Short-latency Activation Research Articles

Postural control adapts by changing temporal neuromuscular control rather than movement strategy complexity after mild perturbation during stance

When the arm of a standing human is perturbed in an unpredictable direction, postural muscles are activated at latencies as short as 50–110 ms. While the motion of the body clearly progresses in hand-to-leg sequence, there is no systematic muscle activation sequence from the arm to the leg muscles, suggesting that the activation of the muscles is not likely the result of local stretch reflexes. In fact, the lower limb muscles are activated before the upright posture is significantly disturbed. The short-latency activation amplitude and the activation probability are clearly tuned to the direction of the arm perturbation for both rostral and caudal muscles. The effect of central set on the short-latency response has been investigated by manipulating the predictability of the perturbations. Possible underlying neural mechanisms have been discussed.

Postural response characterization of standing humans to multi-directional, predictable and unpredictable perturbations to the arm

When the arm of a standing human is perturbed in an unpredictable direction, postural muscles are activated at latencies as short as 50–110ms. While the motion of the body clearly progresses in hand-to-leg sequence, there is no systematic muscle activation sequence from the arm to the leg muscles, suggesting that the activation of the muscles is not likely the result of local stretch reflexes. In fact, the lower limb muscles are activated before the upright posture is significantly disturbed. The short-latency activation amplitude and the activation probability are clearly tuned to the direction of the arm perturbation for both rostral and caudal muscles. The effect of central set on the short-latency response has been investigated by manipulating the predictability of the perturbations. Possible underlying neural mechanisms have been discussed.

Increased tone-offset response in the lateral nucleus of the amygdala underlies trace fear conditioning

Accumulating evidence suggests that the lateral nucleus of the amygdala (LA) stores associative memory in the form of enhanced neural response to the sensory input following classical fear conditioning in which the conditioned stimulus (CS) and the unconditioned stimulus (US) are presented in a temporally continuous manner. However, little is known about the role of the LA in trace fear conditioning where the CS and the US are separated by a temporal gap. Single-unit recordings of LA neurons before and after trace fear conditioning revealed that the short-latency activity to the CS offset, but not that to the onset, increased significantly and accompanied the conditioned fear response. The increased short-latency activity was evident in two aspects: the number of offset-responsive neurons was increased and the latency of the neuronal response to the CS offset was shortened. On the contrary, changes in the firing rate to either the onset or the offset were negligible following unpaired presentations of the CS and US. In sum, our results suggest that increased synaptic efficacy in the CS offset pathway in the LA might underlie the association between temporally distant stimuli in trace fear conditioning.

Short latency activation of cortex by clinically effective thalamic brain stimulation for tremor

Deep brain stimulation (DBS) relieves disabling symptoms of neurologic and psychiatric diseases when medical treatments fail, yet its therapeutic mechanism is unknown. We hypothesized that ventral intermediate (VIM) nucleus stimulation for essential tremor activates the cortex at short latencies, and that this potential is related to the suppression of tremor in the contralateral arm. We measured cortical activity with electroencephalography in 5 subjects (seven brain hemispheres) across a range of stimulator settings, and reversal of the anode and cathode electrode contacts minimized the stimulus artifact, allowing visualization of brain activity. Regression quantified the relationship between stimulation parameters and both the peak of the short latency potential and tremor suppression. Stimulation generated a polyphasic event-related potential in the ipsilateral sensorimotor cortex, with peaks at discrete latencies beginning less than 1 ms after stimulus onset (mean latencies 0.9 ± 0.2, 5.6 ± 0.7, and 13.9 ± 1.4 ms, denoted R1, R2, and R3, respectively). R1 showed more fixed timing than the subsequent peaks in the response (P < 0.0001, Levene's test), and R1 amplitude and frequency were both closely associated with tremor suppression (P < 0.0001, respectively). These findings demonstrate that effective VIM thalamic stimulation for essential tremor activates the cerebral cortex at approximately 1 ms after the stimulus pulse. The association between this short latency potential and tremor suppression suggests that DBS may improve tremor by synchronizing the precise timing of discharges in nearby axons and, by extension, the distributed motor network to the stimulation frequency or one of its subharmonics.

