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P D Cheney

Publications and source records attributed to P D Cheney.

At least 19 recordsLinked to original sources
PubMed2004

Severe subcortical degeneration in macaques infected with neurovirulent simian immunodeficiency virus.

Infection with human immunodeficiency virus-1 (HIV-1), the causative agent of acquired immunodeficiency syndrome (AIDS) in humans, causes a spectrum of neuropathology that includes alterations in behavior, changes in evoked potentials, and neuronal degeneration. In the simian immunodeficiency virus (SIV) model of HIV infection, affected monkeys show clinical symptoms and neurological complications that mimic those observed in human neuro-AIDS. To investigate the relationship between morphological correlates and neurophysiological deficits, unbiased stereology was used to assess total neuron number, volume, and neuronal density for all neurons in the globus pallidus (GP) and for dopamine (DA)-containing neurons in the substantia nigra (SN) in eight macaques inoculated with macrophage-tropic, neurovirulent SIV (SIVmac R71/17E), and five control animals. There was a significant difference between rapid progressors and controls for both neuron number (P < .01) and neuronal density (P < .05) in the GP, and for neuron number (P < .05) in the SN. Neuron loss ranged from 6% to 70% in the GP and from 10% to 50% in the SN. Neuropathological analyses confirmed neuroAIDS-like changes in brain, including microglial nodules, extensive perivascular cuffing and/or the presence of multinucleated giant cells, and alterations in neuronal morphology in the majority of the rapid progressors. By comparison, slow progressors showed little, if any, neuropathology. These neuropathological changes in SIV-infected monkeys indicate that neuron death and morphological alterations in the basal ganglia may contribute to the motor impairments reported in the SIV model and, by analogy, in the subset of patients afflicted with motor impairment in human neuro-AIDS.

Animals↗
PubMed2004

Manifestations of SIV-induced ocular pathology in macaque monkeys.

Simian immunodeficiency virus has been shown to cause acquired immunodeficiency syndrome in macaque monkeys. Data gathered from clinical examination and fundus photography have shown that the lentivirus is capable of the induction of choroidal lesions and retinal hemorrhages in the macaque. These findings demonstrate the potential value of the macaque monkey eye as a model of the retinal pathology routinely seen in human AIDS patients.

Animals↗
PubMed2001

Consistent features in the forelimb representation of primary motor cortex in rhesus macaques.

The purpose of this study was to systematically map the forelimb area of primary motor cortex (M1) in rhesus macaques in an effort to investigate further the organization of motor output to distal and proximal muscles. We used stimulus-triggered averaging (StTAing) of electromyographic activity to map the cortical representation of 24 simultaneously recorded forelimb muscles. StTAs were obtained by applying 15 microA stimuli to M1 sites while the monkey performed a reach and prehension task. Motor output to body regions other than the forelimb (e.g., face, trunk, and hindlimb) was identified using repetitive intracortical microstimulation to evoke movements. Detailed, muscle-based maps of M1 revealed a central core of distal (wrist, digit, and intrinsic hand) muscle representation surrounded by a "horseshoe"-shaped zone of proximal (shoulder and elbow) muscle representation. The core distal and proximal zones were separated by a relatively large region representing combinations of both distal and proximal muscles. On the basis of its size and characteristics, we argue that this zone is not simply the result of stimulus-current spread, but rather a distinct zone within the forelimb representation containing cells that specify functional synergies of distal and proximal muscles. Electrode tracks extending medially from the medial arm of the proximal muscle representation evoked trunk and hindlimb responses. No distal or proximal muscle poststimulus effects were found in this region. These results argue against the existence of a second, major noncontiguous distal or proximal forelimb representation located medially within the macaque M1 representation.

Animals↗
PubMed2000

Sensory evoked potentials in SIV-infected monkeys with rapidly and slowly progressing disease.

