Mean Onset Latency Research Articles

Activity of barosensitive neurons in the caudal ventrolateral medulla that send axonal projections to the rostral ventrolateral medulla in rabbits

In urethane-anesthetized rabbits, we successfully recorded unit activity of four neurons in the caudal ventrolateral medulla (CVLM) that were excited by orthodromic stimulation of the aortic nerve and by antidromic stimulation of the rostral ventrolateral medulla (RVLM). The sum of mean onset latency of excitation to stimulation of the aortic nerve (37.5 ms) and mean conduction time of antidromic spikes (10.5 ms) was close to the mean onset latency of inhibition of reticulospinal neurons in the RVLM to stimulation of the aortic nerve (47.1 ms) as previously reported by us. Three of 4 neurons received excitatory input from carotid sinus baroreceptors as well. Our results provide strong evidence for the hypothesis that neurons in the CVLM subserve the arterial baroreceptor-sympathetic vasomotor reflex.

Sympathetic skin response: normal results in different experimental conditions

1. (1) The sympathetic skin response (SSR) is a slow wave, generated in deep layers of the skin, resulting from reflex activation of the sudomotor sympathetic efferent fibres. The aim of this study was to define experimental conditions, best stimulation and recording procedures, and the criteria for validation of the responses. 2. (2) Thirty normal subjects (aged 25–56) were tested. The stimulation was an electrical pulse train applied to the median nerve at the wrist, a binaural tone burst, or both simultaneously. Records were made with surface electrodes on hand and foot contralateral to the stimulated median nerve. 3. (3) Response shape was most often biphasic in feet, biphasic or triphasic in hands. SSR amplitude was 3.1 ± 1.8 mV in hands, 1.4 ± 0.8 mV in feet. Normal mean onset latency was 1.5 ± 0.08 sec for hand response, 2.05 ± 0.10 sec for foot response. The mean conduction velovity along peripheral sympathetic nerve fibres was 1.40 ± 0.14 m/sec in lower limbs. 4. (4) Bimodal stimulation (burst + median) provided responses of larger amplitude. The influence of stimulation intensity was also investigated. A decrease in amplitude and lengthening of latencies were observed after 15–20 min of testing. 5. (5) The criteria for validation of responses are discussed. The importance of central processing time in the response delay is pointed out. In good methodological conditions, SSR would appear to be a simple, effective means of assessing sympathetic sudomotor outflow in central and peripheral nervous system disorders.

Postnatal development of the electrical activity of rat nigrostriatal dopaminergic neurons

Extra- and intracellular recordings were obtained in vivo from dopaminergic nigrostriatal neurons in rat pups ranging in age from postnatal day (PD) 1 to PD28, and in adult rats. Neurons from PD1— rats were active at very low rates in a random pattern, rarely showed bursting activity, and often exhibited long periods of up to several minutes of silence. Spontaneous spikes were of relatively low amplitude and long duration. The mean firing rate increased and became more regular over time, and short bursts consisting of only 2 spikes were observed. By the second postnatal week, the initial segment component of the spontaneous spike resembled that seen in adults, but the somadendritic component was still relatively small, and there was often a very marked temporal delay between the two. Near the end of the second postnatal week, neurons exhibited a transient phase of pacemaker-like activity. Mean firing rates continued to increase with time, as did the incidence and complexity of bursting activity. The spontaneous firing rate, pattern and spike morphology approached adult values by the fourth postnatal week. Antidromic responses from neostriatum were obtained as early as PD1, and consisted of a significantly greater proportion of full initial segment-soma dendritic spikes compared to nigrostriatal neurons from adult rats. There was usually a long delay between the initial segment and somadendritic components of the spike. Mean antidromic latency and mean antidromic threshold did not vary significantly from PD1 — to adults. Axonal conduction velocity reached maximal adult values by PD16— 21. Neostriatal-evoked orthodromic responses consisted principally of a poststimulus inhibition whose duration decreased from PD1 through adulthood. Pure excitatory responses were very rarely observed at any age. Intracellular recordings from PD2, PD3 and PD5 rats revealed striatal-evoked inhibitory postsynaptic potentials in non-dopaminergic nigral neurons with a mean onset latency (9.8 ± 3.8 ms) which did not differ from that previously reported for adult rats.

