Responses of mitral/tufted cells to orthodromic and antidromic electrical stimulation in the olfactory bulb of the tiger salamander

1988 ◽  
Vol 59 (6) ◽  
pp. 1736-1755 ◽  
Author(s):  
K. A. Hamilton ◽  
J. S. Kauer

1. Responses evoked by electrical stimulation of the olfactory nerve and olfactory tracts were analyzed in 46 output cells of the salamander olfactory bulb, in vivo. Labeling of several cells with horseradish peroxidase indicated that they were mitral and/or tufted neurons. The responses contained reproducible sequences of depolarizing and hyperpolarizing potentials, which changed with increases in stimulus intensity. 2. Stimulation of the nerve with intensities subthreshold for evoking spikes in the recorded cell resulted in a small depolarization followed by a period of hyperpolarization, during which spontaneous spikes were suppressed. With suprathreshold stimulus intensities, a single spike or often a burst of spikes was evoked, followed by a complex prolonged hyperpolarization. When full spikes were blocked by injecting hyperpolarizing current through the recording electrode, an excitatory postsynaptic potential (EPSP) with two major components and sometimes a fast prepotential were observed at the beginning of the response. Amplitudes of the EPSP and hyperpolarization increased with graded increases in stimulus intensity. In tests with paired stimulus volleys, spike generation was inhibited for at least 1 s and often for several seconds during the hyperpolarization. 3. Stimulation of the tracts with intensities subthreshold for evoking spikes in the recorded cell resulted in a complex prolonged hyperpolarization. With suprathreshold stimulus intensities, a single spike was evoked, followed by a similar period of hyperpolarization. When full spikes were blocked by injecting hyperpolarizing current through the recording electrode, a small antidromic spike, presumably generated in the axon or initial segment, was often observed. Amplitude of the hyperpolarization increased with graded increases in stimulus intensity. In tests with paired volleys, generation of a full antidromic spike was inhibited for a period that usually began 20-30 ms, following the spike evoked by the conditioning stimulus and lasted 100-500 ms. Full antidromic spikes were evoked prior to the period of inhibition and small antidromic spikes were evoked during the period. 4. The mean latencies of single evoked spikes or the first spikes of bursts decreased from 22 to 17 ms with increases in the intensity of nerve stimulation and from 7 to 6 ms with increases in the intensity of tract stimulation. Only decreases in orthodromic latency were significant at P less than or equal to 0.05, as determined by one-sided t tests between the means of responses subdivided according to response pattern and relative stimulus intensity.(ABSTRACT TRUNCATED AT 400 WORDS)

1999 ◽  
Vol 46 (4) ◽  
pp. 461-469 ◽  
Author(s):  
C.Q. Huang ◽  
R.K. Shepherd ◽  
P.M. Center ◽  
P.M. Seligman ◽  
B. Tabor

1983 ◽  
Vol 244 (4) ◽  
pp. E317-E322 ◽  
Author(s):  
F. Rohner-Jeanrenaud ◽  
A. C. Hochstrasser ◽  
B. Jeanrenaud

In vivo glucose-induced insulin secretion was greater in preweaned preobese 17-day-old Zucker rats than in the corresponding controls. This hypersecretion of insulin was reversed to normal by acute pretreatment with atropine. A short-lived (30 s) electrical stimulation of the vagus nerve preceding a glucose load potentiated the in vivo glucose-induced insulin release in adult animals (6-9 wk) and more so in obese Zucker (fa/fa) than in lean rats. This suggested the existence of enhanced sensitivity and/or responsiveness of the B cells of obese animals to the parasympathetic system. That the parasympathetic tone was increased in adult obese Zucker (fa/fa) rats was corroborated by the observation that acute vagotomy of these animals resulted in a significant decrease in glucose-induced insulin secretion, whereas no such effect was seen in lean rats. Also, perfused pancreases from adult obese (fa/fa) rats oversecreted insulin during a stimulation by arginine when compared with controls, an oversecretion that was restored toward normal by superimposed infusion of atropine. It is concluded that a) the increased insulin secretion of preobese Zucker fa/fa rats is an early abnormality that is mediated by the vagus nerve, and b) increased secretion of insulin in adult obese fa/fa rats continues to be partly vagus-nerve mediated, although a decreased sympathetic tone and other unknown defects could conceivably play a role as well.


2020 ◽  
Vol 21 (7) ◽  
pp. 2390
Author(s):  
Masamichi Shinoda ◽  
Satoshi Fujita ◽  
Shiori Sugawara ◽  
Sayaka Asano ◽  
Ryo Koyama ◽  
...  

We evaluated the mechanisms underlying the spinal cord stimulation (SCS)-induced analgesic effect on neuropathic pain following spared nerve injury (SNI). On day 3 after SNI, SCS was performed for 6 h by using electrodes paraspinally placed on the L4-S1 spinal cord. The effects of SCS and intraperitoneal minocycline administration on plantar mechanical sensitivity, microglial activation, and neuronal excitability in the L4 dorsal horn were assessed on day 3 after SNI. The somatosensory cortical responses to electrical stimulation of the hind paw on day 3 following SNI were examined by using in vivo optical imaging with a voltage-sensitive dye. On day 3 after SNI, plantar mechanical hypersensitivity and enhanced microglial activation were suppressed by minocycline or SCS, and L4 dorsal horn nociceptive neuronal hyperexcitability was suppressed by SCS. In vivo optical imaging also revealed that electrical stimulation of the hind paw-activated areas in the somatosensory cortex was decreased by SCS. The present findings suggest that SCS could suppress plantar SNI-induced neuropathic pain via inhibition of microglial activation in the L4 dorsal horn, which is involved in spinal neuronal hyperexcitability. SCS is likely to be a potential alternative and complementary medicine therapy to alleviate neuropathic pain following nerve injury.


1959 ◽  
Vol 196 (2) ◽  
pp. 327-329 ◽  
Author(s):  
Raymond R. Walsh

A single, short-duration electrical stimulus delivered to one olfactory bulb evokes a potential in the contralateral bulb. As recorded with a unipolar electrode, the potential is negative central to, and positive peripheral to the external plexiform layer. Bipolar recordings from multiple sites show that the potential is not actively propagated. The potential summates in response to tetanic stimulation and is blocked by anoxia and dimethyl ether d-tubocurarine. In addition to confirming the existence of an interolfactory bulb system, the electrophysiological evidence in conjunction with known anatomical relationships strongly suggests that the evoked potential is a postsynaptic potential of the internal granular cells.


1998 ◽  
Vol 80 (4) ◽  
pp. 1623-1629 ◽  
Author(s):  
A. Kapur ◽  
L. B. Haberly

Kapur, A. and L. B. Haberly. Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting. J. Neurophysiol. 80: 1623–1629, 1998. Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with θ-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 ± 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1–2 h after induction (70% loss in 1.5 h, on average). The N-methyl-d-aspartate (NMDA)-receptor antagonists d-APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of γ-aminobutyric acid–mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, θ-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 ± 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (≤6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.


2020 ◽  
Vol 2 (4) ◽  
pp. 391-398
Author(s):  
Damián Hernández ◽  
Rodney Millard ◽  
Anne M. Kong ◽  
Owen Burns ◽  
Priyadharshini Sivakumaran ◽  
...  

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