Short latency activation of cortex during clinically effective subthalamic deep brain stimulation for Parkinson's disease

Subthalamic deep brain stimulation (DBS) is superior to medical therapy for the motor symptoms of advanced Parkinson's disease (PD), and additional evidence suggests that it improves refractory symptoms of essential tremor, primary generalized dystonia, and obsessive-compulsive disorder. Despite this, its therapeutic mechanism is unknown. We hypothesized that subthalamic stimulation activates the cerebral cortex at short latencies after stimulus onset during clinically effective stimulation for PD. In 5 subjects (six hemispheres), EEG measured the response of cortex to subthalamic stimulation across a range of stimulation voltages and frequencies. Novel analytical techniques reversed the anode and cathode electrode contacts and summed the resulting pair of event-related potentials to suppress the stimulation artifact. We found that subthalamic brain stimulation at 20 Hz activates the somatosensory cortex at discrete latencies (mean latencies: 1.0 ± 0.4, 5.7 ± 1.1, and 22.2 ± 1.8 ms, denoted as R1, R2, and R3, respectively). The amplitude of the short latency peak (R1) during clinically effective high-frequency stimulation is nonlinearly dependent on stimulation voltage (P < 0.001; repeated-measures analysis of variance), and its latency is less variable than that of R3 (1.02 versus 19.46 ms; P < 0.001, Levene's test). We conclude that clinically effective subthalamic brain stimulation in humans with PD activates the cerebral cortex at 1 ms after stimulus onset, most likely by antidromic activation. These findings suggest that alteration of the precise timing of action potentials in cortical neurons with axonal projections to the subthalamic region may be an important component of the therapeutic mechanism of subthalamic brain stimulation.

Effects of hypoxia on genioglossus and scalene reflex responses to brief pulses of negative upper-airway pressure during wakefulness and sleep in healthy men

Hypoxia can depress ventilation, respiratory load sensation, and the cough reflex, and potentially other protective respiratory reflexes such as respiratory muscle responses to increased respiratory load. In sleep-disordered breathing, increased respiratory load and hypoxia frequently coexist. This study aimed to examine the effects of hypoxia on the reflex responses of 1) the genioglossus (the largest upper airway dilator muscle) and 2) the scalene muscle (an obligatory inspiratory muscle) to negative-pressure pulse stimuli during wakefulness and sleep. We hypothesized that hypoxia would impair these reflex responses. Fourteen healthy men, 19-42 yr old, were studied on two separate occasions, approximately 1 wk apart. Bipolar fine-wire electrodes were inserted orally into the genioglossus muscle, and surface electrodes were placed overlying the left scalene muscle to record EMG activity. In random order, participants were exposed to mild overnight hypoxia (arterial oxygen saturation approximately 85%) or medical air. Respiratory muscle reflex responses were elicited via negative-pressure pulse stimuli (approximately -10 cmH(2)O at the mask, 250-ms duration) delivered in early inspiration during wakefulness and sleep. Negative-pressure pulse stimuli resulted in a short-latency activation followed by a suppression of the genioglossus EMG that did not alter with hypoxia. Conversely, the predominant response of the scalene EMG to negative-pressure pulse stimuli was suppression followed by activation with more pronounced suppression during hypoxia compared with normoxia (mean +/- SE suppression duration 64 +/- 6 vs. 38 +/- 6 ms, P = 0.006). These results indicate differential sensitivity to the depressive effects of hypoxia in the reflex responsiveness to sudden respiratory loads to breathing between these two respiratory muscles.

