Cardioacceleration produced by close intra-arterial injection of neurotensin into the stellate ganglion of the cat

1988 ◽  
Vol 66 (4) ◽  
pp. 408-412 ◽  
Author(s):  
M. Bachoo ◽  
C. Polosa
Keyword(s):  
Heart Rate ◽  
Rise Time ◽  
Time Course ◽  
Ganglion Cells ◽  
Stellate Ganglion ◽  
Appreciable Effect ◽  
Cholinergic Transmission ◽  
Onset Latency ◽  
Slow Time ◽  
Preganglionic Stimulation

The effect on heart rate of close i.a. injection of neurotensin (NT), substance P (SP), and vasoactive intestinal peptide (VIP) into the decentralized right stellate ganglion was tested in anaesthetized spinal cats. These peptides are present in the stellate ganglion and may mediate the stellate ganglion cell excitation underlying a previously described slow cardioacceleration evoked by preganglionic stimulation during block of cholinergic transmission. NT (Tyr11-NT) at doses of 25–200 μg produced increases in heart rate of 10–125 beats/min (bpm) and of slow time course. At the dose of 100 μg, NT produced a cardioacceleration of 56 ± 8.4 bpm(mean ± SEM, n = 13) with an onset latency of 23 ± 4 s, a slow rise to peak (rise time 62 ± 4.5 s), and a half decay of 167 ± 14 s. A cardioacceleration of comparable magnitude (78 ± 3.8 bpm) caused by close i.a. administration of acetylcholine (100 μg, n = 13) had an onset latency of 2 ± 1 s, a fast rise to a sharp peak (rise time 3 ± 1 s), and a half decay of 23 ± 4 s. The analogues, Phe11-NT and Trp11-NT, as well as the stereoisomer, D-Tyr11-NT, had no effect on heart rate when injected at doses up to 400 μg. The NT-evoked cardioacceleration was blocked by propranolol or by section of the inferior cardiac nerve and may therefore be attributed to prolonged excitation of stellate ganglion cells. Administration of hexamethonium and atropine was without effect on the NT response. Intravenous injection of NT at the same doses used by intra-arterial injection (25–200 μg) was without appreciable effect on heart rate. At doses of up to 400 μg by close i.a. injection, VIP and SP had no effect on heart rate. Two observations suggest that NT is a likely candidate as mediator of noncholinergic excitation of stellate ganglion cells. One is the finding, reported here, of a similarly slow time course for the NT-evoked cardioacceleration and for the slow cardioacceleration evoked by preganglionic stimulation during block of cholinergic transmission. The other is the previously reported finding that NT-like immunoreactivity in the stellate ganglion is depleted by prolonged stimulation causing loss of the neurally evoked slow cardioacceleration.

Slow cardioacceleration mediated by noncholinergic transmission in the stellate ganglion of the cat

1988 ◽  
Vol 66 (8) ◽  
pp. 1066-1074 ◽  
Author(s):  
Manjit Bachoo ◽  
Ehud Isacoff ◽  
Canio Polosa
Keyword(s):  
Heart Rate ◽  
Rate Increase ◽  
Stellate Ganglion ◽  
Low Frequency ◽  
Low Frequency Stimulation ◽  
Frequency Stimulation ◽  
Preganglionic Stimulation ◽  
Slow Onset ◽  
Inferior Cardiac Nerve ◽  
Stimulation Of

In C1-spinal, pentobarbital-anaesthetized or anemically decerebrated cats, the preganglionic input to the acutely decentralized right stellate ganglion was stimulated with 10- to 30-s trains at 20–40 Hz. Electrical stimulation consistently produced an increase in heart rate in the presence of blocking doses of hexamethonium and atropine or after depletion of acetylcholine from the preganglionic axons by prolonged low frequency stimulation in the presence of hemicholinium. The increase in heart rate had a delayed slow onset, lasted several minutes, and was abolished by propranolol or by section of the inferior cardiac nerve. The magnitude and duration of the heart rate increase were related to intensity, frequency, and duration of preganglionic stimulation. The response to stimulation of a given white ramus was progressively attenuated, and eventually irreversibly lost, during prolonged continuous stimulation of that ramus, while the response to stimulation of a different unstimulated ramus was unchanged. We conclude that the slow cardioacceleration results from a slow and prolonged excitation of postganglionic neurons by a noncholinergic transmitter released by the preganglionic axons.

