DOCSLIB.ORG

Inhibitory Postsynaptic Potential in Mammalian Sympathetic Ganglia (Disynaptic Event/Catecholamine Hyperpolarization/Small Intensely Fluorescent Cells) N

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Inhibitory Postsynaptic Potential in Mammalian Sympathetic Ganglia (Disynaptic Event/Catecholamine Hyperpolarization/Small Intensely Fluorescent Cells) N Proc. Natl. Acad. Sci. USA Vol. 75, No. 8, pp. 4029-4032, August 1978 Neurobiology Involvement of an interneuron in the generation of the slow inhibitory postsynaptic potential in mammalian sympathetic ganglia (disynaptic event/catecholamine hyperpolarization/small intensely fluorescent cells) N. J. DUN AND A. G. KARCZMAR Department of Pharmacology, Loyola University, Stritch School of Medicine, Maywood, Illinois 60153 Communicated by George B. Koelle, May 19,1978 ABSTRACT Acetylchoine (AcCho) was applied electro- causes a hyperpolarizing response resembling the slow ipsp and phoretically to cells of isolated rabbit superior cervical ganglia, that this response is disynaptic in nature. and the response was recorded by means of intracellular re- cording techniques. In the presence of d-tubocurarine (5 M&M), MATERIALS AND METHODS AcCho applied by tetanic current pulses elicited three distinct membrane potential changes: a slow depolarization, a slow Young white rabbits of either sex, weighing 1.5-2.0 kg, were hyperpolarization, and a biphasic response consisting of an used throughout this study. The superior cervical ganglia were initial hyperpolarization followed by a depolarization. Atropine rapidly excised from the rabbits after they were killed by air (I gM) abolished all the membrane potential changes elicited by AcCho. On the other hand, superfusion with a low-Ca/ embolism. Each ganglion was transferred to the recording high-Mg solution, tetrodotoxin (0.1 &M), or haloperidol (0.1 MM) chamber and superfused continuously with Krebs solution (8). selectively and reversibly blocked AcCho-induced hyperpolar- The intracellular recording and iontophoretic techniques used ization without appreciably affecting the depolarization. The have been described (8). Glass microelectrodes filled with 3 M membrane resistance remained relatively constant during the KC1 (tip resistance, 30-50 MO) were used for intracellular re- course of hyperpolarization. Application of steady depolarizing cording and stimulation. The micropipettes used for ionto- and hyperpolarizing currents decreased and increased, re- spectively, the amplitude of hyperpolarization. These results phoretic application of AcChoCl (2 M) had tip resistances of demonstrate that the hyperpolarization elicited by AcCho is about 75-100 MQ; braking currents of about 3-5 nA were used. electrophysiologically and pharmacologically similar to the slow In experiments concerning the effects of tetrodotoxin upon the inhibitory postsynaptic potential induced by nerve stimulation; response to antidromic stimulation, the postginglionic fibers furthermore, they support the view that the slow inhibitory were drawn into a small capillary; repetitive stimuli at 0.3 Hz postsynaptic potential elicited by presynaptic stimulation is a were applied via a pair of platinum electrodes. disynaptic phenomenon involving the release of a second transmitter, possibly dopamine, from an interneuron. RESULTS In the autonomic ganglia, the stimulation of preganglionic Characteristics of Various Potentials Induced by AcCho. nerve elicits, in addition to the familiar fast excitatory postsy- After a ganglion cell was satisfactorily impaled by a micro- naptic potential, slow excitatory and inhibitory postsynaptic electrode, the AcCho-filled .pipette was manipulated into close potentials (1-3). The genesis of the slow excitatory postsynaptic proximity to the ganglion cell. Under these circumstances, potential (slow epsp) is reasonably certain; most likely it can be AcCho discharged by a brief current pulse (<10 msec) caused accounted for in terms of direct activation