Human immunodeficiency virus (HIV-1) infects the central nervous system (CNS) early in the course of disease progression and leads to some form of neurological disease in 40-60% of cases. Both symptomatic and asymptomatic HIV-infected subjects also show abnormalities in evoked potentials. As part of an effort to further validate an animal model of the neurological disease associated with lentiviral infection, we recorded multimodal sensory evoked potentials (EPs) from nine rhesus macaques infected with passaged strains of SIVmac (R71/E17), prior to and at 1 month intervals following inoculation. The latencies of forelimb and hindlimb somatosensory evoked potentials (SEP) and flash visual evoked potentials (VEP) were measured. Within 14 weeks of inoculation, all but two animals had progressed to end-stage disease (rapid progressors). The two animals with slowly progressing disease (AQ15 and AQ94) had postinoculation life spans of 109 and 87 weeks, respectively. No significant changes were observed in evoked potentials recorded during the control period or at any time in the animals with slowly progressing disease. However, all of the monkeys with rapidly progressing disease exhibited increases in latency for at least one evoked potential type. The overall mean increases in somatosensory and visual evoked potential peak latencies for the rapid progressors were 22.4 and 25.3%, respectively. For comparison, the changes in slow progressors were not significant (1.8 and -1.9%, respectively). These results, coupled with our previous finding of slowed motor evoked potentials in the same cohort of macaques (Raymond et al.: J Neurovirol 1999;5:217-231), demonstrate a broad and somewhat variable pattern of viral injury to both sensory and motor system structures, resembling the findings in HIV-infected humans. These results coupled with our earlier work demonstrating cognitive and motor behavioral impairments in the same monkeys support the use of the SIVmac-infected rhesus macaque as a model of AIDS-related neurological disease.

Animals↗
PubMed2000

Chronic recording of EMG activity from large numbers of forelimb muscles in awake macaque monkeys.

Studies of the neural control of movement often require or benefit from long-term recording of EMG activity from large numbers of muscles involved in a particular motor task. While chronic recording of EMG activity has been described in a number of previous monkey studies, the number of muscles recorded has been somewhat limited and the implantation approach has been highly invasive procedures. This paper presents two EMG implant fabrication and surgical implantation methods that are suitable for use in monkeys, relatively non-traumatic and capable of simultaneous recording from 24 or more muscles.

Animals↗
PubMed2000

Correlations between corticomotoneuronal (CM) cell postspike effects and cell-target muscle covariation.

The presence of postspike facilitation (PSpF) in spike-triggered averages of electromyographic (EMG) activity provides a useful means of identifying cortical neurons with excitatory synaptic linkages to motoneurons. Similarly the presence of postspike suppression (PSpS) suggests the presence of underlying inhibitory synaptic linkages. The question we have addressed in this study concerns the extent to which the presence and strength of PSpF and PSpS from corticomotoneuronal (CM) cells correlates with the magnitude of covariation in activity of the CM cell and its target muscles. For this purpose, we have isolated cells during a reach and prehension task during which the activity of 24 individual proximal and distal forelimb muscles was recorded. These muscles show broad coactivation but with a highly fractionated and muscle specific fine structure of peaks and valleys. Covariation was assessed by computing long-term (2 s) cross-correlations between CM cells and forelimb muscles. The magnitude of cross-correlations was greater for muscles with facilitation effects than muscles lacking effects in spike-triggered averages. The results also demonstrate a significant relationship between the sign of the postspike effect (facilitation or suppression) and the presence of a peak or trough in the cross-correlation. Of all the target muscles with facilitation effects in spike-triggered averages (PSpF, PSpF with synchrony, or synchrony facilitation alone), 89.5% were associated with significant cross-correlation peaks, indicating positively covarying muscle and CM cell activity. Seven percent of facilitation effects were not associated with a significant effect in the cross-correlation, whereas only 3.4% of effects were associated with correlation troughs. In contrast, of all the muscles with suppression effects in spike-triggered averages, 38.9% were associated with significant troughs in the cross-correlation, indicating an inverse relation between CM cell and muscle activity consistent with the presence of suppression. Fifty-five percent of suppression effects was associated with correlation peaks, whereas 5.6% was not associated with a significant effect in the cross-correlation. Limiting the analysis to moderate and strong facilitation effects, the magnitude of PSpF was correlated weakly with the magnitude of the cell-muscle cross-correlation peak. Nevertheless, the results show that although many CM cell-target muscle pairs covary during the reach and prehension task in a way consistent with the sign and strength of the CM cell's synaptic effects on target motoneurons, many exceptions exist. The results are compatible with a model in which control of particular motoneuron pools reflects not only the summation of signals from many CM cells but also signals from additional descending, sensory afferent, and intrinsic spinal cord neurons. Any one neuron will make only a small contribution to the overall activity of the motoneuron pool. In view of this, it is not surprising that relationships between postspike effects and CM cell-target muscle covariation are relatively weak with many apparent incongruities.

Animals↗
PubMed2000

Plasticity in the distribution of the red nucleus output to forearm muscles after unilateral lesions of the pyramidal tract.