Noxious somatic stimuli excite neurosecretory vasopressin cells via A1 cell group

Activation of nociceptive somatic afferents excites hypothalamic neurosecretory cells and stimulates the release of vasopressin. To investigate the possibility that relevant afferent information is relayed through the A1 norepinephrine cell group of the caudal ventrolateral medulla, single-unit recording experiments were performed in pentobarbital sodium-anesthetized rats. The effects of somatic nerve stimulation, application of noxious somatic stimuli, and A1 region stimulation on the activity of putative vasopressin-secreting neurosecretory cells of the supraoptic nucleus were compared. The predominant effect of femoral and sciatic nerve stimulation on these cells was excitation, 54% (n tested = 113) displaying a marked increase in discharge probability, which had a mean onset latency of 72 +/- 3 ms and a mean duration of 114 +/- 9 ms. Almost all cells (96%) responding to somatic nerve stimulation were also excited by pinching of the ipsilateral or contralateral hindlimb paw, and the majority (84%) displayed a matching but shorter latency response to A1 region stimulation (mean onset 35 +/- 4 ms, duration 55 +/- 9 ms). A1 region injections of the inhibitory neurotransmitter gamma-aminobutyric acid reversibly blocked the effects of both somatic nerve stimulation (n = 14) and paw pinch (n = 9) on putative vasopressin cells. These results indicate that excitation of vasopressinergic neurosecretory cells by noxious somatic stimuli requires activation of neurons of the caudal ventrolateral medulla and hence are consistent with the proposal of a role for the A1 norepinephrine cell group.

Corticomotoneuronal postspike effects in averages of unrectified EMG activity.

1. Spike-triggered averaging (SpTA) of rectified electromyograms (EMGs) in awake monkeys is recognized as an effective means of establishing causal relations between cortical/cell discharge and muscle activity. The appearance of postspike facilitation (PSF) in averages of rectified EMG activity is interpreted as evidence of an underlying excitatory synaptic linkage between the trigger cell and motoneurons. Cells producing PSF are referred to as corticomotoneuronal (CM) cells. Similarly, postspike suppression (PSS) is interpreted as evidence of underlying inhibitory synaptic linkages. Studies to date have focused almost exclusively on averages of full-wave rectified EMG activity. Because the potential utility of SpTA of unrectified EMG activity has not been systematically examined, we compared postspike effects in SpTAs of rectified and unrectified EMGs for 44 cortical cells yielding 293 cell-target muscle pairs (CMPs). 2. Clear PSF was found in 110 of 293 averages of rectified EMG activity from 28 known CM cells. Forty-nine of these 110 CMPs (45%) also showed clear postspike effects (PSE) in the corresponding averages of unrectified EMGs activity. Loss of effects in averages of unrectified EMGs can be attributed to cancellation of the negative and positive phases of motor unit potentials. Mean onset latencies were similar for effects in rectified and unrectified EMGs [6.9 +/- 1.8 (SD) ms vs. 6.6 +/- 1.2 (SD) ms]. Overall, the magnitudes of effects measured as peak-to-noise ratios were also similar for effects in the two groups (8.8 vs. 8.7). The 61 CMPs that showed clear PSF in rectified EMGs but no effects in corresponding unrectified EMGs had, as a group, longer and more dispersed onset latencies and were weaker in magnitude than those that showed effects in both rectified and unrectified EMGs. Moreover, the occurrence of clear effects in averages of unrectified EMGs was correlated with the strength of PSF (75% of strong but only 29% of weak PSFs showed clear PSEs in averages of unrectified EMG activity). 3. Clear PSS was observed in 24 (8%) averages of rectified EMGs derived from nine cells. Remarkably, clear PSEs were found in 12 of the corresponding averages of unrectified EMG activity.(ABSTRACT TRUNCATED AT 400 WORDS)

A1 cell group mediates solitary nucleus excitation of supraoptic vasopressin cells.

