections of cat VN were used to quantify GABA-ir by an image analysing system measuring GABA-positive punctate structures and the number of GABA-positive neurons. Both the lesioned and intact sides were analysed in three populations of UVN cats killed at different times after injury (1 week, 3 weeks and 1 year). These data were compared to those collected in normal unlesioned and sham-operated cats. Results showed a spatial distribution of GABA-ir in the control cats that confirmed previous studies. GABA-ir neurons, fibres and nerve terminals were scattered in all parts of the VN. A higher concentration of GABA-positive neurons (small cells) was detected in the medial and inferior VN (MVN and IVN) and in the dorsal part of the lateral VN (LVNd). A higher level of GABA-positive punctate structures was observed in the MVN and in the prepositus hypoglossi (PH) nucleus. Lesion-induced changes were found at each survival time. One week after injury the number of GABA-positive neurons was significantly increased in the MVN, the IVN and the dorsal part of the LVN on the lesioned side and in the ventral part of the LVN on the intact side. One year later a bilateral increase in GABA-positive neurons was detected in the MVN whilst a bilateral decrease was observed in both the SVN and the ventral part of the LVN. Changes in the GABA-staining varicosities did not strictly coincide with the distribution of GABA-ir cells, suggesting that GABA-ir fibres and nerve terminals were also modified. One week and later after injury, higher GABA-staining varicosities were seen unilaterally in the ipsilateral MVN. In contrast, bilateral increases (in PH) and bilateral decreases (in SVN and the ventral part of the LVN) were recorded in the nearly (3 weeks) or fully (1 year) compensated cats. At this stage GABA-staining varicosities were significantly increased in the lesioned side of the MVN. These findings demonstrate the reorganization of the GABAergic system in the VN and its possible role in recovery process after UVN in the cat. The changes seen during the acute stage could be causally related to the VN neuron deafferentation, contributing to the static vestibular deficits. Those found in the compensated cats would be more functionally implicated in the dynamic aspects of vestibular compensation.

Analysis of firing correlations between sympathetic premotor neuron pairs in anesthetized cats.

The activity of sympathetic premotor neurons in the rostral ventrolateral medulla (subretrofacial nucleus) supports sympathetic vasomotor tone, but the factors that drive these premotor neurons' activity have not been determined. This study examines whether either direct interconnections between subretrofacial neurons or synchronizing common inputs to them are important for generating their tonic activity. Simultaneous extracellular single-unit recordings were made from 32 pairs of sympathetic premotor neurons in the subretrofacial nucleus of chloralose-anesthetized cats. Paired spike trains were either separated by spike shape from a single-electrode recording (14 pairs) or recorded from two electrodes less than 250 microm apart (18 pairs). All neurons were inhibited by carotid baroreceptor stimulation and most had a spinal axon proven by antidromic stimulation from the spinal cord. Autocorrelation, inter-spike interval, and cardiac cycle-triggered histograms were constructed from the spontaneous activity of each neuron, and cross-correlation histograms covering several time scales were generated for each neuron pair. No significant peaks or troughs were found in short-term cross-correlation histograms (2 ms bins, +/-100 ms range), providing no support for important local synaptic interactions. On an intermediate time scale (20 ms bins, +/-1 s range), cross-correlation revealed two patterns indicating shared, synchronizing inputs. Repeating peaks and troughs (19/32 pairs) were due to the two neurons' common cardiac rhythmicity, of presumed baroreceptor origin. Single, zero time-spanning peaks of 40--180 ms width were seen in 5/32 cases. Calculations based on the prevalence and strength of these synchronizing inputs indicate that most of the ensemble spike activity of the subretrofacial neuron population is derived from asynchronous sources (be they intrinsic or extrinsic). If synchronizing sources such as neuronal oscillators were responsible for more than a minor part of the drive, they would be multiple, dispersed, and weak.

Suppressive effects of oxcarbazepine on tooth pulp-evoked potentials recorded at the trigeminal spinal tract nucleus in cats.