Somatosensory cell response to an auditory cue in a haptic memory task

Neurons in the monkey’s anterior parietal cortex (Brodmann’s areas 3a, 3b, 1, and 2) have been reported to retain information from a visual cue that has been associated with a tactile stimulus in a haptic memory task. This cross-modal transfer indicates that neurons in somatosensory cortex can respond to non-tactile stimuli if they are associated with tactile information needed for performance of the task. We hypothesized that neurons in somatosensory cortex would be activated by other non-tactile stimuli signaling the haptic movements—of arm and hand—that the task required. We found such cells in anterior parietal areas. They reacted with short-latency activity changes to an auditory signal (a click) that prompted those movements. Further, some of those cells changed their discharge in temporal correlation with the movements themselves, with the touch of the test objects, and with the short-term memory of those objects for subsequent tactile discrimination. These findings suggest that cells in the somatosensory cortex participate in the behavioral integration of auditory stimuli with other sensory stimuli and with motor acts that are associated with those stimuli.

Activation of Ventral Tegmental Area Cells by the Bed Nucleus of the Stria Terminalis: A Novel Excitatory Amino Acid Input to Midbrain Dopamine Neurons

We examined the role of excitatory amino acids (EAAs) in the activation of midbrain dopaminergic (DA) neurons evoked by stimulation of the ventromedial and ventrolateral (subcommissural) bed nucleus of the stria terminalis (vBNST). Using anesthetized rats and extracellular recording techniques, we found that 84.8% of ventral tegmental area (VTA) DA neurons were activated synaptically by single-pulse electrical stimulation of the vBNST. In contrast, similar stimulation did not affect the activity of presumed GABA neurons in the VTA. Three characteristic responses were observed in VTA DA neurons: short latency activation (<25 msec; 55.1% of cells), long latency activation (>65 msec; 56% of cells), and inhibition (61.8% of cells, usually followed by long latency excitation). Microinfusion of antagonists of EAA receptors (3 mm kynurenic acid, 100 microm AP-5, or 50 microm CNQX) from a micropipette adjacent to the recording electrode significantly reduced both short and long latency activations evoked in DA neurons by vBNST stimulation. Specific responses were attenuated similarly by AP-5 alone, CNQX alone, or a cocktail of AP-5+CNQX, indicating that joint activation of NMDA plus non-NMDA receptors was required. Stimulation of the vBNST by local microinfusion of glutamate increased the firing and bursting activity of VTA DA neurons. Similar microinfusion of GABA decreased bursting of VTA DA neurons without altering their firing rate. Retrograde and anterograde labeling and antidromic activation of vBNST neurons by VTA stimulation confirmed a direct projection from the vBNST to the VTA. These results reveal that inputs from the vBNST exert a strong excitatory influence on VTA DA neurons mediated by both NMDA and non-NMDA receptors.

Instigation and control of treadmill locomotion in high decerebrate cats by stimulation of the hook bundle of Russell in the cerebellum

In high decerebrate cats, pulse train microstimulation of a restricted region of the midline cerebellar white matter produced a generalized increase in postural muscle tone in the neck, trunk, and limb extensor muscles, and air-stepping of all four legs on a stationary surface. On the moving belt of a treadmill, such stimulation produced well coordinated, fore- and hindlimb locomotion as evoked by stimulating the mesencephalic locomotor region (MLR). Microinjection of a neural tracer into the cerebellar locomotion-inducing site resulted in a bilateral retrograde labeling of cells limited to the fastigial nuclei simultaneously with anterograde labeling of fibers projecting bilaterally to the medial pontomedullary reticular formation (mPMRF) the vestibular complex and upper cervical segments. These results have led to our proposition that the effective cerebellar locomotor region (CLR) corresponds to the midline region of the hook bundle of Russell. Passing through this structure are crossed fastigioreticular and fastigiovestibular fibers, together with fastigiospinal fibers. Subsequently, we showed that CLR stimulation resulted in simultaneous short-latency synaptic activation of long-descending reticulospinal and vestibulospinal cells with high synaptic security. Clearly, the fastigial nucleus possesses potential capability to recruit and regulate posture- and locomotor-related subprograms which are distributed within the brainstem and spinal cord by the in-parallel activation of fastigiospinal, fastigioreticular, and fastigiovestibular pathways.