Stimulation of the nucleus tractus solitarius (NTS) excites putative vasopressin-secreting cells of the supraoptic nucleus (SON) via a catecholaminergic projection to hypothalamus. Despite recent evidence of a direct catecholaminergic projection from NTS to SON, we have performed single-unit recording experiments in pentobarbital sodium-anesthetized rats to investigate the possibility that NTS stimulation effects on SON vasopressin cells are indirect, being relayed via the A1 noradrenergic cell group of the caudal ventrolateral medulla. The effects of single-pulse NTS and A1 region stimulation on the activity of antidromically identified SON neurosecretory cells that had been functionally characterized as vasopressin secreting were compared. NTS stimulation excited 81% of all putative vasopressin-secreting cells tested (n = 83), with a mean onset latency of 51 +/- 1 ms. A1 region stimulation excited 76% of all cells tested and 90% of units responsive to NTS stimulation, with a mean latency of 39 +/- 1 ms. Consistent with previous work NTS stimulation excited only a minority of oxytocin cells tested (3/13), and of these two-thirds also responded to A1 stimulation. Bilateral electrolytic lesions of the A1 region abolished the effects of NTS stimulation on putative vasopressin cells. Ipsilateral A1 region injections of the inhibitory neurotransmitter gamma-amino-butyric acid reversibly blocked NTS stimulation effects on putative vasopressin cells in animals where the contralateral A1 region had already been lesioned. These results support the proposal that excitation of SON vasopressin-secreting cells after NTS stimulation is due to activation of a relay projection through the A1 noradrenergic cell group of the caudal ventrolateral medulla.

Long-term potentiation and N-methyl-D-aspartate receptors in the visual cortex of young rats.

1. Long-term potentiation (LTP) of synaptic transmission following tetanic stimulation of the white matter was studied by recording extracellular field potentials and intracellular synaptic potentials from layer II/III of visual cortical slices from young rats ranging in age from 21 to 40 days. 2. Single shocks applied to the white matter at 0.1 Hz, used as test stimuli, elicited field potentials that consisted of primary and secondary components. The removal of Ca2+ ions from the perfusate allowed identification of the secondary component as originating postsynaptically and the primary one as reflecting a mixture of antidromic and postsynaptic potentials. 3. Tetanic stimulation at 5 Hz for 60 s was delivered to the white matter and field potentials were observed for 20 min to 9 h after the tetanus. LTP was defined as being present when the response displayed more than a 20% increase in amplitude of the Ca2+-sensitive components 20 min after the tetanus. LTP was induced in twelve of twenty-three slices tested, and this potentiation lasted throughout the period of observation. The average magnitude of potentiation was 147.8 +/- 28.4% of the control value for the twelve slices. 4. Administration of D,L-2-amino-5-phosphonovalerate (APV), an antagonist selective for N-methyl-D-aspartate (NMDA)-preferring receptors, slightly reduced the amplitudes of Ca2+-sensitive components of the field potentials. The average magnitude of reduction was 80.2 +/- 15.3% of the pre-drug control values. In the presence of APV, LTP was induced in only one slice of twelve tested. 5. Stable intracellular recordings were obtained from twenty-three cells from layer II/III. Excitatory postsynaptic potentials (EPSPs) evoked by white matter stimulation had mean onset and peak latencies of 4.1 and 11.3 ms, respectively. In some cells these fast EPSPs were followed by another slow EPSP with a much longer latency and higher amplitude. Administration of APV revealed further that the fast EPSPs consisted of two components, i.e. early and late components. 6. Tetanization of the white matter induced long-lasting enhancement of EPSPs in eight of twelve cells tested. In five of these eight cells, fast EPSPs were enhanced in amplitude and in the remaining three cells, slow EPSPs appeared de novo after the tetanus. 7. APV reduced the amplitudes of the fast EPSPs and abolished the slow EPSPs if present. The average magnitude of reduction for the fast EPSPs was 65.6 +/- 15.1% and this reduction was due mainly to an elimination of the late component.(ABSTRACT TRUNCATED AT 400 WORDS)

