scholarly journals Saccade-Related Inhibitory Input to Pontine Omnipause Neurons: An Intracellular Study in Alert Cats

1999 ◽  
Vol 82 (3) ◽  
pp. 1198-1208 ◽  
Author(s):  
Kaoru Yoshida ◽  
Yoshiki Iwamoto ◽  
Sohei Chimoto ◽  
Hiroshi Shimazu

Omnipause neurons (OPNs) are midline pontine neurons that are thought to control a number of oculomotor behaviors, especially saccades. Intracellular recordings were made from OPNs in alert cats to elucidate saccade-associated postsynaptic events in OPNs and thereby determine what patterns of afferent discharge impinge on OPNs to cause their saccadic inhibition. The membrane potential of impaled OPNs exhibited steep hyperpolarization before each saccade that lasted for the whole period of the saccade. The hyperpolarization was reversed to depolarization by intracellular injection of Cl− ions, indicating it consisted of temporal summation of inhibitory postsynaptic potentials (IPSPs). The duration of the saccade-related hyperpolarization was almost equal to the duration of the concurrent saccades. The time course of the hyperpolarization was similar to that of the radial eye velocity except for the initial phase. During the falling phase of eye velocity, the correlation between the instantaneous amplitude of hyperpolarization and the instantaneous eye velocity was highly significant. The amplitude of hyperpolarization at the eye velocity peak was correlated significantly with the peak eye velocity. The time integral of the hyperpolarization was correlated with the radial amplitude of saccades. The initial phase disparity between the hyperpolarization and eye velocity was due to the relative constancy of peak time (∼20 ms) of the initial steep hyperpolarization regardless of the later potential profile that covaried with the eye velocity. The initial steep hyperpolarization led the beginning of saccades by 15.9 ± 3.8 (SD) ms, which is longer than the lead time for medium-lead burst neurons. These results demonstrate that the pause of activity in OPNs is caused by IPSPs initiated by an abrupt, intense input and maintained, for the whole duration of the saccade, by afferents conveying eye velocity signals. We suggest that the initial sudden inhibition originates from central structures such as the superior colliculus and frontal eye fields and that the eye velocity-related inhibition originates from the burst generator in the brain stem.

1989 ◽  
Vol 32 (3) ◽  
pp. 681-687 ◽  
Author(s):  
C. Formby ◽  
B. Albritton ◽  
I. M. Rivera

We describe preliminary attempts to fit a mathematical function to the slow-component eye velocity (SCV) over the time course of caloric-induced nystagmus. Initially, we consider a Weibull equation with three parameters. These parameters are estimated by a least-squares procedure to fit digitized SCV data. We present examples of SCV data and fitted curves to show how adjustments in the parameters of the model affect the fitted curve. The best fitting parameters are presented for curves fit to 120 warm caloric responses. The fitting parameters and the efficacy of the fitted curves are compared before and after the SCV data were smoothed to reduce response variability. We also consider a more flexible four-parameter Weibull equation that, for 98% of the smoothed caloric responses, yields fits that describe the data more precisely than a line through the mean. Finally, we consider advantages and problems in fitting the Weibull function to caloric data.


1995 ◽  
Vol 74 (3) ◽  
pp. 1367-1372 ◽  
Author(s):  
G. Cheron ◽  
S. Saussez ◽  
N. Gerrits ◽  
E. Godaux

1. Properties of nucleus incertus (NIC) neurons projecting to the cerebellar flocculus were studied in alert cats by using chronic unit and eye movement recording and antidromic activation. Projection of these neurons onto the flocculus was verified with retrograde transport of horseradish peroxidase after injections in the flocculus. 2. Bipolar stimulation electrodes were implanted into the "middle" zone of each flocculus because this zone is known to be involved in the control of horizontal eye movements. The dorsomedial aspect of the pontine tegmentum was explored with microelectrodes during stimulation of both flocculi. The majority of neurons antidromically activated from the flocculus were found in the caudal part of the NIC. 3. Of the 69 neurons activated from the flocculus, 44 were classified as burst-tonic (BT) neurons; 34 discharged in relation with horizontal movements of the eye, 10 in relation with vertical movements. Of the 14 remaining neurons, 6 were not related to eye movements and 8 were classified as burst neurons. The BT neurons of the NIC displayed a great sensitivity to both horizontal eye position and horizontal eye velocity. 4. This study demonstrates the presence of a new group of horizontal eye movement related BT neurons situated in the NIC. The fact that they project to the horizontal floccular zone emphasizes the importance of the functional specialization of the different Purkinje cell zones.