Neuronal firing activity in the dorsal hippocampus during the auditory discrimination oddball task in awake rats: relation to event-related potential generation

In order to investigate the roles of the hippocampus in event-related potential (ERP) generation, extracellular neuronal firings in the dorsal hippocampus were recorded together with the ERPs on the cortical surface and at the hippocampus during the auditory discrimination task in awake rats. The major ERP components on the cortical surface in response to the target tone were the P2, N2, and P3 with the latencies being approximately 100, 200 and 450 ms, respectively. For the non-target tone, the N2 and P3 components were not clearly observed. Local ERP at the hippocampus exhibited similar wave-forms to that on the cortex in response to the target and non-target tones. In the hippocampus, 11 of 21 neuronal firings showed a long-latency sustained activation from 113.6±89.7 ms to 539.1±208.6 ms with the peak being 281.6±167.4 ms after the target tone onset. This increase was not observed after the non-target tone, and was not prominent when the rat did not perform the task. It was not time-locked to lever pressing behavior, and was not affected by the intensity of the tone stimulus. These features in relation to behavioral and paradigm indices were similar to the long-latency ERP components, N2 and P3. Possible involvement of the hippocampus in ERP generation was further suggested by the correlation between the magnitude of the long-latency activation and the amplitudes of N2 and P3 in some hippocampal firings. On the other hand, seven neuronal firings showed a short-latency transient activation with the peak at 36.3±14.4 ms accompanied by the early components of local ERP in the hippocampus both after the target and non-target tones. This response was more conspicuous when the rat did not perform the task and its amplitude was positively affected by the stimulus intensity. These findings imply that there are two types of hippocampal neuronal activation during the auditory discrimination oddball task. One is the short-latency activation that is related to information processing of the exogenous stimulus property. The second is the long-latency activation that may be involved in execution of the cognitive task, and in generation of long-latency ERP components.

Various strategies of forelimb movement during contact placing reactions elicited by tactile stimulation of the different aspects of a cat's paw.

Forelimb trajectory and the activity of eight muscles operating at the elbow, wrist and digit joints were analyzed during contact placing (CP) reactions elicited by tactile stimuli applied to the lateral (L) or medial (M) side of the cat's forepaw to verify whether a common movement strategy was used in these reactions. A tactile stimulus applied to the lateral side of the paw led, most frequently, to a short-latency activation of the elbow flexor muscles and flexor carpi radialis. Stimulation of the medial side of the paw produced either a short-latency activation of the elbow flexors or both the elbow flexor and extensor muscles. At the distal joints it most frequently activated extensor carpi ulnaris and flexor carpi radialis muscles. Different patterns of activation of the muscles during LCP and MCP reactions led to a diverse involvement of elbow flexion and extension movements at the beginning of the reactions. LCP was usually initiated by the elbow flexion movement whereas during MCP reactions the elbow flexion often appeared with a delay due to a brief co-contraction of the elbow flexor and extensor muscles which temporarily locked the elbow joint. The latter reaction was initiated by a backward/upward movement at the proximal joints accompanied by an ulnar deviation and a palmar flexion of the paw. The medio-lateral components of the movement were also clearly different in LCP and MCP reactions, both at the proximal and distal joints. The results indicate that various strategies of movement are used in CP reactions depending on the site of tactile stimulation.