Timing and distribution of flash-evoked activity in the lateral geniculate nucleus of the alert monkey

Simultaneous recording of activity from multiple cortical laminae in alert monkeys, using multichannel electrodes, has been used to identify the intracranial generators of surface-recorded, visually evoked potentials (VEP) to stroboscopic flash. Beyond their clinical implications, these results offer an unique view of the timing and sequence of cortical visual processing in the alert monkey, including the somewhat surprising findings of an extremely short-latency response in lamina IVA, a contra- over ipsilateral latency advantage throughout lamina IV, and the lack of a consistent flash-evoked response in the major cortical recipient of the magnocellular system, lamina IVCa. The present study used similar techniques to examine flash-evoked activity in LGN and in optic tract, both to elucidate the role of the subcortical pathways in establishing this pattern, and to provide a parallel, detailed view of the timing of visual activity in LGN and optic tract in the alert monkey. Flash-evoked responses are robust in both parvo- and magnocellular laminae, but these responses differ along several dimensions: (1) parvocellular multiunit activity (MUA) is 1 4 to 1 2 the amplitude of magnocellular MUA; (2) oscillatory activity is higher in frequency and shorter in duration in parvo- than in magnocellular responses; (3) inhibitory processes appear less prominent and diverse in parvo- than in magnocellular activity; (4) mean onset latencies of MUA are longer in parvo- than in magnocellular laminae, but there is extensive overlap in these distributions. Latencies encountered in ipsilateral lamina 3, and at laminar borders dorsal to 3, group more clearly with those of the magnocellular laminae than with those of the other parvocellular laminae. As a result, in the parvocellular division as a whole, the average latency to ipsilateral stimulation is shorter than that to contralateral stimulation. The optic tract exhibits a dorsal-to-ventral progression of onset latency and oscillation frequency consistent with a dorsal/ventral segragation of the inputs to parvo- and magnocellular layers. Comparison of optic tract and LGN data reveals that while many LGN response characteristics are initiated in the retina, significant modification of retinal output occurs at LGN. The techniques used here permit a particularly sensitive and reliable assessment of the timing and distribution of visual responses in the optic tract and LGN of alert monkeys. Our data support the view that in the alert monkey, the surface-VEP to passive, binocular flash primarily reflects activation of parvocellular thalamorecipient laminae of Area 17. Short-latency responses, in parvocellular lamina 3, and at laminar borders in the parvocellular division, may promote the early activation of striate lamina IVA. This in turn, may be important in shaping the laminar profile of activation in Area 17 as a whole. However, both the reported failure of binocular flash to activate magnocellular terminal zones, and the contra-/ipsilateral latency advantage appear to stem from processes operating at the cortical level.

Rapid and transient excitation of respiration mediated by central chemoreceptor.

We evaluated rapid and transient changes in phrenic nerve (PN) and internal intercostal (IIC) activities when 0.2-0.5 ml of saline saturated with 100% CO2 was injected into the vertebral artery during various respiratory phases in decerebrated spontaneously breathing cats. The injections evoked an initial transient inhibition of ongoing PN or IIC activity with a mean onset latency of 0.17 s, followed by excitation of subsequent respiratory activities with an onset latency ranging from 0.4 to 2.7 s; the average onset latency of expiratory excitation (1.49 s) was significantly longer than that of inspiratory facilitation (0.89 s). The initial inhibitory responses were analogous to reflex effects of injections of phenyl biguanide, indicating that the initial inhibition was due to activation of vascular nociceptors and the subsequent excitation was due to stimulation of the central chemoreceptors. In addition, CO2-saline injections during hypocapnic apnea developed a quick reappearance of respiratory rhythm, and the first facilitatory effect appeared in tonic IIC activity, which became more active before rhythm started. In summary, the present study, by use of a technique of vertebral arterial injections of 100% CO2-saline, revealed dynamic properties of respiratory control system mediated by central chemoreceptors and vascular nociceptors.

Neuronal pathways for the lingual reflex in the Japanese toad.