2001 ◽  
Vol 281 (3) ◽  
pp. H1093-H1103 ◽  
Author(s):  
Damiano Baldassarre ◽  
Mauro Amato ◽  
Carlo Palombo ◽  
Carmela Morizzo ◽  
Linda Pustina ◽  
...  

Ultrasonic studies have shown that arterial compliance increases after prolonged ischemia. The objective of the present study was to develop an alternative plethysmographic method to investigate compliance, exploring validity and clinical applicability. Forearm pulse volume (FPV) and blood pressure (BP) were used to establish the FPV-BP relationship. Forearm arterial compliance (FAC) was measured, and the area under the FAC-BP curve (FACAUC) was determined. The time course curve of compliance changes during reactive hyperemia was obtained by continuous measurements of FACAUCfor 20 s before and for 300 s after arterial occlusion. This technique allows us to effectively assess compliance changes during reactive hyperemia. Furthermore, the selected measurement protocol indicated the necessity for continuous measurements to detect “true” maximal FACAUCchanges. On multivariate analysis, preischemic FACAUCwas mainly affected by sex, peak FACAUCwas affected by sex and systolic BP, percent changes were affected by plasma high-density and low-density lipoprotein cholesterol, peak time was affected by age and body mass index, and descent time was affected by plasma triglyceride levels. The proposed technique is highly sensitive and well comparable with the generally accepted echotracking system. It may thus be considered as an alternative tool to detect and monitor compliance changes induced by arterial occlusion.


2003 ◽  
Vol 90 (4) ◽  
pp. 2163-2170 ◽  
Author(s):  
Frank Richter ◽  
Sven Rupprecht ◽  
Alfred Lehmenkühler ◽  
Hans-Georg Schaible

Spreading depression (SD), a neuronal mechanism involved in brain pathophysiology, occurs in brain areas with high neuronal density such as the cerebral cortex. By contrast, the brain stem is thought to be resistant to SD. Here we show that DC shifts resembling cortical SD can be elicited in rat brain stem by topical application of KCl but not by pricking the brain stem. However, this was only possible until postnatal day 13, and, in addition, susceptibility for SD had to be enhanced. The latter was achieved by superfusion of the brain stem for 45 min with a solution containing acetate instead of chloride ions. Transient asphyxia or hypoxia by 2 min breathing 6% O2 in N2 had a similar effect. Negative brain stem DC deflections were paralleled by an increase of extracellular potassium concentration ≤40 mM and were spreading, but unlike cortical SD they were not inducible by glutamate and N-methyl-d-aspartate (NMDA). Time course and slope of brain stem SD either resembled cortical SD or were long-lasting and sustained. The latter stopped normal breathing. Different from cortical SD, negative brain stem DC deflections were changed in their slope (mostly converted into sustained shape, peak time was significantly prolonged, decline-time and duration were prolonged), but not abolished by the NMDA receptor blocker MK-801. Thus we demonstrate that the immature brain stem has the capacity to generate negative DC shifts, which could be relevant as a risk factor in newborn brain stem function.


1995 ◽  
Vol 268 (2) ◽  
pp. G355-G360 ◽  
Author(s):  
D. Grundy ◽  
V. Bagaev ◽  
K. Hillsley

The aim of the present study was to investigate electrophysiologically the effect of systemic cholecystokinin (CCK) on the discharge of vagal gastric mechanoreceptors. Twenty-two single vagal afferent fibers were selected for the investigation of responses to intravenous CCK octapeptide (CCK-8) on the basis of a positive response to gastric distension. Resting discharge in these afferent fibers was 1.3 +/- 0.3 impulses.s-1 and increased to 9.2 +/- 0.9 impulses.s-1 during distension (P < 0.0001), CCK (20-100 pmol iv) caused a gastric relaxation of 2.1 +/- 0.2 cmH2O and inhibition of phasic motility. The discharge of 20/22 of vagal tension receptors closely followed the magnitude and time course of the fall in pressure. Mean discharge before and after CCK (50 pmol) was 7 +/- 0.9 and 3.9 +/- 0.8 impulses.s-1, respectively (P < 0.001, n = 22). Both the pressure response and the concomitant changes in afferent discharge were abolished by L-364,718 (1.2 mg/kg iv). Only two afferent units failed to show a decrease in firing following CCK (50 pmol), and at 500 pmol the discharge of these units was augmented. In conclusion, CCK (50 pmol) has predominantly indirect effects on gastric mechanoreceptors, which decrease their firing in association with gastric relaxation.