Spinal NK1 receptors contribute to the increased excitability of the nociceptive flexor reflex during persistent peripheral inflammation

Hyperalgesia is a characteristic of inflammation and is mediated, in part, by an increase in the excitability of spinal neurons. Although substance P does not appear to mediate fast synaptic events that underlie nociception in the spinal cord, it may contribute to the hyperalgesia and increased excitability of spinal neurons during inflammation induced by complete Freund's adjuvant. We examined the role of endogenous substance P in changes in the excitability of spinal neurons during adjuvant-induced, peripheral inflammation by determining the effect of a selective NK1 receptor antagonist (RP67580) on the nociceptive flexor reflex in adult rats. Experiments were conducted 2 or 3 days after injection of adjuvant. Animals exhibited moderate thermal hyperalgesia at this time. The flexor reflex was evoked by electrical stimulation of the sural nerve and was recorded in the ipsilateral hamstring muscles. The flexor reflex ipsilateral to the inflamed hindpaw was enhanced approximately two-fold compared to the flexor reflex evoked in untreated animals as determined by the number of potentials and the duration of the reflex. The enhanced reflex in adjuvant-treated animals was most likely due to an increase in the excitability of spinal interneurons because short-latency activity in the hamstring muscles did not differ between untreated animals and adjuvant-treated animals following electrical stimulation of the L5 dorsal root or the nerve innervating the muscle with a stimulus that was 1.3–1.5 times the threshold for excitation of A-fibers. Intrathecal administration of RP67580 (2.3 and 6.8 nmol) attenuated the flexor reflex evoked in adjuvant-treated animals, but had no effect in untreated animals. Intravenous or intraplantar injection of RP67580 (6.8 nmol) did not affect the flexor reflex in adjuvant-treated animals indicating a spinal action of the drug following intrathecal administration. RP68651, the enantiomer of RP67580, was without effect at doses up to 6.8 nmol, indicating that the effects of comparable doses of RP67580 were due to an action of the drug at NK1 receptors. However, intrathecal administration of 23 nmol of both drugs attenuated the reflex in adjuvant-treated and control animals indicating that effects of RP67580 at this dose were not mediated entirely by its action at NK1 receptors. Overall, these data suggest that endogenous substance P has a role in the increased excitability of spinal interneurons observed during persistent inflammation and support the hypothesis that substance P released in the spinal cord contributes to the hyperalgesia that accompanies adjuvant-induced persistent, peripheral inflammation.

Activation of cells of cochlear nucleus by electrical stimulation of lateral hypothalamus.

Effects of electrical stimulation of the lateral hypothalamus (HS) were examined in 67 cells of the dorsal or ventral cochlear nucleus. Both short latency activity in the 10-20 ms post-stimulus period and late activity in the > 20 ms post-stimulus period were elicited in response to HS. A greater percentage of units exhibited the short latency response in dorsal (89%) than ventral (68%) cochlear nucleus. It was not previously recognized that stimulation of the hypothalamus could elicit increases in spike activity in this auditory relay nucleus. The hypothalamus is known to play a role in visceral-emotional functions, including feeding, fleeing, fighting and reproductive behavior. These results suggest a means by which neural activities supporting these functions could influence acoustic relay transmissions.

Site of interaction between saccade signals and vestibular signals induced by head rotation in the alert cat: functional properties and afferent organization of burster-driving neurons.