Inhibition in ON-OFF directionally selective ganglion cells of the rabbit retina

1993 ◽  
Vol 69 (6) ◽  
pp. 2174-2187 ◽  
Author(s):  
F. R. Amthor ◽  
N. M. Grzywacz
Keyword(s):  
Receptive Field ◽  
Apparent Motion ◽  
Rise Time ◽  
Time Course ◽  
Ganglion Cells ◽  
Rabbit Retina ◽  
Null Direction ◽  
Field Center ◽  
Receptive Field Center ◽  
Light Flashes

1. We have investigated the inhibitory mechanisms modulating the extracellularly recorded responses of ON-OFF directionally selective (DS) ganglion cells of the rabbit retina. Our investigations used both moving spots and apparent motion. The latter was produced by both prolonged light steps, which simulate movement of an edge, and light flashes, which simulate movement of a spot or slit. 2. Within the excitatory receptive-field center of DS ganglion cells, apparent motion with prolonged light steps elicits null-direction inhibition whose strength rises to 90% of maximum in 160 +/- 110 ms (7 cells) and then decays slowly, remaining above baseline longer than 2,000 ms for short interslit distances. 3. Prolonged light steps are generally effective for inhibiting any given excitatory receptive-field locus from an ovate-shaped area that extends asymmetrically in the direction that would be previously traversed by null-direction moving objects. This inhibitory area is typically larger than one-half the size of the receptive-field center. The strength of the inhibition is greater at short than long distances within this area. 4. The rise and fall times of the null-direction inhibition elicited by apparent motion using prolonged light steps are somewhat faster at large than short interslit distances. 5. Short light flashes (at sufficiently long interslit delays) elicit inhibition not only from the same asymmetric, ovate-shaped inhibitory field as long steps of light, but also from loci completely surrounding the second slit. This implies that the asymmetric, null-direction-specific inhibition is due to a temporally sustained mechanism. The symmetric inhibition elicited by short flashes may be due to the presence of the antagonistic surround mechanism within the receptive-field center. The apparent absence of this surround inhibition for preferred-direction apparent motion during prolonged light steps may be due to masking by facilitation that is strongly evoked by long steps, but not flashes of light (see accompanying paper). 6. The relatively slow rise time and sustained time course of the inhibition elicited by null-direction apparent motion within the excitatory receptive field center appears to distinguish it from the inhibition elicited by stimulation within the receptive field surround, which has a much faster rise time and more transient time course. However, the sustained, null-direction inhibitory mechanism that can be elicited by prolonged light steps within the excitatory receptive field center extends into the surround on the side of the receptive-field center previously traversed during null-direction motion.(ABSTRACT TRUNCATED AT 400 WORDS)

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

scholarly journals Uptake and Distribution of Administered Bone Marrow Mesenchymal Stem Cell Extracellular Vesicles in Retina

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 730
Author(s):  
Biji Mathew ◽  
Leianne A. Torres ◽  
Lorea Gamboa Gamboa Acha ◽  
Sophie Tran ◽  
Alice Liu ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Extracellular Vesicles ◽  
Time Course ◽  
Ganglion Cells ◽  
Ex Vivo ◽  
Dependent Manner ◽  
Paracrine Effects

Cell replacement therapy using mesenchymal (MSC) and other stem cells has been evaluated for diabetic retinopathy and glaucoma. This approach has significant limitations, including few cells integrated, aberrant growth, and surgical complications. Mesenchymal Stem Cell Exosomes/Extracellular Vesicles (MSC EVs), which include exosomes and microvesicles, are an emerging alternative, promoting immunomodulation, repair, and regeneration by mediating MSC’s paracrine effects. For the clinical translation of EV therapy, it is important to determine the cellular destination and time course of EV uptake in the retina following administration. Here, we tested the cellular fate of EVs using in vivo rat retinas, ex vivo retinal explant, and primary retinal cells. Intravitreally administered fluorescent EVs were rapidly cleared from the vitreous. Retinal ganglion cells (RGCs) had maximal EV fluorescence at 14 days post administration, and microglia at 7 days. Both in vivo and in the explant model, most EVs were no deeper than the inner nuclear layer. Retinal astrocytes, microglia, and mixed neurons in vitro endocytosed EVs in a dose-dependent manner. Thus, our results indicate that intravitreal EVs are suited for the treatment of retinal diseases affecting the inner retina. Modification of the EV surface should be considered for maintaining EVs in the vitreous for prolonged delivery.