2006 ◽  
Vol 96 (3) ◽  
pp. 1370-1382 ◽  
Author(s):  
James C. Beck ◽  
Paul Rothnie ◽  
Hans Straka ◽  
Susan L. Wearne ◽  
Robert Baker

Elucidating the causal role of head and eye movement signaling during cerebellar-dependent oculomotor behavior and plasticity is contingent on knowledge of precerebellar structure and function. To address this question, single-unit extracellular recordings were made from hindbrain Area II neurons that provide a major mossy fiber projection to the goldfish vestibulolateral cerebellum. During spontaneous behavior, Area II neurons exhibited minimal eye position and saccadic sensitivity. Sinusoidal visual and vestibular stimulation over a broad frequency range (0.1–4.0 Hz) demonstrated that firing rate mirrored the amplitude and phase of eye or head velocity, respectively. Table frequencies >1.0 Hz resulted in decreased firing rate relative to eye velocity gain, while phase was unchanged. During visual steps, neuronal discharge paralleled eye velocity latency (∼90 ms) and matched both the build-up and the time course of the decay (∼19 s) in eye velocity storage. Latency of neuronal discharge to table steps (40 ms) was significantly longer than for eye movement (17 ms), but firing rate rose faster than eye velocity to steady-state levels. The velocity sensitivity of Area II neurons was shown to equal (±10%) the sum of eye- and head-velocity firing rates as has been observed in cerebellar Purkinje cells. These results demonstrate that Area II neuronal firing closely emulates oculomotor performance. Conjoint signaling of head and eye velocity together with the termination pattern of each Area II neuron in the vestibulolateral lobe presents a unique eye-velocity brain stem-cerebellar pathway, eliminating the conceptual requirement of motor error signaling.


1979 ◽  
Vol 73 (3) ◽  
pp. 265-286 ◽  
Author(s):  
D F Wunk ◽  
F S Werblin

The postsynaptic potentials (PSPs) that form the ganglion cell light response were isolated by polarizing the cell membrane with extrinsic currents while stimulating at either the center or surround of the cell's receptive field. The time-course and receptive field properties of the PSPs were correlated with those of the bipolar and amacrine cells. The tiger salamander retina contains four main types of ganglion cell: "on" center, "off" center, "on-off", and a "hybrid" cell that responds transiently to center, but sustainedly, to surround illumination. The results lead to these inferences. The on-ganglion cell receives excitatory synpatic input from the on bipolars and that synapse is "silent" in the dark. The off-ganglion cell receives excitatory synaptic input from the off bipolars with this synapse tonically active in the dark. The on-off and hybrid ganglion cells receive a transient excitatory input with narrow receptive field, not simply correlated with the activity of any presynaptic cell. All cell types receive a broad field transient inhibitory input, which apparently originates in the transient amacrine cells. Thus, most, but not all, ganglion cell responses can be explained in terms of synaptic inputs from bipolar and amacrine cells, integrated at the ganglion cell membrane.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Bernardo Neme Ide ◽  
Lázaro Alessandro Soares Nunes ◽  
René Brenzikofer ◽  
Denise Vaz Macedo

The purpose of this study was to observe the time course of muscle damage and inflammatory responses following an eccentric overload resistance-training (EO) program. 3 females (23.8 ± 2.6 years; 70.9 ± 12.7 kg; 1.6 ± 0.08 m) and 5 males (23.8 ± 2.6 years; 75.1 ± 11.2 kg; 1.8 ± 0.1 m) underwent thirteen training sessions (4 × 8–10 eccentric-only repetitions—80% of eccentric 1RM, one-minute rest, 2x week−1, during 7 weeks, for three exercises). Blood samples were collected prior to (Pre) and after two (P2), seven (P7), nine (P9), eleven (P11), and thirteen (P13) sessions, always 96 hours after last session. The reference change values (RCV) analysis was employed for comparing the responses, and the percentual differences between the serial results were calculated for each subject and compared with RCV95%. Four subjects presented significant changes for creatine kinase at P2, and another two at P13; six for C-reactive protein at P2, and three at P11; two for neutrophils at P2, P4, and P13, respectively; and only one for white blood cells at P2, P4, P7, and P9, for lymphocyte at P7, P9, and P13, and for platelet at P4. We conclude that EO induced high magnitude of muscle damage and inflammatory responses in the initial phase of the program with subsequent attenuation.