1. The purpose of the present study was to evaluate the antinociceptive effect of oxcarbazepine, a keto derivitive of carbamazepine (an anticonvulsant), in an animal model. To evoke a nociceptive response, we electrically stimulated the maxillary canine tooth pulp (MCTP) in anaesthetized (allobarbital-urethane), spontaneously breathing cats. 2. The evoked potentials were recorded from the superficial layers of the caudal part of the trigeminal spinal tract nucleus (5ST). We examined a slow component with a large amplitude (the P3 component) in evoked compound potentials; its mean conduction velocity was 1.7 m/s, suggesting a response mediated by C-fibres. 3. To confirm that the P3 component was related to pain sensation, we used morphine, a most efficacious antinociceptive agent, in the present study. The P3 component was significantly suppressed by intravenous administration of morphine (3 mg/kg) and was also suppressed by microinjection of morphine (2 microg) into the recording site of the 5ST. These results suggest that the P3 component is involved in the transmission of nociceptive information. 4. We compared the effect of oxcarbazepine with mexiletine; both are known to block neuronal Na+ channels. Intravenous administration of mexiletine suppressed the P3 component at a dose of 5 mg/kg. Microinjection of mexiletine (10 microg) into the recording site of the 5ST tended to suppress the P3 component, but this effect was not significant. 5. Intravenous administration of oxcarbazepine (1-10 mg/kg) caused a dose-dependent inhibition of the P3 component, which was significantly suppressed at 10 mg/kg oxcarbazepine. Intravenous administration of 10,11-dihydro-10-hydroxy-5H-dibenz[b,f]azepine-5-carboxamide (MHD), a metabolite of oxcarbazepine, at doses of 3-30 mg/kg caused a dose-dependent inhibition of the P3 component. Oxcarbazepine was not available for the microinjection study because it is not water soluble. We used MHD for the microinjection study instead of oxcarbazepine, because MHD can be dissolved in water up to 3 mg/mL. Microinjections of MHD (6 microg) into the recording site of the 5ST suppressed the P3 component. These results indicate that oxcarbazepine has an antinociceptive action.

Activation of skeletal muscle afferents evokes release of glutamate in the subretrofacial nucleus (SRF) of cats

The subretrofacial nucleus (SRF) is a region of the rostral ventrolateral medulla known to play a crucial role in sympathoexcitation. SRF neurons send direct projections to the intermediolateral cell columns of the spinal cord where they form synaptic contact with preganglionic sympathetic motor neurons. Activation of this neural pathway increases sympathetic outflow to the heart and blood vessels affecting cardiac function and vasomotor tone. Previous studies utilizing electrophysiological recording techniques and c-Fos expression have established that the activity of SRF neurons is increased during skeletal muscle contraction. However, the excitatory neurotransmitter mediating this increased activity remains in question. In the present study, static contraction of the triceps surae was induced by electrical stimulation of L7 and S1 ventral roots in anesthetized cats ( n=12). Endogenous release of glutamate (Glu) from the SRF was recovered by microdialysis and measured by HPLC. Static muscle contraction for 4 min increased mean arterial pressure (MAP) 38±4 mmHg from a control level of 102±12 mmHg ( P<0.05). During muscle contraction the extracellular concentration of Glu recovered from the SRF increased from 623±117 to 1078±187 nM ( P<0.05). To determine the effect of muscle contraction on Glu release in the absence of synaptic input from other reflexogenic areas, contraction was repeated following acute sinoaortic denervation and vagotomy. Following this denervation, muscle contraction increased MAP 41±4 mmHg ( P<0.05) and Glu concentration from 635±246 to 1106±389 nM ( P<0.05). Muscle paralysis prevented the increases in MAP and Glu concentration during ventral root stimulation. These results suggest that: (i) Glu is released in the SRF during activation of contraction-sensitive skeletal muscle afferent fibers in the cat; and (ii) synaptic input from other reflexogenic areas appears to be ineffective in modulating the release of Glu in the SRF during static muscle contraction.

Survival of retinal ganglion cells after transection of the optic nerve in adult cats: a quantitative study within two weeks.

We have previously reported that a small number of retinal ganglion cells (RGCs) of adult cats survive 2 months after transection of the optic nerve (ON) and that alpha cells have the greatest ability to survive among different types of RGCs (Watanabe et al., 1995). Here we report the time course of RGC survival within 15 days after ON transection using retrograde labeling with DiI injected into the bilateral lateral geniculate nuclei of cats. The density of DiI-labeled RGCs in the central retina as well as in the periphery did not change until day 3 after ON transection, then decreased rapidly, to 43% of the original density on day 7, and falling to 19% by day 14. We then intracellularly injected Lucifer yellow into the DiI-labeled RGCs to examine the difference in the time course between surviving alpha and beta cells. Similar to the density change in total surviving RGCs, the proportion of surviving beta cells did not change until day 3, then decreased rapidly to 65% of the original density on day 4, falling to 12% by day 14. By contrast, 64% of alpha cells survived for 14 days after axotomy. Analysis of regression lines for survival time courses indicated that death of beta cells was characterized with a rapid period phase from day 3 to day 7 after axotomy whereas that of alpha cells lacked it. Axon-like sprouting from surviving beta cells was first recognized in the nerve fiber layer on day 3, and were later more conspicuous.