It has been hypothesized that the magnocellular red nucleus (RNm) contributes to compensation for motor impairments associated with lesions of the pyramidal tract. To test this hypothesis, we used stimulus triggered averaging (StTA) of electromyographic (EMG) activity to characterize changes in motor output from the red nucleus after lesions of the pyramidal tract. Three monkeys were trained to perform a reach and prehension task. EMG activity was recorded from 11 forearm muscles including one elbow, five wrist, and five digit muscles. Microstimulation (20 microA at 20 Hz) was delivered throughout the movement task to compute StTAs. Two monkeys served as controls. In a third monkey, 65% of the left pyramidal tract had been destroyed by an electrolytic lesion method five years before recording. The results demonstrate a clear pattern of postlesion reorganization in red nucleus-mediated output effects on forearm muscles. The normally prominent extensor preference in excitatory output from the RNm (92% in extensors) was greatly diminished in the lesioned monkey (59%). Similarly, suppression effects, which are normally much more prominent in flexor than in extensor muscles (90% in flexors), were also more evenly distributed after recovery from pyramidal tract lesions. Because of the limited excitatory output from the RNm to flexor muscles that normally exists, loss of corticospinal output would leave control of flexors particularly weak. The changes in RNm organization reported in this study would help restore function to flexor muscles. These results support the hypothesis that the RNm is capable of reorganization that contributes to the recovery of forelimb motor function after pyramidal tract lesions.

Action Potentials↗
PubMed1999

Simple and choice reaction time performance in SIV-infected rhesus macaques.

It is well established that HIV infection can lead to motor/cognitive disorders in humans. A number of studies have shown that simian immunodeficiency virus (SIV) infection in rhesus macaques parallels many aspects of HIV disease in humans. The purpose of this study was to define further the SIV-infected rhesus macaque as a model of neuro-AIDS. Our objective was to detect movement-related impairments in behaviorally trained, SIV-infected macaques using both simple and choice reaction time tasks. Reaction times (RTs), movement times (MTs), and error types were examined. Nine monkeys were infected with neurovirulent strains of SIVmac, four of which served initially as controls before their inoculation. Seven of the nine monkeys developed simian AIDS within 4 months of inoculation (rapid progressors), while two monkeys survived for more than 1 year postinoculation (slow progressors). Of the rapid progressors, four exhibited slowed reaction times and six showed movement time slowing. One rapid progressor showed evidence of a strategy shift to overcome impaired motor abilities. Monkeys with rapidly progressing SIV-related disease consistently show behavioral abnormalities reflecting underlying neuronal injury. Although the slow progressors also showed RT and/or MT slowing, a role for nonspecific factors related to late-stage simian AIDS could not be ruled out in these cases. The results demonstrate that motor impairments associated with SIV infection in rhesus macaques can be detected using RT and MT measures, further establishing the SIVmac-infected macaque monkey as a viable model of neuro-AIDS.

Animals↗
PubMed1999

Microglial activation and neurological symptoms in the SIV model of NeuroAIDS: association of MHC-II and MMP-9 expression with behavioral deficits and evoked potential changes.

HIV-1 causes cognitive and motor deficits and HIV encephalitis (HIVE) in a significant proportion of AIDS patients. Neurological impairment and HIVE are thought to result from release of cytokines and other harmful substances from infected, activated microglia. In this study, the quantitative relationship between microglial activation and neurological impairment was examined in the simian immunodeficiency model of HIVE. Macaque monkeys were infected with a passaged, neurovirulent strain of simian immunodeficiency virus, SIV(mac)239(R71/17E). In concurrent studies, functional impairment was assessed by motor and auditory brainstem evoked potentials and by measurements of cognitive and motor behavioral deficits. Brain tissue was examined by immunohistochemistry using two markers of microglia activation, MHC-II and matrix metalloproteinase-9 (MMP-9). The inoculated animals formed two groups: rapid progressors, which survived 6-14 weeks postinoculation, and slow progressors, which survived 87-109 weeks. In the rapid progressors, two patterns of MHC-II expression were present: (1) a widely disseminated pattern of MHC-II expressing microglia and microglial nodules in cortical gray matter and subcortical white matter, and (2) a more focal pattern in which MHC-II expressing microglia were concentrated into white matter. Animals exhibiting both patterns of microglial activation showed mild to severe changes in cognitive and motor behavior and evoked potentials. All rapid progressors showed expression of MMP-9 in microglia located in subcortical white matter. In the slow progressors MHC-II and MMP-9 staining was similar to uninoculated control macaques, and there was little or no evidence of HIVE. These animals showed behavioral deficits at the end of the disease course, but little changes in evoked potentials. Thus, increases in MHC-II and MMP-9 expression are associated with development of cognitive and motor deficits, alterations in evoked potentials, and rapid disease progression.