1. Anuran tongue is controlled by visual stimuli for releasing the prey-catching behavior ('snapping') and also by the intra-oral stimuli for eliciting the lingual reflex. To elucidate the neural mechanisms controlling tongue movements, we analyzed the neuronal pathways from the glossopharyngeal (IX) afferents to the hypoglossal (XII) tongue-muscle motoneurons. 2. Field potentials were recorded from the bulbar dorsal surface over the fasciculus solitarius (fsol) to the electrical stimulation of the ipsilateral IX nerve. They were composed of three successive negative waves: S1, S2 and N wave. The S1 and S2 waves followed successive stimuli applied at short intervals (10 ms or less), whereas the N wave was strongly suppressed at intervals shorter than 500 ms. Furthermore, the S1 wave had lower threshold than the S2 wave. 3. Orthodromic action potentials were intra-axonally recorded from IX afferent fibers in the fsol to the ipsilateral IX nerve stimuli. Two peaks found in the latency distribution histogram of these action potentials well coincided with the negative peaks of the S1 and the S2 waves of the simultaneously recorded field potentials. Therefore, the S1 and S2 waves should represent the compound action potentials of two groups of the IX afferent fibers with different conduction velocities. 4. Ipsilateral IX nerve stimuli elicited excitatory postsynaptic potentials (EPSPs) in the tongue-protractor motoneurons (PMNs) and the tongue-retractor motoneurons (RMNs). Inhibitory postsynaptic potentials were not observed. 5. The EPSPs recorded in PMNs had mean onset latencies of 6.4 ms measured from the negative peaks of the S1 wave. The EPSPs were facilitated when paired submaximal stimuli were applied at intervals shorter than 20 ms, but were suppressed at intervals longer than 30 ms. Furthermore, the EPSPs were spatially facilitated when peripherally split two bundles of the IX nerve were simultaneously stimulated. 6. On the other hand, the EPSPs recorded in RMNs had shorter onset latencies, averaging 2.5 ms. In 14 of 43 RMNs, early and late EPSP components could be reliably discriminated. The thresholds for the early EPSP components were as low as those for the S1 waves, whereas for the late EPSP components the thresholds were usually higher than those for the S2 waves.(ABSTRACT TRUNCATED AT 400 WORDS)

Normal latency values of early cortical somatosensory evoked potentials in children

Somatosensory evoked potentials (SEPs) after median and posterior tibial nerve stimulation were studied in 172 children ranging in age from 1 day to 16 years for the purpose of obtaining normal reference values, for use in analysing pathological cases. The mean onset and peak latencies of the N wave after median nerve stimulation and of the P wave after posterior tibial nerve stimulation were calculated for 12 age groups. N and P latencies decreased from birth to 3 years of age, when they reached their minimal values. The latencies then increased with age, the increased being greater for posterior tibial nerve SEPs than for median nerve SEPs. By contrast the ascending time (the interval between onset and peak latencies) decreased) progressively with age from to adolescence.

Saccade-related and visual activities in the pulvinar nuclei of the behaving rhesus monkey.

We studied three subdivisions of the pulvinar: a retinotopically organized inferior area (PI), a retinotopically mapped region of the lateral pulvinar (PL), and a separate, visually responsive component of the lateral pulvinar (Pdm). Single neurons were recorded in these regions from awake, trained rhesus monkeys, and we correlated the discharge patterns of the cells with eye movements. About 60% of the neurons discharged after saccadic eye movements in an illuminated environment and had either excitatory, inhibitory, or biphasic (inhibitory-excitatory) response patterns. These responses were most often transient in nature. Neurons with excitatory activity had a mean onset latency of 72 ms after the termination of the eye movement. Latencies for cells with inhibitory responses averaged 58 ms. In sharp contrast, the cells with biphasic response patterns became active before the termination of the eye movement. A unique set of these neurons termed saccade cells, were active with visually guided eye movements in the light, with the same eye movements made to a briefly pulsed target in the dark, and for similar eye movements made spontaneously in total darkness. The activity was present with the appropriate saccade, independent of the beginning eye position. Biphasic response patterns were typical of these saccade cells. Saccade cells were most common in Pdm and PI. About half of the saccade cells also had some visual response that was independent of eye movement. A second group of cells was active with saccadic eye movements in the light but not in the dark. Some of these cells had clear visual responses that could account for their activity following eye movements; others had no clear visual receptive field.(ABSTRACT TRUNCATED AT 250 WORDS)

