Paired-pulse stimulation of an electric-hydraulic pump used to replace the mammalian heart

1968 ◽  
Vol 35 (1) ◽  
pp. 41-47
Author(s):  
S. D. Moulopoulos ◽  
M. J. Crosby ◽  
Y. Nose ◽  
W. J. Kolff
1993 ◽  
Vol 70 (6) ◽  
pp. 2241-2250 ◽  
Author(s):  
M. K. Floeter ◽  
A. Lev-Tov

1. The excitation of lumbar motoneurons by reticulospinal axons traveling in the medial longitudinal fasciculus (MLF) was investigated in the newborn rat using intracellular recordings from lumbar motoneurons in an in vitro preparation of the brain stem and spinal cord. The tracer DiI (1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine) was introduced into the MLF of 6-day-old littermate rats that had been fixed with paraformaldehyde to evaluate the anatomic extent of this developing pathway. 2. Fibers labeled from the MLF by DiI were present in the cervical ventral and lateral white matter and a smaller number of labeled fibers extended to the lumbar enlargement. Patches of sparse terminal labeling were seen in the lumbar ventral gray. 3. In the in vitro preparation of the brain stem and spinal cord, MLF stimulation excited motoneurons through long-latency pathways in most motoneurons and through both short-(< 40 ms) and long-latency connections in 16 of 40 motoneurons studied. Short- and longer-latency components of the excitatory response were evaluated using mephenesin to reduce activity in polysynaptic pathways. 4. Paired-pulse stimulation of the MLF revealed a modest temporal facilitation of the short-latency excitatory postsynaptic potential (EPSP) at short interstimulus intervals (20–200 ms). Trains of stimulation at longer interstimulus intervals (1–30 s) resulted in a depression of EPSP amplitude. The time course of the synaptic depression was compared with that found in EPSPs resulting from paired-pulse stimulation of the dorsal root and found to be comparable. 5. The short-latency MLF EPSP was reversibly blocked by 6-cyano-7-nitroquinoxaline (CNQX), an antagonist of non-N-methyl-D-aspartate glutamate receptors, with a small CNQX-resistant component. Longer-latency components of the MLF EPSP were also blocked by CNQX, and some late components of the PSP were sensitive to strychnine. MLF activation of multiple polysynaptic pathways in the spinal cord is discussed.


1998 ◽  
Vol 779 (1-2) ◽  
pp. 324-328 ◽  
Author(s):  
Y Fueta ◽  
H Kawano ◽  
T Ono ◽  
T Mita ◽  
K Fukata ◽  
...  

2016 ◽  
Vol 10 ◽  
Author(s):  
Poli Daniele ◽  
Thiagarajan Srikanth ◽  
DeMarse Thomas ◽  
Wheeler Bruce ◽  
Brewer Gregory

1994 ◽  
Vol 72 (2) ◽  
pp. 592-604 ◽  
Author(s):  
L. Brodin ◽  
O. Shupliakov ◽  
V. A. Pieribone ◽  
J. Hellgren ◽  
R. H. Hill

1. The glutamatergic synapses formed between the unbranched giant reticulospinal axons onto spinal neurons in lamprey offer a central vertebrate synapse in which the presynaptic element can be impaled with one or several microelectrodes, which may be used for recording as well as microinjection of different substances. To provide a basis for the use of this synapse in studies of release mechanisms, we have examined the use-dependent modulation of the synaptic response under conditions of conventional cell body stimulation, and during direct stimulation of the presynaptic axon. 2. To examine the stability of the mixed electrotonic and chemical reticulospinal excitatory postsynaptic potential (EPSP) over time, action potentials were evoked at a rate of 1 Hz for 800–1000 trials. In three out of seven synapses the chemical component remained at a similar amplitude, while in four cases a progressive decrease (up to 35%) occurred. The electrotonic component remained at a similar amplitude in all cases. 3. During paired pulse stimulation of the reticulospinal cell body (pulse interval 65 ms) the chemical EPSP component showed a net facilitation in all cases tested [from 0.64 +/- 0.35 to 0.89 +/- 0.48 (SD) mV, n = 13], while the peak amplitude of the electrotonic component was unchanged (1.37 +/- 0.68 and 1.36 +/- 0.66 mV, respectively). Recording of the axonal action potential during paired pulse stimulation showed that the width of the first and second action potential did not differ [1/2 width (2.48 +/- 0.39 ms and 2.48 +/- 0.42 ms, respectively; n = 8)]. 4. The degree of facilitation varied markedly between different synapses, ranging from an increase of a few percent to a two-fold increase (24 +/- 16% mean change of total EPSP amplitude, corresponding to 44 +/- 26% mean change of chemical EPSP amplitude). This type of variability was also observed in synapses made from the same unbranched reticulospinal axon onto different postsynaptic cells. 5. When paired pulse stimulation was applied to the reticulospinal axon in the very vicinity of the synaptic area (0.1–1 mm) a net depression of the chemical component occurred in 11 out of 19 cases, and in the remaining cases the level of net facilitation was lower as compared with cell body stimulation (range between +17 and -23% change of total EPSP amplitude; mean -5%; n = 19). 6. To test if the change of the EPSP plasticity during local stimulation correlated with an increased transmitter release, two microelectrodes were placed in the same reticulospinal axon at different distances from the synaptic area.(ABSTRACT TRUNCATED AT 400 WORDS)


2001 ◽  
Vol 86 (5) ◽  
pp. 2231-2245 ◽  
Author(s):  
Maria J. Denslow ◽  
Tore Eid ◽  
Fu Du ◽  
Robert Schwarcz ◽  
Eric W. Lothman ◽  
...  