AIDS Dementia Complex↗
PubMed1999

Morphological correlates of neurological dysfunction in macaques infected with neurovirulent simian immunodeficiency virus.

The pattern of neurological disease caused by human immunodeficiency virus (HIV) infection of the central nervous system (CNS) was investigated using a macaque model of acquired immune defiency syndrome (AIDS). Seven of nine macaques inoculated with neurovirulent simian imunodeficiency virus (SIVmac ) developed AIDS within 3 months. Four of these had clinically obvious neurological disease and extensive conduction defects in the form of latency increases in evoked potential (EP) responses. Neuropathologically, all four animals had disseminated white matter disease in the form of multifocal, perivascular and nodular parenchymal mononuclear cell infiltrates, along with extensive involvement of the cortical grey matter, leptomeninges and intracranial portions of cranial nerves. A brisk multinucleated giant cell (MGC) response was a frequent accompaniment in the affected areas. Three of the animals in this group also showed spongiform vacuolation in the occipital grey matter, a lesion described only rarely in HIV encephalitis. In the remaining three animals, there was only minimal evidence of overt neurological impairment or conduction defects. These animals had only mild to moderate neuropathological changes and lesions were virtually confined to the white matter regions of the brain. MGC responses were rare or absent in the CNS of these animals. Neuropathological findings in this SIVmac model have therefore shown good correlation with the severity of clinical and neurophysiological changes, and are reminiscent of HIV-1 encephalitis. More importantly, white matter involvement was a consistent finding in the affected macaques, regardless of the duration and severity of disease, or type of virus inoculated, suggesting an unusual susceptibility for lentiviral infection in these regions of the macaque CNS.

Animals↗
PubMed1999

Motor skill impairment in SIV-infected rhesus macaques with rapidly and slowly progressing disease.

A number of studies have shown that simian immunodeficiency virus (SIV) infection in rhesus macaques parallels many aspects of HIV disease in humans. The purpose of this study was to further characterize the rhesus macaque infected with neurovirulent SIV as a model of neuroAIDS. Using a motor skill task, our objective was to detect SIV-related movement impairments in behaviorally trained macaques. The motor skill task required retrieval of a food pellet from a cup in a rotating turntable across a range of speeds. Nine monkeys were infected with neurovirulent strains of SIVmac (R71/17E): four monkeys served initially as controls pre-inoculation. Seven monkeys developed simian AIDS within 4 months of inoculation (rapid progressors), and two survived more than 18 months post-inoculation (slow progressors). Of the rapid progressors, five exhibited significant deficits in this task, most showing a gradual decline in performance terminating in a sharp drop to severely impaired levels of performance. One slow progressor (AQ15) showed no performance declines. The other slow progressor (AQ94) showed a significant decrease in maximum speed that was concurrent with the onset of clinical signs. For AQ94, the role of sickness behavior related to late stage simian AIDS could not be ruled out. These results demonstrate that motor system impairment can be detected early in the course of SIV infection in rhesus macaques, further establishing the SIVmac-infected macaque monkey as a viable model of neuroAIDS.

Animals↗
PubMed1999

Motor evoked potentials in a rhesus macaque model of neuro-AIDS.

Previous work using bone marrow passaged SIVmac239 (simian immunodeficiency virus) has shown that macrophage tropic strains of this virus enter the rhesus macaque brain early following inoculation (Sharma et al, 1992; Desrosiers et al, 1991; Zhu et al, 1995; and Narayan et al, 1997). As part of an effort to more fully characterize the extent of neurologic impairment associated with SIV infection of the brain, we used transcranial electrical stimulation of motor cortex and the spinal cord to evoke EMG potentials in two forelimb (EDC and APB) and two hindlimb (LG and AH) muscles. The latencies, magnitudes and thresholds of motor evoked potentials (MEPs) recorded from nine monkeys infected with neurovirulent SIVmac R71/17E were compared to pre-inoculation records from the same monkeys. Seven of nine monkeys developed simian AIDS within 4 months of inoculation and were euthanized. Two monkeys remained free of AIDS-related clinical illness for over 18 months following inoculation. Six of the seven monkeys with rapidly progressing disease showed post-inoculation latency increases ( > or = 2 s.d. of control) in at least one cortical MEP. Increases in cortical MEP latency ranged from 21-97% in different monkeys. All seven rapidly progressing animals showed post-inoculation increases in at least one spinal cord MEP latency. Maximum spinal cord MEP latency increases ranged from 22-147%. Increases in central conduction time (CCT) ranged up to 204% and exceeded two standard deviations of control in four monkeys. Neither of the two monkeys with slowly progressing disease showed significant increases in either cortical or spinal cord MEP latency or CCT. Only the monkeys with rapidly progressing disease exhibited classic AIDS-related neuropathology, although there was no consistent relationship between the severity of neuropathology and the extent of MEP abnormalities. In conclusion, our results demonstrate clear deficits in the functional integrity of both central and peripheral motor system structures associated with SIV infection and further support the use of SIV-infected rhesus macaques as a model of neuro-AIDS.