Effects of bicuculline on direction-sensitive relay cells in the dorsal lateral geniculate nucleus (LGNd) of cats

The direction sensitivity of relay cells in the cat’s dorsal lateral geniculate (LGNd) was measured using sinusoidal grating stimuli before and during local bicuculline administration. One hundred and twenty-eight LGNd relay cells were recorded in laminae A and A1, of which 44 relay cells (34%) were found to be sensitive to direction of stimulus movement. The direction-sensitive LGNd relay cells could be differentiated into two subgroups based on different measures of their response amplitude. Type I cells exhibited their direction sensitivity when the fundamental Fourier component (FFC) of the poststimulus time histograms (PSTHs) was used as response measure, but did not show significant direction sensitivity when mean firing rate was used. Type II cells exhibited their direction sensitivity, no matter whether the FFC or mean firing rate was used as the measure. Of 35 cells analyzed, 27 cells remained direction sensitive during bicuculline administration. At the population level, the direction bias of type I cells did not change systematically, while the direction bias of type II cells decreased significantly during bicuculline administration. These results suggest that the direction bias of these two types of relay cells are mediated by different neural mechanisms. The direction bias of type I cells may involve multiple inputs from spatio-temporally separate subunits within retinal ganglion cells receptive fields. The direction bias of type II cells may involve GABAergic neuronal circuits within the LGNd.

Distribution of terminals from pedunculopontine tegmental nucleus and synaptic organization in lateralis medialis-suprageniculate nucleus of cat's thalamus: anterograde tracing, immunohistochemical studies, and quantitative analysis.

The cat's lateralis medialis-suprageniculate nuclear complex (LM-Sg) in the thalamus receives input from various brain regions such as the superior colliculus, brain stem, and spinal cord, as well as from visual association cortex. In a previous study, we demonstrated that LM-Sg receives cholinergic fibers from the pedunculopontine tegmental nucleus (PPT) and that cholinergic terminals make synaptic contacts with the dendrites of glutamatergic projection neurons and of GABAergic interneurons (Hoshino et al., 1997). In this study, we investigate the distribution and the organization of PPT terminals by means of a combined anterograde tracer (biotinylated dextran amine, BDA) and immunohistochemical methods. When stained by acetylcholinesterase (AChE), the LM-Sg is not uniformly immunoreactive, but rather is patchily labeled and shows a streaming type of reactivity. The tissue content appears high in enzyme activity in AChE-positive zones and is much lighter in activity in AChE-negative zones. We compared the synaptic organization between AChE-positive and AChE-negative portions of the LM-Sg in separate groups of electron-microscopic material: four types of vesicle containing profiles (RS, RL, F1, and PSD) as well as synaptic glomeruli were observed in this nucleus. Among these, the PSD profiles were observed more frequently in AChE-positive portions than in AChE-negative zones. Furthermore, the number of glomeruli was significantly higher in AChE-positive than in AChE-negative zones. Following the injection of BDA into PPT, labeled terminals within LM-Sg were rather more concentrated in the AChE-positive portion. Although the majority of PPT terminals made synaptic contacts with dendrites in the neuropil, a few terminals were involved in the synaptic glomeruli. The present results show that the synaptic organization is distinctly different between the AChE-positive and AChE-negative portions of LM-Sg. These results suggest that the AChE-positive portions of LM-Sg are relatively more involved in integrating information arising from a diverse set of inputs and processing that information within glomeruli in a complex manner than occurs in the AChE-negative portion of LM-Sg.

Mathematical models for the spatial receptive-field organization of nonlagged X-cells in dorsal lateral geniculate nucleus of cat.