1. Extracellular spikes of burster-driving neurons (BDNs) were recorded within and immediately below the prepositus hypoglossi nucleus in the alert cat. BDNs were characterized by short-latency activation after stimulation of the contralateral vestibular nerve (latency: 1.4-2.7 ms) and the ipsilateral superior colliculus (latency: 1.7-3.5 ms). Convergence of vestibular and collicular inputs was found in all of 85 BDNs tested. Firing of BDNs increased during contralateral horizontal head rotation and decreased during ipsilateral rotation. A burst of spikes was induced in association with contralateral saccades and quick phases of nystagmus. 2. BDNs showed irregular tonic discharges during fixation. There was no significant correlation between the firing rate during fixation and horizontal or vertical eye position in most BDNs. During horizontal sinusoidal head rotation, the change in firing rate was approximately proportional to and in phase with contralateral head velocity. The phase lag of the response relative to head angular velocity was 13.8 +/- 20.1 degrees (mean +/- SD) at 0.5 Hz and 7.2 +/- 13.5 degrees at 0.2 Hz on the average. The gain was 0.88 +/- 0.25 (spikes/s)/(degrees/s) at 0.5 Hz and 1.19 +/- 0.49 (spikes/s)/(degrees/s) at 0.2 Hz. 3. Quantitative analysis of burst activity associated with saccades or quick phases indicated that the ON direction of BDNs was contralateral horizontal. The number of spikes in the burst was linearly related to the amplitude of the contralateral component of rapid eye movements. The slope of regression line was, on the average, 1.14 +/- 0.48 spikes/deg. There was no significant difference between the mean slopes for saccades and quick phases. The number of spikes depended on the difference between initial and final horizontal eye positions and not on the absolute eye position in the orbit. The mean burst firing rate was proportional to the mean velocity of the contralateral component of rapid eye movements. The slope of the regression line was 0.82 +/- 0.34 (spikes/s)/(degrees/s). Significant correlation was also found between intraburst instantaneous firing rate and instantaneous component eye velocity. 4. Objects presented in the contralateral visual field elicited a brief burst of spikes in BDNs independent of any eye movement. Contralateral saccades to the target were preceded by an early response to the visual stimulus and subsequent response associated with eye movement. 5. Excitation of BDNs produced by stimulation of the ipsilateral superior colliculus was facilitated by contralateral horizontal head rotation. Therefore saccadic signals from the superior colliculus to BDNs may be augmented by vestibular signals during head rotation.(ABSTRACT TRUNCATED AT 400 WORDS)

Cerebellar influence on olivary excitability in the cat.

This study examines the influence of the cerebellum on the excitability of inferior olivary neurons in the cat. Two major pathways from the cerebellar nuclei to the inferior olive have been investigated by electrophysiological and anatomical techniques. The first, excitatory pathway connects the cerebellar nuclei through nuclei at the mesodiencephalic junction with the inferior olive. The second is the direct, GABAergic, nucleo-olivary pathway. Intra- as well as extracellular recordings obtained in the rostral part of the medial accessory and principal olives revealed that electrical stimulation with a short burst of three pulses delivered at the mesodiencephalic junction results in short-latency activation (4-8 ms) of most olivary neurons. More than half of the units showed, in addition to the short-latency activation, a consistent response with a much longer latency (approximately 180 ms). Many units (66%) that responded to mesodiencephalic stimulation could also be activated by superior cerebellar peduncle stimulation with a similar stimulation paradigm (latency 9-15 ms). However, in such cases consistent long-latency responses were only rarely recorded (7%). To distinguish between the effect of the two pathways, both of which are activated by superior cerebellar peduncle stimulation, an electrolytic lesion of the nucleo-olivary fibres was made in the brainstem in six experiments. The effect of this lesion was verified in three cases by retrograde horseradish peroxidase tracing from the rostral inferior olive at the end of the experiment. This time only extracellular recordings were made. Stimulation of the mesodiencephalic junction still resulted in easily activated olivary units which showed an increased probability of firing a long-latency action potential. Stimulation of the superior cerebellar peduncle now resulted in a 50% decrease in probability of activating olivary units in the short-latency range. However, a five-fold increase in the chance of triggering action potentials in the long-latency interval was noted, implying that many units reacted only with a long-latency action potential. The results obtained with our experimental paradigm appear enigmatic since it is well established that the nucleo-olivary pathway is GABAergic and thus, by convention, should be inhibitory to the olivary neurons. However, it is possible to explain these results in terms of dynamic coupling of olivary neurons. This concept ascribes an important role to the nucleo-olivary pathway in regulating the degree of electrotonic coupling between olivary neurons (probably by a shunting mechanism) and as such may be an important instrument in the regulation of synchronous and rhythmic olivary discharges.(ABSTRACT TRUNCATED AT 400 WORDS)

Patterned light flash evoked short latency activity in the visual system of visually normal and in amblyopic subjects