Visual response latency of X- and Y-cells in the dorsal lateral geniculate nucleus of the cat

Visual response latencies and rise times of X- and Y-cells in the dorsal lateral geniculate nucleus (dLGN) of anaesthetized, paralyzed cats were measured during repeated stimulation with sinusoidal grating patterns. Measurements were restricted to individual stimulus trials on which the instantaneous discharge rate exceeded a criterion amplitude defined in terms of the baseline activity of each cell. The latencies of response onsets and response peaks were systematically related to the spatial frequency and contrast of the grating stimuli. Response latencies of Y-cells were shortest for gratings of low spatial frequency (0.17 c/deg) and increased monotonically with increases in spatial frequency. Response latencies of X-cells were shortest for gratings of intermediate spatial frequency (0.75 c/deg) and longer for lower and higher spatial frequencies. Latencies decreased monotonically with increases in stimulus contrast from 5 to 40% for both X- and Y-cells. In general, short-latency responses were less variable than long-latency responses. This was true for absolute as well as relative measures of variability. The mean onset and peak latencies of Y-cell responses were 10–15 msec shorter than the corresponding latencies of X-cell responses to stimuli of optimal spatial frequency and contrast. The rise times (latency of response peak minus latency of response onset) of Y-cell responses were consistently shorter than those of X-cells in spite of the higher peak responses of Y-cells. The results of this study are consistent with the idea that low spatial frequency information is passed through the lateral geniculate nucleus more quickly than is high spatial frequency information. These data provide support for models of visual processing wherein a coarse, global analysis of the visual scene by Y-cells precedes a finer, local analysis by X-cells.

Supratrigeminal neurons mediate the shortest, disynaptic pathway from the central amygdaloid nucleus to the contralateral trigeminal motoneurons in the rat

1. 1. Stimulation of the supratrigeminal area (STA) of the rat induced a monosynaptic EPSP in most mylohyoid-digastric motoneurons and a monosynaptic IPSP or EPSP in the majority of masseteric ones, contralaterally. 2. 2. Stimulation of the central amygdaloid nucleus induced the ipsilateral STA activity immediately followed by the contralateral mylohyoid nerve activities. 3. 3. The same amygdaloid stimulation excited 19 of 46 STA neurons, which were antidromically identified to project to the contralateral trigeminal motor nucleus. Nine of these were monosynaptically excited. 4. 4. The mean of the antidromic and monosynaptic latencies of these neurons explains the mean onset latencies of the amygdaloid influences on the contralateral trigeminal motoneurons. 5. 5. Therefore, the shortest crossing amygdalo-motoneuronal pathway is probably disynaptic and mediated by commissural STA neurons.

Afferent renal nerve stimulation excites supraoptic vasopressin neurons

Single-unit recording experiments were performed in pentobarbital-anesthetized rats to investigate the effects of afferent renal nerve (ARN) stimulation on the activity of neurosecretory vasopressin cells of the supraoptic nucleus (SON). Neurosecretory SON cells were identified by antidromic invasion from the neurohypophysis and classified either as vasopressin (AVP) or oxytocin (OXY) secreting on the basis of their spontaneous activity patterns and response to activation of arterial baroreceptors. Fifty-three spontaneously active units were identified bilaterally in the SON: 40 putative AVP and 13 putative OXY neurons. Most putative AVP neurons (14/14 contralateral, 18/26 ipsilateral) were excited by ARN stimulation (mean onset latency 189 +/- 5 ms, mean response duration 237 +/- 17 ms). In contrast, ARN stimulation had no effect on the firing frequency of the 13 putative OXY neurons. These data indicate that sensory information originating in the kidney selectively alters the activity of SON AVP neurons and suggest that afferent information from the kidney is important in the coordination of neural and hormonal activity concerned with body fluid balance and the regulation of arterial pressure.