Previous studies have revealed a loss of neurons in layer III of the entorhinal cortex (EC) in patients with temporal lobe epilepsy. These neurons project to the hippocampus and may activate inhibitory interneurons, so that their loss could disrupt inhibitory function in the hippocampus. The present study evaluates this hypothesis in a rat model in which layer III neurons were selectively destroyed by focal injections of the indirect excitotoxin, aminooxyacetic acid (AOAA). Inhibitory function in the hippocampus was assessed by evaluating the discharge of CA1 neurons in response to stimulation of afferent pathways in vivo. In control animals, stimulation of the temporo-ammonic pathway leads to heterosynaptic inhibition of population spikes generated by subsequent stimulation of the commissural projection to CA1. This heterosynaptic inhibition was substantially reduced in animals that had received AOAA injections 1 mo previously. Stimulation of the commissural projection also elicited multiple population spikes in CA1 in AOAA-injected animals, and homosynaptic inhibition in response to paired-pulse stimulation of the commissural projection was dramatically diminished. These results suggest a disruption of inhibitory function in CA1 in AOAA-injected animals. To determine whether the disruption of inhibition occurred selectively in CA1, we assessed paired-pulse inhibition in the dentate gyrus. Both homosynaptic inhibition generated by paired-pulse stimulation of the perforant path, and heterosynaptic inhibition produced by activation of the commissural projection to the dentate gyrus appeared largely comparable in AOAA-injected and control animals; thus abnormalities in inhibitory function following AOAA injections occurred relatively selectively in CA1. Electrolytic lesions of the EC did not cause the same loss of inhibition as seen in animals with AOAA injections, indicating that the loss of inhibition in CA1 is not due to the loss of excitatory driving of inhibitory interneurons. Also, electrolytic lesions of the EC in animals that had been injected previously with AOAA had little effect on the abnormal physiological responses in CA1, suggesting that most alterations in inhibition in CA1 are not due to circuit abnormalities within the EC. Comparisons of control and AOAA-injected animals in a hippocampal kindling paradigm revealed that the duration of afterdischarges elicited by high-frequency stimulation of CA3, and the number of stimulations required to elicit kindled seizures were comparable. Taken together, our results reveal that the selective loss of layer III neurons induced by AOAA disrupts inhibitory function in CA1, but this does not create a circuit that is more prone to at least one form of kindling.


1966 ◽  
Vol 71 (2) ◽  
pp. 143-145 ◽  
Author(s):  
Brian F. Hoffman ◽  
Paul F. Cranefield

2002 ◽  
Vol 88 (5) ◽  
pp. 2477-2489 ◽  
Author(s):  
Christian H. Lemon ◽  
Patricia M. Di Lorenzo

Despite evidence for an abundance of inhibitory synaptic processes within the taste-responsive portion of the brain stem, little is known about how these processes are activated or modulated. In this context, this study tested the hypothesis that activation of the chorda tympani nerve (CT) invokes inhibition that influences gustatory neural information processing in the rostral nucleus of the solitary tract (NTS). Stimulating electrodes were implanted in the middle ear of urethane-anesthetized rats to enable the passage of current across the CT. Electrophysiological responses to sucrose, NaCl, HCl, and quinine were recorded from single NTS neurons both individually and immediately following tetanic electrical stimulation of the CT. Additionally, NTS field responses to paired pulse stimulation of the CT were recorded. Electrical pulses delivered to the CT were found to produce a compound action potential with four components. Taste-responsive units in the NTS showed tetanus-evoked responses that varied in latency and strength. Those cells that showed strong, short latency responses to CT stimulation showed large magnitude responses to NaCl and were relatively narrowly tuned. Units with longer latencies generally responded more broadly to taste stimuli and with lower response magnitudes. Following tetanus, taste responses in 20 (43%) of the 46 units were reversibly altered in a stimulus-selective manner. Taste responses in 18 units were both enhanced and attenuated following tetanic stimulation, although attenuation was much more common. Additionally, tetanus was found to affect the temporal organization of spikes within taste responses to one stimulus in seven units (15%), four of which also showed changes in response magnitude to a different stimulus following tetanus. The influence of tetanus on taste responses was shown to be reliable and repeatable in neurons from which stimulus trials were recorded more than once. Across all units, responses to quinine were most dramatically and frequently attenuated following tetanus, while those to NaCl were least susceptible to change. NTS field responses evoked by paired pulse stimulation of the CT suggested that the initial pulse evoked an inhibitory influence in the NTS that decayed and returned to baseline by 2 s. These data are consistent with the idea that afferent input to the NTS normally activates inhibitory synaptic activity. As with other sensory systems, such inhibition may serve to facilitate contrast in the neural representation of different stimulus qualities.


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