Latency of Repeated Responses to Single-Pulse Stimulation of Schaffer Collaterals Recorded in Hippocampal Field CA1 in Rats during Sleep

2016 ◽  
Vol 46 (9) ◽  
pp. 1047-1058
Author(s):  
V. A. Zosimovskii ◽  
V. A. Korshunov
1991 ◽  
Vol 260 (2) ◽  
pp. R290-R297 ◽  
Author(s):  
D. H. Huangfu ◽  
P. G. Guyenet

The central pathway mediating a sympatholytic response to stimulation of the superior laryngeal nerve (SLN) was studied in halothane-anesthetized, paralyzed rats. Single-pulse stimulation of SLN inhibited lumbar sympathetic nerve discharge (LSND) with onset latency of 113 +/- 1.7 ms. LSND inhibition was markedly attenuated by bilateral microinjection of kynurenic acid (Kyn, glutamate receptor antagonist, 4.5 nmol/side) into the caudal ventrolateral medulla (CVL) or by bilateral administration of bicuculline methiodide (Bic; gamma-aminobutyric acid-receptor antagonist, 225 pmol/side) into the rostral ventrolateral medulla (RVL). In 13 of 14 cases, the baroreceptor reflex was also severely reduced. Injections of Bic or Kyn elsewhere in the medullary reticular formation were ineffective. Single-pulse stimulation of SLN inhibited 19 of 26 RVL reticulospinal barosensitive cells (onset latency 46 +/- 1.4 ms). This inhibition was attenuated (from 92 +/- 6 to 14 +/- 12%) by iontophoretic application of Bic (n = 7), which also reduced the cells' inhibitory response to aortic coarctation. The remaining seven barosensitive neurons were unaffected by SLN stimulation. In conclusion, the sympathetic baroreflex and the sympathoinhibitory response to SLN stimulation appear to be mediated by similar medullary pathways.


1996 ◽  
Vol 271 (4) ◽  
pp. R1054-R1062 ◽  
Author(s):  
F. Hayashi ◽  
D. R. McCrimmon

It was hypothesized that, because rats appear to lack a prominent disynaptic projection from the dorsal respiratory group to phrenic motoneurons (Phr), they would lack the short-latency excitation of Phr output seen in cats in response to stimulation of some cranial nerve afferents. Single-pulse superior laryngeal nerve (SLN) stimulation elicited a short-latency bilateral excitation of glossopharyngeal (IX) and hypoglossal (XII) nerves and an ipsilateral excitation of pharyngeal branch of vagus (PhX) in 67% of rats, but no excitation of Phr. Vagus (X) stimulation elicited a bilateral excitation of Phr and a predominantly ipsilateral excitation of IX and PhX. Single-pulse stimulation of SLN or X also elicited longer-latency, bilateral decreases in activity of all recorded nerves. Repetitive stimulation (50 Hz) of SLN or X suppressed inspiratory activity and prolonged expiration. Lung inflation (7.5 cmH2O) inhibited Phr and PhX activity; X stimulation inhibited Phr but prolonged PhX activity. In conclusion, rats predictably lack the SLN-induced short latency Phr excitation but exhibit other short latency reflexes for which the underlying circuitry is not clear.


1989 ◽  
Vol 13 (2) ◽  
pp. 116-122 ◽  
Author(s):  
Anton Moritz ◽  
Sharon Grundfest-Broniatowski ◽  
Laszlo Ilyes ◽  
Jerry Kasick ◽  
Gordon Jacobs ◽  
...  

2001 ◽  
Vol 85 (6) ◽  
pp. 2639-2642 ◽  
Author(s):  
Kaoru Yoshida ◽  
Yoshiki Iwamoto ◽  
Sohei Chimoto ◽  
Hiroshi Shimazu

We investigated the synaptic organization responsible for the inhibition of omnipause neurons (OPNs) following stimulation of the superior colliculus (SC) in alert cats. Stimulation electrodes were implanted bilaterally in the rostral and caudal SC where a short-pulse train induced small and large saccades, respectively. Effects of single-pulse stimulation on OPNs were examined with intracellular and extracellular recordings. In contrast to monosynaptic excitatory postsynaptic potentials, which were induced by rostral SC stimulation, inhibitory postsynaptic potentials were induced with disynaptic latencies (1.3–1.9 ms) from both the rostral and caudal SC in most OPNs. Analysis of a larger extracellular sample complemented intracellular observations. Monosynaptic activation of OPNs was elicited more frequently from rostral sites than from caudal sites, whereas spike suppression with disynaptic latencies was induced by caudal as well as rostral stimulation with similar frequencies. The results imply that disynaptic inhibition is produced by activation of SC cells that are distributed over wide regions related to saccades of different sizes. We suggest that signals from these neurons initiate a saccadic pause of OPNs through single inhibitory interneurons.


1959 ◽  
Vol 196 (2) ◽  
pp. 335-339
Author(s):  
Torquato Gualtierotti

Single pulse stimulation of the lateral geniculate body and other optic centers in the brain stem, in addition to evoking potentials in the visual area, induced a widespread afterdischarge on the cortical surface of the brain of the cat. This discharge consists of a number of 7–13/sec. surface-positive waves. It starts from an extravisual trigger area and spreads intracortically at a speed of 0.5 mm/sec. Extracortically an afterdischarge made up of waves at half the frequency of the cortical afterdischarge was recorded from the deep nuclei of the cerebellum and from the inferior olive. This activity is induced by the cortical afterdischarges. No change occurred in pyramidal tracts activity during the afterdischarges. Sensory evoked potentials and afterdischarges did not interfere with one another. The afterdischarge did not alter the gross behavior of the animal.


1996 ◽  
Vol 75 (6) ◽  
pp. 2658-2661 ◽  
Author(s):  
S. Chimoto ◽  
Y. Iwamoto ◽  
H. Shimazu ◽  
K. Yoshida

1. Extracellular recordings were made from medium-lead burst neurons (MLBNs) in the paramedian pontomedullary reticular formation rostral and caudal to the abducens nucleus in the alert cat. 2. Single-pulse stimulation of the contralateral superior colliculus during intersaccadic intervals evoked no response in most MLBNs. When collicular stimulation was applied at the beginning of saccades, spikes of MLBNs were consistently evoked with short latencies. The shortest latency was 0.8 ms, indicating monosynaptic activation of MLBNs from the superior colliculus. 3. Results suggest that monosynaptic excitatory effects from the colliculus are concealed by inhibitory input from omnipause neurons (OPNs) during intersaccadic intervals and that the monosynaptic collicular activation is disclosed when this inhibition is removed by a pause in OPN activity at the beginning of saccades.


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