Spatial receptive fields of relay cells in dorsal lateral geniculate nucleus (dLGN) have commonly been modeled as a difference of two Gaussian functions. We present alternative models for dLGN cells which take known physiological couplings between retina and dLGN and within dLGN into account. The models include excitatory input from a single retinal ganglion cell and feedforward inhibition via intrageniculate interneurons. Mathematical formulas describing the receptive field and response to circular spot stimuli are found both for models with a finite and an infinite number of ganglion-cell inputs to dLGN neurons. The advantage of these models compared to the common difference-of-Gaussians model is that they, in addition to providing mathematical descriptions of the receptive fields of dLGN neurons, also make explicit contributions from the geniculate circuit. Moreover, the model parameters have direct physiological relevance and can be manipulated and measured experimentally. The discrete model is applied to recently published data (Ruksenas et al., 2000) on response versus spot-diameter curves for dLGN cells and for the retinal input to the cell (S-potentials). The models are found to account well for the results for the X-cells in these experiments. Moreover, predictions from the discrete model regarding receptive-field sizes of interneurons, the amount of center-surround antagonism for interneurons compared to relay cells, and distance between neighboring retinal ganglion cells providing input to interneurons, are all compatible with data available in the literature.

Effects of inactivation of the anterior interpositus nucleus on the kinematic and dynamic control of multijoint movement.

We previously showed that inactivating the anterior interpositus nucleus in cats disrupts prehension; paw paths, normally straight and accurate, become curved, hypometric, and more variable. In the present study, we determined the joint kinematic and dynamic origins of this impairment. Animals were restrained in a hammock and trained to reach and grasp a cube of meat from a narrow food well at varied heights; movements were monitored using the MacReflex analysis system. The anterior interpositus nucleus was inactivated by microinjection of the GABA agonist muscimol (0.25-0.5 microgram in 0.5 microliter saline). For each joint, we computed the torque due to gravity, inertial resistance (termed self torque), interjoint interactions (termed interaction torque), and the combined effects of active muscle contraction and passive soft tissue stretch (termed generalized muscle torque). Inactivation produced significant reductions in the amplitude, velocity, and acceleration of elbow flexion. However, these movements continued to scale normally with target height. Shoulder extension was reduced by inactivation but wrist angular displacement and velocity were not. Inactivation also produced changes in the temporal coordination between elbow, shoulder, and wrist kinematics. Dynamic analysis showed that elbow flexion both before and during inactivation was produced by the combined action of muscle and interaction torque, but that the timing depended on muscle torque. Elbow interaction and muscle torques were scaled to target height both before and during inactivation. Inactivation produced significant reductions in elbow flexor interaction and muscle torques. The duration of elbow flexor muscle torque was prolonged to compensate for the reduction in flexor interaction torque. Shoulder extension was produced by extensor interaction and muscle torques both before and during inactivation. Inactivation produced a reduction in shoulder extension, primarily by reduced interaction torque, but without compensation. Wrist plantarflexion, which occurred during elbow flexion, was driven by plantarflexor interaction and gravitational torques both before and during inactivation. Muscle torque acted in the opposite direction with a phase lead to restrain the plantarflexor interaction torque. During inactivation, there was a reduction in plantarflexor interaction torque and a loss of the phase lead of the muscle torque. Our findings implicate the C1/C3 anterior interpositus zone of the cerebellum in the anticipatory control of intersegmental dynamics during reaching, which zone is required for coordinating the motions of the shoulder and wrist with those of the elbow. In contrast, this cerebellar zone does not play a role in scaling the movement to match a target.

Age-dependent changes in the midsized neurofilament subunit in sensory-motor systems of the cat brainstem: an immunocytochemical study.

This study documents age-related changes in the immunoreactivity of the medium-molecular weight subunit of neurofilaments in sensory and motor neurons in the brainstem of the cat. In old age, there was a clear decrease in immunoreactivity in the following brainstem sensory and motor nuclei: sensory trigeminal, gracile, cuneate, and facial motor. Only a few neuronal perikarya and dendrites were labeled in these nuclei in old cats; moreover, when present, the labeling was weak. In contrast, in adult cats, these nuclei contained intensely stained neuronal perikarya and dendrites. In other sensory and motor nuclei of the brainstem, there was an obvious age-related increase in the immunoreactivity of the medium-molecular weight subunit of neurofilaments in the perikarya. Despite different patterns of age-related alterations in immunoreactivity within perikarya and dendrites in distinct brainstem regions, most sensory and motor axons in old cats were smaller than those in adult cats. A decrease in the medium-molecular weight neurofilament subunit in the dendrites may be the basis for the dendritic atrophy that has been shown to occur in sensory nuclei in old animals. The decrease in axonal size is likely to be one of the causes of the decrease in axonal conduction velocity, in these neurons, that was reported in our previous studies.