In a previous experimental study on anaesthetized cat it was shown that a short latency (35-40 ms) cortical potential changed polarity due to the presence or absence of a pattern in the flash stimulus. The results suggested one pathway of neuronal activation in the cortex to a pattern that was within the level of resolution and another to patterns that were not. It was implied that a similar difference in impulse transmission to pattern and non-pattern stimuli may be recorded in humans. The present paper describes recordings of the short-latency visual evoked response to varying light flash checkerboard pattern stimuli of high intensity in visually normal and amblyopic children and adults. When stimulating the normal eye a visual evoked response potential with a peak latency between 35 to 40 ms showed a polarity change to patterned compared to non-patterned stimulation. The visual evoked response resolution limit could be correlated to a visual acuity of 0.5 and below. In amblyopic eyes the shift in polarity was recorded at the acuity limit level. The latency of the pattern depending potential was increased in patients with amblyopia compared to normal, but not directly related to amblyopic degree. It is concluded that the short latency, visual evoked response that mainly represents the retino-geniculo-cortical activation may be used to estimate visual resolution below 0.5 in acuity level.(ABSTRACT TRUNCATED AT 250 WORDS)

Latencies of response of eye movement-related neurons in the region of the interstitial nucleus of Cajal to electrical stimulation of the vestibular nerve in alert cats

Recent studies have shown that the interstitial nucleus of Cajal (INC) in the midbrain reticular formation is involved in the conversion of vertical semicircular canal signals into eye position during vertical vestibulo-ocular reflexes. Secondary vestibulo-ocular relay neurons related to the vertical canals, which constitute the majority of output neurons sending signals from the vestibular nuclei directly to the oculomotor nuclei, have been shown to project axon collaterals to the region within and near the INC. To understand how the INC is involved in the signal conversion, latencies of response of neurons in the INC region to electrical stimulation of the vestibular nerve were examined in alert cats. The responses of 96 cells whose activity was clearly modulated by sinusoidal pitch rotation (at 0.31 Hz) were analyzed. These included 41 cells whose activity was closely correlated with vertical eye movement (38 burst-tonic and 3 tonic neurons), and 55 other cells (called pitch cells as previously). Twenty nine of the 96 cells (30%) were activated at disynaptic latencies following single shock stimulation of the contralateral vestibular nerve. Disynaptically activated cells were significantly more frequent for pitch cells than for eye movement-related cells (25/55 = 45% vs 4/41 = 10%; p less than 0.001, Chi-square test). Conversely, cells that did not receive short-latency activation (less than 6 ms) were more frequent among eye movement-related cells than pitch cells (26/41 = 63% vs 13/55 = 24%; p less than 0.001, Chi-square test).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of lingual nerve and chewing cortex stimulation upon activity of the swallowing neurons located in the region of the hypoglossal motor nucleus

This study focuses on motoneurons and interneurons in the region of the hypoglossal nucleus (XIIth) related to swallowing and chewing. In sheep anesthetized with halothane, we have used extracellular microelectrodes to study the effects of stimulation of the superior laryngeal nerve (SLN), the lingual nerve (LN) and the chewing cortex (CCx) upon activities of the swallowing neurons (SNs). Ipsilateral stimulation (1-5 pulses at 500 Hz) of the peripheral afferents or CCx did not generally induce a short latency activation of the hypoglossal swallowing motoneurons (Group I SNs) since only 4 motoneurons (69 tested) were activated by the SLN, 4 motoneurons (56 tested) by the LN and none by the CCx. In contrast, the same stimulations were more effective with swallowing interneurons (Group II SNs) located in the reticular formation close to the XIIth motor nucleus since 12 neurons (30 tested) were activated with short latencies (9 +/- 1.8 ms; mean latency +/- S.D.) by the SLN, 9 neurons (21 tested) by the LN (latency; 8 +/- 1.8 ms) and 5 neurons (18 tested) by the CCx (latency: 13 +/- 1.7 ms). Seven neurons were activated by two or three modes of stimulation indicating the existence of convergent inputs upon some Group II SNs. During chewing movements induced by a prolonged stimulation (20-40 Hz) of the CCx, 10 Group I SNs (16 tested) versus only one Group II SN (8 tested) were found to fire in association with the jaw opening. Moreover, 3 motoneurons and 4 interneurons inactive during swallowing discharged during chewing movements.(ABSTRACT TRUNCATED AT 250 WORDS)