scholarly journals Rapid multi-directed cholinergic transmission in the central nervous system

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Santhosh Sethuramanujam ◽  
Akihiro Matsumoto ◽  
Geoff deRosenroll ◽  
Benjamin Murphy-Baum ◽  
J Michael McIntosh ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Ganglion Cells ◽  
Release Site ◽  
Amacrine Cells ◽  
Global Scale ◽  
Cholinergic Transmission ◽  
Data Set ◽  
The Central Nervous System ◽  
Synaptic Mechanisms

AbstractIn many parts of the central nervous system, including the retina, it is unclear whether cholinergic transmission is mediated by rapid, point-to-point synaptic mechanisms, or slower, broad-scale ‘non-synaptic’ mechanisms. Here, we characterized the ultrastructural features of cholinergic connections between direction-selective starburst amacrine cells and downstream ganglion cells in an existing serial electron microscopy data set, as well as their functional properties using electrophysiology and two-photon acetylcholine (ACh) imaging. Correlative results demonstrate that a ‘tripartite’ structure facilitates a ‘multi-directed’ form of transmission, in which ACh released from a single vesicle rapidly (~1 ms) co-activates receptors expressed in multiple neurons located within ~1 µm of the release site. Cholinergic signals are direction-selective at a local, but not global scale, and facilitate the transfer of information from starburst to ganglion cell dendrites. These results suggest a distinct operational framework for cholinergic signaling that bears the hallmarks of synaptic and non-synaptic forms of transmission.

Paired-pulse facilitation in the dentate gyrus: a patch-clamp study in rat hippocampus in vitro

1994 ◽  
Vol 72 (1) ◽  
pp. 326-336 ◽  
Author(s):  
M. Andreasen ◽  
J. J. Hablitz
Keyword(s):  
Patch Clamp ◽  
Dentate Gyrus ◽  
Time Constant ◽  
Rise Time ◽  
Time Course ◽  
Nmda Antagonist ◽  
Paired Pulse ◽  
Stimulation Intensity ◽  
Paired Pulse Facilitation ◽  
Epsc Amplitude

1. Whole-cell patch-clamp recordings were used to study paired-pulse facilitation (PPF) of the lateral perforant path input to the dentate gyrus in thin hippocampal slices. 2. Orthodromic stimulation of the lateral perforant pathway evoked a excitatory postsynaptic current (EPSC) with a latency of 3.3 +/- 0.1 ms (mean +/- SE) that fluctuated in amplitude. The EPSC had a rise time (10-90%) of 2.79 +/- 0.06 ms (n = 35) and decayed with a single exponential time course with a time-constant of 9.14 +/- 0.24 ms (n = 35). No correlation was found between the amplitude of the EPSC and the rise time or decay time-constant. The non-N-methyl-D-aspartate (NMDA) antagonist 6-cyano-7-nitroquinoxaline-2,3-dione completely blocked the EPSC whereas the NMDA antagonist D-aminophosphonovaleric acid (APV) had modest effects. 3. When a test (T-)EPSC was preceded at an interval of 100 ms by a conditioning (C-)EPSC, a significant increase in the amplitude of the T-EPSC was seen in 38 out of 44 trials analyzed from a total of 27 granule cells. The average amount of PPF was 35.7 +/- 2.1%. There was no apparent correlation between the amount of PPF and the stimulation intensity or mean amplitude of the C-EPSC. The time course of the facilitated T-EPSC was not significantly different from that of the C-EPSC. 4. No correlation was found between the amplitude of the C-EPSC and that of the T-EPSC. Estimates of quantal content (mcv) were determined by calculating the ratio of the squared averaged EPSC amplitude (from 48 responses) to the variance of these responses (M2/sigma 2) whereas quantal amplitudes (qcv) were estimated by calculating the ratio of the response variance to average EPSC amplitude (sigma 2/M). PPF was found to be associated with an average increase in mcv of 64.8 +/- 7.2% (n = 38) whereas qcv was decreased by 12.1 +/- 3.8%. 5. The time course of PPF was studied by varying the interval between the C- and T-pulse from 10 to 400 ms while keeping the stimulation intensity constant. Maximal facilitation of the T-EPSC was obtained with interpulse intervals < or = 25 ms where the average facilitation amounted to approximately 70% (n = 6). The decline of facilitation was nearly exponential and was no longer evident with intervals > 350 ms.(ABSTRACT TRUNCATED AT 400 WORDS