Patterns of facilitation and suppression of antagonist forelimb muscles from motor cortex sites in the awake monkey.

Patterns of excitatory and inhibitory effects were produced in antagonistic forelimb muscles by single intracortical microstimuli (S-ICMS) applied to motor cortex sites in macaque monkeys performing ramp-and-hold wrist movements. Stimulus-triggered averages (stimulus-TAs) of rectified electromyographic (EMG) activity revealed poststimulus facilitation and/or suppression in identified flexor and extensor muscles of the wrist and fingers. At 22 cortical sites the action potentials of single cells were also recorded and used to compute spike-triggered averages (spike-TAs) of covarying muscles. The set of muscles activated during the movement in which the cell was active are referred to here as "agonists"; those muscles active during wrist movement in the opposite direction are called "antagonists." (At sites where cells were not isolated the muscles showing poststimulus facilitation were called agonists.) Poststimulus effects in agonist muscles typically consisted of facilitation in a subset of the agonists. For 48 sites from which poststimulus effects were tested on both flexors and extensors, the following combinations of effects were observed: 1) pure facilitation of agonist muscles with no effect on antagonists; 2) facilitation of both agonists and antagonists; 3) facilitation of agonist muscles with reciprocal suppression of antagonists; 4) "mixed" facilitation and suppression of synergist muscles; and 5) pure suppression of some muscles with no effect on their antagonists. The suppression effects appeared most commonly in flexor muscles; conversely, facilitation was generally stronger in extensors. Cortical sites eliciting pure suppression of flexor muscles with no facilitation of extensor muscles were found in two monkeys. These purely suppressive effects were observed not only in stimulus-TAs but also in spike-TAs computed from single cells at these sites. Some of these cells increased their activity during wrist extension (but had no detectable effect on the extensor muscles); others discharged during flexion. Several observations suggest that the cortically evoked suppression is mediated by polysynaptic relays. The mean onset latency of the postspike suppression (7.4 ms) produced by inhibitory cells was longer than the mean onset latency of postspike facilitation (6.7 ms) produced by CM cells. Similarly, the mean onset latency of poststimulus suppression (8.9 ms) was longer than that of poststimulus facilitation (8.0 ms). Moreover, suppression was usually weaker than facilitation in the spike-TAs, as well as in stimulus-TAs compiled for the same stimulus intensity.(ABSTRACT TRUNCATED AT 400 WORDS)

Excitatory input from sensory motor cortex to neostriatum and its modification by conditioning stimulation of the substantia nigra

Extracellular single unit responses were recorded from 381 neurons in the neostriatum of urethane-anesthetized rats. Single pulse stimulation of the sensory motor cortex produced strong excitatory responses in neostriatal neurons with a mean onset latency of 7.9 ms. A train of 10 pulses (0.15 ms, 300–600 μA) at 10 Hz delivered to the substantia nigra 100 ms before cortical stimulation attenuated the original excitatory response of 22 of 53 striatal neurons tested and enhanced the excitatory response of 12 of these neurons. These attenuating and enhancing effects were reduced or abolished by the systemic administration of haloperidol, a dopamine antagonist. Single pulse nigral stimulation 100 ms before the cortical stimulation had little or no effect on the excitatory response of neostriatal neurons. The iontophoretic application of dopamine also had attenuation and enhancement effects on the excitatory response of striatal neurons to cortical stimulation. The results suggest that the attenuation and enhancement of the excitatory responses of striatal neurons to cortical stimulation which resulted from nigral conditioning stimulation is mediated by nigrostriatal dopaminergic neurons.