POTENTIALS EVOKED IN HUMAN AND MONKEY CEREBRAL CORTEX BY STIMULATION OF THE MEDIAN NERVE

Somatosensory evoked potentials (SEPs) are generated in afferent pathways, subcortical structures and various regions of cerebellar and cerebral cortex by stimulation of somatic receptors or electrical stimulation of peripheral nerves. This review summarizes current knowledge of SEPs generated in cerebral cortex by stimulation of the median nerve, the most common form of stimulation for human research and clinical investigations. Major sources of data for the review are intracranial recordings obtained from patients during diagnostic or neurosurgical procedures, and similar recordings in monkeys. Short-latency cortical SEPs in the 20-40 ms latency range consist of P20 and N30, recorded from motor cortex and frontal scalp; P25 and N35, recorded from cortex near the central sulcus and central scalp; and N20 and P30, recorded from somatosensory cortex and parietal scalp. Several lines of evidence including cortical surface and intracerebral recordings, neuromagnetic recordings and lesion studies in humans and monkeys, strongly support the conclusion that these potentials are generated in contralateral somatosensory cortex in areas 3b and 1, in contrast to the conclusion of many previous studies that SEPs recorded from the frontal scalp are generated in motor cortex and other frontal lobe areas. These potentials are primarily mediated by cutaneous afferents of the dorsal column-medial lemniscal system; the contribution of muscle afferents has not been completely resolved but appears to be small. There is currently no evidence that short-latency SEPs are generated in cortex other than primary somatosensory cortex. Recordings from the vicinity of the second somatosensory area, from the supplementary motor and sensory areas and from surface cortex other than sensorimotor cortex have not detected reliable short-latency activity, although some of these regions generate long-latency potentials. Consequently, short-latency SEPs recorded from the scalp are similar to those recorded from the surface of sensorimotor cortex. Old World monkeys such as Macaca mulatta and M. fascicularis provide an excellent model for human short-latency SEPs. All the potentials described above in humans have corresponding monkey analogues, with similar distributions over the cortical surface. The squirrel monkey, a New World species, exhibits the same potentials, but due to the different morphology of sensorimotor cortex, the surface distribution of SEPs is quite different.

Corticospinal projections to upper and lower limb spinal motoneurons in man

The pattern of muscle activation produced by magnetic stimulation over the human motor cortex has been examined in normal subjects. Magnetic stimulation elicited short latency compound muscle action potentials (CMAPs) from upper limb muscles contralateral to the stimulus and from lower limb muscles bilaterally. In the upper limb, the hand and forearm muscles had the lowest thresholds for activation and the largest CMAPs. There was little or no activation of the more proximal muscles, biceps and triceps. In the lower limb the extensor digitorum brevis and tibialis anterior had low thresholds and large CMAPs. There was little or no short latency activation of solcus. This pattern of muscle activation remained the same even when the stimulating coll was moved to various locations within a radius of 3 cm from the vertex. Recordings from individual tibialis anterior and soleus motor units indicated that the differential activation of these muscles reflected the relative amplitudes of the short latency postsynaptic potentials produced by magnetic stimulation in their motoneurons. The ‘jitter’ in the activation of single muscles fibers by magnetic stimulation suggests that these projections are monosynaptic. It is argued that the pattern of muscle activation reflects the projections from the cortex to motoneurons rather than the projections of afferents onto cortical neurons. We conclude that magnetic stimulation can be used to identify the projections of the corticospinal pathways in man.