A mathematical model of cardiovascular dynamics for the diagnosis and prognosis of hemorrhagic shock

2021 ◽  
Author(s):  
Laura D’Orsi ◽  
Luciano Curcio ◽  
Fabio Cibella ◽  
Alessandro Borri ◽  
Lilach Gavish ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Hemorrhagic Shock ◽  
Time Course ◽  
Differential Algebraic Equations ◽  
Model Parameters ◽  
Algebraic Equations ◽  
Cardiovascular Dynamics ◽  
Compensation Mechanisms

Abstract A variety of mathematical models of the cardiovascular system have been suggested over several years in order to describe the time-course of a series of physiological variables (i.e. heart rate, cardiac output, arterial pressure) relevant for the compensation mechanisms to perturbations, such as severe haemorrhage. The current study provides a simple but realistic mathematical description of cardiovascular dynamics that may be useful in the assessment and prognosis of hemorrhagic shock. The present work proposes a first version of a differential-algebraic equations model, the model dynamical ODE model for haemorrhage (dODEg). The model consists of 10 differential and 14 algebraic equations, incorporating 61 model parameters. This model is capable of replicating the changes in heart rate, mean arterial pressure and cardiac output after the onset of bleeding observed in four experimental animal preparations and fits well to the experimental data. By predicting the time-course of the physiological response after haemorrhage, the dODEg model presented here may be of significant value for the quantitative assessment of conventional or novel therapeutic regimens. The model may be applied to the prediction of survivability and to the determination of the urgency of evacuation towards definitive surgical treatment in the operational setting.

Dendritic competition in the developing retina: Ganglion cell density gradients and laterally displaced dendrites

1993 ◽  
Vol 10 (2) ◽  
pp. 313-324 ◽  
Author(s):  
Rafael Linden
Keyword(s):  
Density Gradient ◽  
Cell Density ◽  
Time Course ◽  
Ganglion Cells ◽  
Lateral Displacement ◽  
Optic Tract ◽  
Density Gradients ◽  
Temporal Asymmetry ◽  
Dendritic Arbors ◽  
Contralateral Eye

AbstractDendrites of retinal ganglion cells (RGCs) tend to be distributed preferentially toward areas of reduced RGC density. This, however, does not occur in the retina of normal pigmented rats, in which it has been suggested that the centro-peripheral gradient of RGC density is too shallow to provide directional guidance to growing dendrites. In this study, laterally displaced dendrites of RGCs retrogradely labeled with horseradish peroxidase were related to cell density gradients induced experimentally in the rat retina. Neonatal unilateral lesions of the optic tract produced retrograde degeneration of contralaterally projecting RGCs, but spared ipsilaterally projecting neurons in the same retina. These lesions created an anomalous temporal to nasal gradient of cell density across the decussation line, opposite to the nasal to temporal gradient found along the same axis in either normal rats or rats that had the contralateral eye removed at birth. RGCs in rats that received optic tract lesions had their dendrites displaced laterally toward the depleted nasal retina, while in either normal or enucleated rats there was no naso-temporal asymmetry. The lateral displacement affected both primary dendrites and higher-order branches. However, the gradient of cell density after optic tract lesions was less steep than the gradient in either normal or enucleated rats. To test for the presence of steeper gradients at early stages of development, RGC density gradients were also examined at postnatal day 5 (P5). In normal rats, the RGCs were homogeneously distributed throughout the retina, while rats given optic tract lesions at birth already showed a temporo-nasal density gradient at P5. Still, this anomalous gradient was less steep than that found in normal adults. It is concluded that the time course, rather than the steepness of the RGC density gradient, is the major determinant of the lateral displacement of dendritic arbors with respect to the soma in developing RGCs. The data are consistent with the idea that the overall shape of dendritic arbors depends in part on dendritic competition during retinal development.

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