of muscarinic re- a fast membrane depolarization with a rise time of <30 msec ceptors located on the principal ganglion cells by presynapti- (8). Superfusion of the ganglion with Krebs solution containing cally released acetylcholine (AcCho) (1-3). The generation of d-tubocurarine (5 AM) completely and reversibly blocked the the slow inhibitory postsynaptic potential (slow ipsp), on the fast AcCho potential in <5 min (9). The resting membrane other hand, remains to be established; it may involve either a potential and other membrane electrical properties were not direct muscarinic action (ref. 4; however, see ref. 5) or a cate- significantly affected by d-tubocurarine (10); the average cholamine released from an adrenergic interneuron (1, 6). In resting potential was found to be about -55 mV. The results the superior cervical ganglion of the rabbit, small intensely described hereafter were obtained in the presence of 5 AM fluorescent (SIF) cells with distinct catecholamine fluorescence d-tubocurarine. are located among the principal ganglion cells (7). These small When applied by tetanic current pulses (10-30 Hz, 10 msec neurons are innervated by the cholinergic preganglionic fibers per pulse for 1-2 sec), AcCho elicited three different types of and, in turn, make synaptic contacts with principal ganglion membrane potential change, depending on the neuron. Of the cells (7). Thus, the SIF cells appear morphologically to be likely 94 cells that exhibited satisfactory resting and action potentials, candidates for the status of an adrenergic interneuron, situated the majority of cells, 48, showed slow membrane depolarization in the synaptic pathway and mediating the slow ipsp. Recently, in response to AcCho iontophoresis. The amplitude of the de- we reported (8) that, when dopamine is applied iontophoreti- polarization ranged from 1.2 to 6.8 mV (mean + SD, 3.7 + 1.7 cally to rabbit sympathetic neurons, it elicits a membrane hy- mV) and total duration ranged from 12 to 33 sec (mean, 28 sec). perpolarization that exhibits electrophysiological features Twenty-one cells exhibited a response of another type, con- similar to those of the slow ipsp. To support the hypothesis that sisting of a slow membrane hyperpolarization. The amplitude an adrenergic interneuron mediates the slow ipsp, it should be of hyperpolarization varied from 1.5 to 7.4 mV (mean, 4.9 mV), shown that AcCho applied to the vicinity of the ganglion cells and the duration ranged from 7.2 to 24 sec (mean, 14.4 sec). Both the depolarizing and hyperpolarizing responses showed The costs of publication of this article were defrayed in part by the payment of page charges This article must therefore be hereby marked Abbreviations: AcCho, acetylcholine; SIF, small intensely fluorescent "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate cells; slow ipsp, slow inhibitory postsynaptic potential; slow epsp, slow this fact. excitatory postsynaptic potential. 4029 Downloaded by guest on September 26, 2021 4030 Neurobiology: Dun and Karczmar Proc. Natl. Acad. Sci. USA 75 (1978) A D present study, the effect of haloperidol (0.1 MM) was examined on eight cells that exhibited either hyperpolarizing or biphasic response to AcCho. Haloperidol depolarized the cell membrane by about 2-3 mV and rapidly blocked the AcCho-induced E hyperpolarization (in <2 min). In the case illustrated in Fig. 1, H AcCho elicited a biphasic response; haloperidol selectively blocked the hyperpolarization and affected the depolarizing response only slightly (Fig. 1 B and C). The selective inhibitory C- F I_ action of haloperidol on the hyperpolarizing response was also demonstrated in experiments on cells that exhibited only de- polarizing response to AcCho. As illustrated in Fig. 2B, halop- eridol (0.1 uM) did not appreciably attenuate the depolarization FIG. 1. Effects of superfusing the sympathetic ganglion cell with after 5 min of superfusion. haloperidol, atropine, or low-Ca/high-Mg solution on AcCho hyper- Effects