1991 ◽  
Vol 81 (1) ◽  
pp. 51-58 ◽  
Author(s):  
J. H. A. Dambrink ◽  
B. P. M. Imholz ◽  
J. M. Karemaker ◽  
W. Wieling

1. The magnitude and time course of circulatory adaptation to active standing were investigated in healthy premenarchic girls and boys (n = 24; 10–14 years old) by non-invasive measurement of heart rate and continuous finger blood pressure (Finapres). 2. Four subjects (two girls, two boys) showed presyncopal symptoms after 4–9 min of free standing. 3. In the 20 non-fainting subjects, changes in blood pressure and heart rate upon standing did not differ between girls (n = 10) and boys (n = 10). In the initial phase of standing (first 30 s) systolic and diastolic blood pressures dropped by 22 ± 14 (mean ± sd) and 16 ± 7 mmHg, respectively, at 8 ± 2 s. Blood pressure subsequently recovered and showed an overshoot in all subjects. The transient drop in blood pressure was accompanied by an increase in heart rate of 40 ± 7 beats/min. These characteristic transient changes were not observed with passive head-up tilt. During the early steady-state phase (2 min), systolic blood pressure was similar to the supine value and diastolic blood pressure rose by 11 ± 5 mmHg. Heart rate increased by 25 ± 11 beats/min. In six of the subjects (three girls, three boys) the increase in heart rate exceeded 30 beats/min (postural tachycardia). Little further changes were observed during prolonged (10 min) standing. 4. Typical findings in the four near-fainting subjects were higher supine heart rates, no blood pressure overshoot in the initial phase (in three out of four subjects), postural tachycardia in the early steady-state phase and progressive decreases in blood pressure and heart rate afterwards. 5. In conclusion, for investigation of orthostatic circulatory adaptation in childhood it is important to pay attention to the dynamics of the circulatory response. No important differences appear to exist in orthostatic circulatory control between premenarchic girls and boys: orthostatic tachycardia and fainting appear to be common in both.


1993 ◽  
Vol 70 (04) ◽  
pp. 617-624 ◽  
Author(s):  
H C Hemker ◽  
S Wielders ◽  
H Kessels ◽  
S Béguin

SummaryA method is described by which the time-course of thrombin generation in plasma can be obtained from a continuous optical density recording of p-nitroaniline (pNA) production in a 2:3 diluted plasma. A chromogenic substrate, methylmalonyl-methylanalyl-arginyl-pNA (SQ68), is used that is specifically split by thrombin but at a low rate. The thrombin that appears and disappears in the plasma does not split more than 5% of the substrate added, so the rate of substrate conversion is in good approximation proportional to the amidolytic activity in the plasma over the entire period of thrombin generation. The course of the enzyme concentration can be calculated from the amidolytic activity curve. It is shown that the thrombin generation curves obtained in this way are essentially identical to those obtained via the classical subsampling method.The presence of SQ 68 influences the amount of free thrombin that appears in plasma because it competitively inhibits the inactivation of thrombin by AT III and α2 macroglobulin. The inhibition of the thrombin peak by heparin, relative to an uninhibited control, remains unaltered by the presence of the substrate.From the course of thrombin activity and the prevailing decay constants, the course of prothrombin conversion velocity can be calculated. Prothrombin conversion was seen to be inhibited at high (>500 μM) substrate concentrations only, and experimental conditions are found under which the inhibition of the clotting process by the substrate is negligibleThe amidolytic activity is the sum of the activities of free thrombin and of the α2 macroglobulin-thrombin complex formed. Via a mathematical procedure the amount of SQ 68 that has been split by thrombin alone and not by the a2 macroglobulin-thrombin complex, can be derived from the course of the optical density.The total amount of SQ 68 eventually split by thrombin alone is proportional to the surface under the thrombin generation curve, i. e. to the time-integral of free thrombin. This value, that we call the thrombin potential (TP), directly indicates how much of any physiological substrate can potentially be split by the thrombin being generated in the plasma.


Sign in / Sign up

Export Citation Format

Share Document