Animals↗
PubMed1998

A low-cost, multi-channel, EMG signal processing amplifier.

There is a growing need in studies of movement control to expand the number of muscles from which EMG activity is recorded during performance of motor tasks. Optimal viewing and analysis of this EMG activity requires signal processing which provides adjustable gain and baseline offset as wells as selectable AC coupling, rectification and filtering. This paper presents a low-cost circuit that combines two channels of EMG signal processing capability in one module.

Animals↗
PubMed1998

Neurovirulent simian immunodeficiency virus induces calbindin-D-28K in astrocytes.

Astrocyte activation has been postulated to be a major contributor to functional changes in the brain of AIDS patients. We assessed astrocyte activation in the simian immunodeficiency virus (SIV) model. Four groups of macaque brains were examined: uninoculated controls, animals inoculated with virus that did not cause disease, animals inoculated with virus that caused AIDS but did not cause encephalitis, and animals with SIV encephalitis. We examined expression of calbindin-D-28K, a calcium binding protein that is upregulated in astrocytes during excitotoxic events, as well as glial fibrillary acidic protein (GFAP). The presence of calbindin in astrocytes was confirmed by double-labeling using confocal microscopy. Increases in calbindin staining were most apparent in the white matter, but increases in GFAP staining were most apparent in middle layers of the cerebral cortex. Six of the seven animals with SIV encephalitis had calbindin immunoreactive astrocytes in the subcortical white matter, corpus callosum, internal capsule, cerebral peduncle, pontine white matter, and cerebellar white matter. Very rarely, a few, very lightly calbindin-immunoreactive astrocytes were present in the uninoculated control brains. The increase in calbindin expression by astrocytes in SIV encephalitis suggests that these cells are subject to calcium toxicity. In uninoculated control macaques, and in macaques inoculated with virus that did not cause disease, GFAP-immunoreactive astrocytes were present throughout the subcortical white matter and in layer I, but very few were found in layers III-V of the cerebral cortex. Two animals that died of AIDS without encephalitis had somewhat higher numbers of GFAP immunoreactive astrocytes in middle cortical layers. In seven animals that received passaged neurovirulent virus and developed both AIDS and encephalitis, the number of GFAP-immunoreactive astrocytes in middle cortical layers was high, indicating widespread astrocyte activation.

Animals↗
PubMed1998

Fractionator analysis shows loss of neurons in the lateral geniculate nucleus of macaques infected with neurovirulent simian immunodeficiency virus.

Infection of macaques with neurovirulent strains of simian immunodeficiency virus (SIVmac) is an experimental model for the neurological manifestations of AIDS. Loss of neurons has been reported in the cerebral cortex following immunodeficiency viral infection, but thalamic structures which may contribute to electrophysiological changes and neurological deficits have not been examined. In this study, the lateral geniculate nucleus (LGN) of macaques inoculated with macrophage-tropic, neurovirulent virus SIVmac239 (R71 and 17E) was examined for neuron loss using the optical fractionator method. Estimates of the number of neurons in the P layers of the lateral geniculate nucleus of age-matched control macaques ranged from 1.0 to 1.3 x 10(6), while the number of neurons in SIV infected macaques ranged from 0.8 to 1.1 x 10(6), reflecting neuron loss of up to 28%. Neuron loss was not observed in the magnocellular layer. The total number of glia and glial density were unchanged. Loss of neurons in the lateral geniculate nucleus was correlated with the pattern of neuropathological changes. Neuron loss was most severe in animals with encephalitis concentrated in the brain stem and subcortical white matter and was less apparent in animals with diffuse encephalitis. Neuron loss in the lateral geniculate nucleus did not explain changes observed in the visual evoked potential, which was severely affected in two animals which showed a loss of 24 and 26%, while it was normal in a third animal which showed neuron loss of 28%.