of Low-Ca/High-Mg Solution. The resting mem- polarization and depolarization. The upper tracing ofeach pair rep- brane potential was slightly altered in a low-Ca (0.25 mM)/ resents the current pulses (10 Hz, 10 msec per pulse for 2 sec) used <5 mV. to elicit the AcCho responses. The ganglion was continuously super- high-Mg (12 mM) solution, the change being always fused with Krebs solution containing 5MM d-tubocurarine. (A, D, and Superfusing the ganglion with the low-Ca/high-Mg solution G) Control responses; (B and C) 1 and 2 min after superfusion with rapidly diminished the amplitude of AcCho hyperpolarization haloperidol (0.1 MM), respectively; (E) 4 min after low-Ca (0.25 and abolished it in <5 min (Fig. 1E); this effect was consistently InM)/high-Mg (12 mM) superfusion; (H) 2 min after atropine (1 MAM); observed in all 14 cells examined. Whenever necessary, the (F and I) 10 min after wash with Krebs solution. Records A-F and change in the resting membrane potential due to thesuperfu- G-I were taken from two different ganglion cells. Vertical calibration sion of low-Ca/high-Mg solution was rectified by passing an mark, 10 mV and 1 nA; horizontal calibration mark, 4 sec for records appropriate steady current through the recording microelec- A-F, and 2 sec for records G-I. trode; this maneuver did not unmask AcCho hyperpolarization. a delay of about 100-400 msec from the start of the current The hyperpolarizing response to AcCho returned after the pulses to the initiation of responses. Still another type of response low-Ca/high-Mg solution was replaced with Krebs solution was 9bserved in 16 cells; this response consisted of biphasic (Fig. iF). This clear-cut effect of the low-Ca/high-Mg solution membrane potential change, initial hyperpolarization being on the hyperpolarizing response to AcCho differed dramatically followed by depolarization (Fig. 1A). The amplitude of the from its lack of action
Load more

Recommended publications
  • Electrophysiological Analysis of Potassium and Sodium Movements in Crustacean Nervous System
    J. exp. Biol. (1975), 63, 85-1 15 85 With igfigura Printed in Great Britain ELECTROPHYSIOLOGICAL ANALYSIS OF POTASSIUM AND SODIUM MOVEMENTS IN CRUSTACEAN NERVOUS SYSTEM BY N. JOAN ABBOTT,* R. B. MORETONf AND Y. PICHON Ldboratoire de Neurobiologie Cellulaire de C.N.R.S., Gif-sur-Yvette 91190, France {Received 20 December 1974) SUMMARY 1. An electrophysiological method was used to estimate the half-times for sodium and potassium entry to, and efflux from, the extra-axonal space in peripheral nerve and central nervous connectives of two species of crustacean. Results from crab (marine) and crayfish (fresh water) were qualitatively similar. 2. Peripheral nerve showed no evidence for diffusion barriers, potassium entry and efflux being rapid, and proceeding at comparable rates. 3. In connective, potassium entry was extremely slow, with a half-time greater than 100 min, while potassium efflux was relatively rapid (7\ = 6min). Sodium movements were less restricted, but sodium entry was more rapid than sodium efflux. 4. The potassium experiments were compared with the behaviour of a theoretical model system. Evidence is presented for diffusional restriction to potassium at the connective perineurial layer. The mechanism of restriction may involve changes in permeability or activation of an ion pump in the perineurial layer. 5. The physiological significance of these findings is discussed. INTRODUCTION In studies in the cockroach (Treherne, Lane, Moreton & Pichon, 1970; Pichon & Treherne, 1970; Pichon, Moreton & Treherne, 1971) it was observed that large rapid potential changes could be recorded in intact central nervous connectives, following an elevation of potassium concentration in the bathing medium. As intra- cellularly recorded action potentials showed no equivalent reduction in amplitude, it was suggested that the apparent depolarization ('extraneuronal potential') was not due to depolarization of axon membranes.