Functional relations between the cortical gustatory area and the amygdala: Electrophysiological and behavioral studies in rats

The functional interconnections between the cortical gustatory area (CGA) and the amygdala were examined by electrophysiological and behavioral experiments in rats. The cortical neurons responsive to taste stimuli applied to the anterior part of the tongue were located in the Vth layer of the agranular insular cortex. Of a total of 27 cortical neurons recorded, 10 showed facilitatory and/or inhibitory responses with the mean onset latency of about 20 msec to electrical stimulation of the ipsilateral amygdala. On the other hand, of 18 amygdaloid neurons responsive to taste stimuli, 13 showed facilitatory and/or inhibitory responses to electrical shocks to the ipsilateral CGA, with a mean latency of about 16 ms. No cortical and amygdaloid neurons sampled responded antidromically to the electrical stimulation. These results suggest the existence of mutual polysynaptic fiber connections between the CGA and the amygdala. The behavioral experiment was performed by means of a conditioned taste aversion (CTA) technique. After acquisition of CTA to sucrose solution by pairing it with an i.p. injection of LiCl which produces sickness, bilateral small knife cuts between the CGA and the amygdala in the perirhinal region disrupted retention of CTA. Thus, these interconnections may play some role in association of taste-related cognitive processes with feeding behavior.

A new indirect method for measuring spinal conduction velocity in man

A non-invasive, indirect method for measuring spinal cord mixed afferent-efferent conduction is described. The method is based upon eliciting late reflex responses labelled R1 and R2 from voluntarily contracting thenar and tibialis anterior muscles by preferentially stimulating median and common peroneal sensory nerve fibers. The mean onset latencies of R1 measured 27.5 msec and 30.6 msec recorded from hand and leg muscles respectively. R2 mean onset latencies measured 46.0 msec and 65.1 msec respectively. R1 has characteristics similar to an H-reflex. R2 is a long-loop reflex of unknown pathway assumed to involve similar circuits and rostral turn around points when elicited by both arm and leg stimulation. Mean spinal cord conduction time between the seventh cervical and fifth lumbar spinous processes, is given by (R2 leg − R1 leg) 2 − (R2 arm − R1 arm) 2 It measured 7.95 msec and the calculated mean conduction velocity was 57.9 ± 5.7 m/sec.

Corticomotoneuronal cells contribute to long-latency stretch reflexes in the rhesus monkey.

To test the hypothesis that a transcortical reflex contributes to the stretch-evoked long-latency electromyographic (e.m.g.) response we documented the responses of identified corticomotoneuronal (c.m.) cells and their target muscles to perturbations of active wrist movements. Macaque monkeys performed ramp-and-hold wrist movements against elastic loads, alternating between flexion and extension zones; brief (25 ms) torque pulses were intermittently applied during the hold period. C.m. cells were identified by a clear post-spike facilitation in spike-triggered averages of forelimb muscle e.m.g. activity. Activity of c.m. cells and twelve wrist and digit flexor and extensor muscles was recorded during: (a) active ramp-and-hold wrist movements, (b) passive ramp-and-hold wrist movements, and (c) torque perturbations applied during the hold phase of active flexion and extension which either lengthened or shortened the c.m. cell's target muscles. Muscle-lengthening perturbations evoked a reproducible pattern of average e.m.g. activity in the stretched muscles, consisting of two peaks: the first response (M1) had an onset latency of 11.2 +/- 2.1 ms (mean +/- S.D.), and the second (M2) began at 27.9 +/- 5.1 ms. Torque perturbations which shortened the active muscles also evoked a characteristic e.m.g. response consisting of an initial cessation of activity at 13.5 +/- 3.4 ms followed by a peak beginning at 33.9 +/- 3.0 ms. The responses of twenty-one c.m. cells which facilitated wrist muscles were documented with torque pulse perturbations applied during active muscle contraction. Twenty of twenty-one c.m. cells responded at short latency (23.4 +/- 8.8 ms) to torque perturbations which stretched their target muscles. For each c.m. cell-target muscle pair, transcortical loop time was calculated as the sum of the onset latency of the c.m. cell's response to lengthening perturbations (afferent time) and the onset latency of post-spike facilitation (efferent time). The mean transcortical loop time was 30.4 +/- 10.2 ms, comparable to the mean onset latency of the M2 peak (27.9 +/- 5.1). The duration of a c.m. cell's response to torque perturbations provides a further measure of the extent of its potential contribution to the M2 muscle response. In all cases but two, the c.m. cell response, delayed by the latency of the post-spike facilitation, overlapped the M2 e.m.g. peak.