Animals↗
PubMed1998

Distribution and characteristics of poststimulus effects in proximal and distal forelimb muscles from red nucleus in the monkey.

We used stimulus-triggered averaging (StTA) of electromyographic (EMG) activity to investigate two major questions concerning the functional organization of the magnocellular red nucleus (RNm) for reaching movements in the macaque monkey. The first is whether the clear preference toward facilitation of extensor muscles we have reported in previous studies for distal (wrist and digit) forelimb muscles also exists for proximal muscles (shoulder and elbow). The second question is whether distal and proximal muscles may be cofacilitated from RNm suggesting the representation of functional muscle synergies for coordinated reaching movements. Two monkeys were trained to perform a prehension task requiring multijoint coordination of the forelimb. EMG activity was recorded from 24 forelimb muscles including 5 shoulder, 7 elbow, 5 wrist, 5 digit, and 2 intrinsic hand muscles. Microstimulation (20 microA at 20 Hz) was delivered throughout the movement task. From 137 microstimulation sites in the RNm, a total of 977 poststimulus effects was obtained including 733 poststimulus facilitation effects (PStF) and 244 poststimulus suppression effects (PStS). Of the PStF effects, 58% were obtained from distal muscles; 42% from proximal muscles. Digit muscles were more frequently facilitated (35%) than the wrist, elbow, or shoulder muscles (20, 24, and 18%, respectively). The intrinsic hand muscles were infrequently facilitated (3%). At all joints tested, PStF was more common in extensor muscles than flexor muscles. This extensor preference was very strong for shoulder (85%), wrist (85%), and digit muscles (94%) and weaker for elbow muscles (60%). Of the PStS effects, 65% were in distal muscles and 35% in proximal muscles. Interestingly, the flexor muscles were more frequently inhibited from RNm than extensor muscles. At 72% of stimulation sites, at least two muscles were facilitated. The majority of these sites (61%) cofacilitated both proximal and distal muscles. At the remaining sites (39%), PStF was observed in either the proximal (17%) or distal muscles (22%). Facilitation most often involved combinations of shoulder, elbow, and distal muscles (30%) or shoulder and distal muscles (26%). Only rarely were intrinsic hand muscles part of the total muscle synergy. Our results show that the RNm 1) controls both proximal and distal muscles but the strength of influence is biased toward distal muscles, 2) preferentially controls extensor muscles not only at distal forelimb joints but also at proximal joints, and 3) output zones cofacilitate synergies of proximal and distal muscles involved in the control of forelimb reaching movements.

Animals↗
PubMed1998

Corticomotoneuronal postspike effects in shoulder, elbow, wrist, digit, and intrinsic hand muscles during a reach and prehension task.

We used spike-triggered averaging of rectified electromyographic activity to determine whether corticomotoneuronal (CM) cells produce postspike effects in muscles of both proximal and distal forelimb joints in monkeys performing a reach and prehension task. Two monkeys were trained to perform a self-paced task in which they reached forward from a starting position to retrieve a food reward from a small cylindrical well. We compiled spike-triggered averages from 22 to 24 separate forelimb muscles at both proximal (shoulder, elbow) and distal (wrist, digits, intrinsic hand) joints. Of 174 cells examined, 112 produced postspike effects in at least one of the target muscles. Of those cells, 45.5% produced postspike effects in both proximal and distal forelimb muscles. A nearly equal number (44.7%) produced postspike effects in distal muscles only, whereas a clear minority (9.8%) produced postspike effects in only proximal muscles. The majority of CM cells (71.4%) produced effects in two or more muscles, with an average muscle field of 3.1 +/- 2.1 (mean +/- SD) for facilitation plus suppression. Of 345 postspike effects identified, 70.7% were facilitation effects and 29.3% were suppression effects. The large majority of effects (72.2%) were in distal muscles. When averaged by joint, the latency and peak magnitude of postspike facilitation showed a stepwise increase from proximal to distal joints. The results of this study show that the majority of CM cells engaged in coordinated forelimb reaching movements facilitate and/or suppress muscles at multiple joints, including muscles at both proximal and distal joints. The results also show that CM cells make more frequent and more potent terminations in motoneuron pools of distal compared with proximal muscles.

Action Potentials↗