    [Show full text]
  • Long-Term Potentiation Differentially Affects Two Components of Synaptic
    Proc. Nati. Acad. Sci. USA Vol. 85, pp. 9346-9350, December 1988 Neurobiology Long-term potentiation differentially affects two components of synaptic responses in hippocampus (plasticity/N-methyl-D-aspartate/D-2-amino-5-phosphonovglerate/facilitation) DOMINIQUE MULLER*t AND GARY LYNCH Center for the Neurobiology of Learning and Memory, University of California, Irvine, CA 92717 Communicated by Leon N Cooper, September 6, 1988 (receivedfor review June 20, 1988) ABSTRACT We have used low magnesium concentrations ing electrode was positioned in field CAlb between two and the specific antagonist D-2-amino-5-phosphonopentanoate stimulating electrodes placed in fields CAla and CAlc; this (D-AP5) to estimate the effects of long-term potentiation (LTP) allowed us to activate separate inputs to a common pool of on the N-methyl-D-aspartate (NMDA) and non-NMDA recep- target cells. Stimulation voltages were adjusted to produce tor-mediated components of postsynaptic responses. LTP in- field EPSPs of -1.5 mV and did not elicit population spikes duction resulted in a considerably larger potentiation of non- in any of the responses included for data analysis. NMDA as opposed to NMDA receptor-related currents. In- Paired-pulse facilitation was produced by applying two creasing the size of postsynaptic potentials with greater stimulation pulses separated by 30 or 50 ms to the same stimulation currents or with paired-pulse facilitation produced stimulating electrode and LTP was induced by patterned opposite effects; i.e., those aspects ofthe response dependent on burst stimulation-i.e., 10 bursts delivered at 5 Hz, each NMDA receptor's increased to a greater degree than did those burst being composed of four pulses at 100 Hz (see ref.
    [Show full text]
  • Neurophysiology of Frog Dorsal Root Afferent Fibers and Their Intraspinal Processes
    Loyola University Chicago Loyola eCommons Dissertations Theses and Dissertations 1989 Neurophysiology of Frog Dorsal Root Afferent Fibers and Their Intraspinal Processes Nancy C. Tkacs Loyola University Chicago Follow this and additional works at: https://ecommons.luc.edu/luc_diss Part of the Physiology Commons Recommended Citation Tkacs, Nancy C., "Neurophysiology of Frog Dorsal Root Afferent Fibers and Their Intraspinal Processes" (1989). Dissertations. 2652. https://ecommons.luc.edu/luc_diss/2652 This Dissertation is brought to you for free and open access by the Theses and Dissertations at Loyola eCommons. It has been accepted for inclusion in Dissertations by an authorized administrator of Loyola eCommons. For more information, please contact [email protected]. This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License. Copyright © 1989 Nancy C. Tkacs UBRA~Y·· NEUROPHYSIOLOGY OF FROG DORSAL ROOT AFFERENT FIBERS AND THEIR INTRASPINAL PROCESSES by Nancy C. Tkacs A Dissertation Submitted to the Faculty of the Graduate School of .Loyola University of Chicago in Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy April 1989 DEDICATION To Bill, with deep love and gratitude ii ACKNOWLEDG.EMENTS I would like to thank the faculty of the Department of Physiology for the excellent training I have received. I am particularly grateful to Dr. James Filkins for supporting my dissertation research. My thanks also go to Dr. Charles Webber, Dr. David Euler, Dr. David Carpenter, and Dr. Sarah Shefner for serving on my dissertation committee. Their helpful suggestions added much to the research and the dissertation. My gratitude goes to several individuals who unselfishly shared their time, resources, and expertise.
    [Show full text]
  • Action Potential and Synapses
    SENSORY RECEPTORS RECEPTORS GATEWAY TO THE PERCEPTION AND SENSATION Registering of inputs, coding, integration and adequate response PROPERTIES OF THE SENSORY SYSTEM According the type of the stimulus: According to function: MECHANORECEPTORS Telereceptors CHEMORECEPTORS Exteroreceptors THERMORECEPTORS Proprioreceptors PHOTORECEPTORS interoreceptors NOCICEPTORS STIMULUS Reception Receptor – modified nerve or epithelial cell responsive to changes in external or internal environment with the ability to code these changes as electrical potentials Adequate stimulus – stimulus to which the receptor has lowest threshold – maximum sensitivity Transduction – transformation of the stimulus to membrane potential – to generator potential– to action potential Transmission – stimulus energies are transported to CNS in the form of action potentials Integration – sensory information is transported to CNS as frequency code (quantity of the stimulus, quantity of environmental changes) •Sensation is the awareness of changes in the internal and external environment •Perception is the conscious interpretation of those stimuli CLASSIFICATION OF RECEPTORS - adaptation NONADAPTING RECEPTORS WITH CONSTANT FIRING BY CONSTANT STIMULUS NONADAPTING – PAIN TONIC – SLOWLY ADAPTING With decrease of firing (AP frequency) by constant stimulus PHASIC– RAPIDLY ADAPTING With rapid decrease of firing (AP frequency) by constant stimulus ACCOMODATION – ADAPTATION CHARACTERISTICS OF PHASIC RECEPTORS ALTERATIONS OF THE MEMBRANE POTENTIAL ACTION POTENTIAL TRANSMEMBRANE POTENTIAL
    [Show full text]
  • Fast and Slow Synaptic Potentials Produced Ina Mammalian
    Proc. Nat!. Acad. Sci. USA Vol. 83, pp. 1941-1944, March 1986 Neurobiology Fast and slow synaptic potentials produced in a mammalian sympathetic ganglion by colon distension (visceral afferent/inferior mesenteric ganglion/noncholinergic) STEPHEN PETERS AND DAVID L. KREULEN Department of Pharmacology, University of Arizona Health Sciences Center, Tucson, AZ 85724 Communicated by C. Ladd Prosser, November 1, 1985 ABSTRACT Radial distension of the large intestine pro- way also comprises noncholinergic fibers; indeed, it remains duced a slow depolarization in a population of neurons in the to be determined whether noncholinergic slow EPSPs even inferior mesenteric ganglion of the guinea pig. The slow occur physiologically. potentials often occurred simultaneously with cholinergic fast We report here the discovery of a noncholinergic sensory potentials [(excitatory postsynaptic potentials (EPSPs)] yet pathway that projects from the distal colon to the inferior persisted in the presence of nicotinic and muscarinic choliner- mesenteric ganglion (1MG) of the guinea pig. This pathway, gic antagonists when all fast EPSPs were absent. The amplitude activated by colon distension, produces noncholinergic slow of the distension-induced noncholinergic slow depolarization depolarizations resembling nerve-evoked slow EPSPs in increased with increasing distension pressure. For distensions sympathetic ganglion cells. Often, distension of the colon of 1-min duration at pressures of 10-20 cm of water, the mean produced both an increase in cholinergic EPSPs and a slow depolarization amplitude was 3.4 mV. The slow depolarization depolarization, suggesting a simultaneous action of two was associated with an increase in membrane resistance, and cell. The prolonged periods ofcolon distension resulted in a tachyphylax- different neurotransmitters on a single ganglion is of the depolarization.
    [Show full text]
  • Neural Plasticity in the Brain During Neuropathic Pain
    biomedicines Review Neural Plasticity in the Brain during Neuropathic Pain Myeong Seong Bak 1, Haney Park 1 and Sun Kwang Kim 1,2,* 1 Department of Science in Korean Medicine, Graduate School, Kyung Hee University, Seoul 02447, Korea; [email protected] (M.S.B.); [email protected] (H.P.) 2 Department of Physiology, College of Korean Medicine, Kyung Hee University, Seoul 02447, Korea * Correspondence: [email protected]; Tel.: +82-2-961-0491 Abstract: Neuropathic pain is an intractable chronic pain, caused by damage to the somatosensory nervous system. To date, treatment for neuropathic pain has limited effects. For the development of efficient therapeutic methods, it is essential to fully understand the pathological mechanisms of neuropathic pain. Besides abnormal sensitization in the periphery and spinal cord, accumulating evidence suggests that neural plasticity in the brain is also critical for the development and mainte- nance of this pain. Recent technological advances in the measurement and manipulation of neuronal activity allow us to understand maladaptive plastic changes in the brain during neuropathic pain more precisely and modulate brain activity to reverse pain states at the preclinical and clinical levels. In this review paper, we discuss the current understanding of pathological neural plasticity in the four pain-related brain areas: the primary somatosensory cortex, the anterior cingulate cortex, the periaqueductal gray, and the basal ganglia. We also discuss potential treatments for neuropathic pain based on the modulation of neural plasticity in these brain areas. Keywords: neuropathic pain; neural plasticity; primary somatosensory cortex; anterior cingulate cortex; periaqueductal grey; basal ganglia Citation: Bak, M.S.; Park, H.; Kim, S.K.
    [Show full text]
  • Nervous Tissue
    Nervous Tissue • Controls and integrates all body activities within limits that maintain life • Three basic functions – sensing changes with sensory receptors • fullness of stomach or sun on your face – interpreting and remembering those changes – reacting to those changes with effectors • muscular contractions • glandular secretions 12-1 Major Structures of the Nervous System • Brain, cranial nerves, spinal cord, spinal nerves, ganglia, enteric plexuses and sensory receptors 12-2 Organization of the Nervous System • CNS is brain and spinal cord • PNS is everything else 12-3 Nervous System Divisions • Central nervous system (CNS) – consists of the brain and spinal cord • Peripheral nervous system (PNS) – consists of cranial and spinal nerves that contain both sensory and motor fibers – connects CNS to muscles, glands & all sensory receptors 12-4 Subdivisions of the PNS • Somatic (voluntary) nervous system (SNS) – neurons from cutaneous and special sensory receptors to the CNS – motor neurons to skeletal muscle tissue • Autonomic (involuntary) nervous systems – sensory neurons from visceral organs to CNS – motor neurons to smooth & cardiac muscle and glands • sympathetic division (speeds up heart rate) • parasympathetic division (slow down heart rate) • Enteric nervous system (ENS) – involuntary sensory & motor neurons control GI tract – neurons function independently of ANS & CNS 12-5 Neurons • Functional unit of nervous system • Have capacity to produce action potentials – electrical excitability • Cell body • Cell processes = dendrites
    [Show full text]
  • Bi 360 Week 4 Discussion Questions: Electrical and Chemical Synapses
    Bi 360 Week 4 Discussion Questions: Electrical and Chemical Synapses 1a) What is the difference between a non-rectifying electrical synapse and a rectifying electrical synapse? A non-rectifying electrical synapse allows information to flow between two cells in either direction (presynaptic cell postsynaptic cell and postsynaptic cell presynaptic cell). A rectifying electrical synapse allows information to flow in only one direction; positive current will flow in one direction which is equivalent to negative current flowing in the opposite direction. 1b) You are conducting a voltage clamp experiment to determine the properties of a synapse within the central nervous system. You conduct the experiment as follows: 1) You depolarize the presynaptic cell and record the voltage in both the pre- and the postsynaptic cell. 2) You hyperpolarize the presynaptic cell and record from the pre- and postsynaptic cell. 3) You depolarize the postsynaptic cell and record from the pre- and postsynaptic cell. 4) You hyperpolarize the postsynaptic cell and record from the pre- and postsynaptic cell. Analyze each piece of data shown below and determine what kind of synapse this is. How did you draw your conclusion? This is a rectifying electrical synapse. When you depolarize the presynaptic cell, there is a response in both the pre and post synaptic cell. When the postsynaptic cell is depolarized, however, there is a depolarization in the postsynaptic cell but no response in the presynaptic cell. A similar trend can be seen in the hyperpolarizing data but in the opposite direction. This means there must be a voltage dependent gate allowing positive current to flow in one direction while preventing it from flowing in the other.
    [Show full text]
  • 11 Introduction to the Nervous System and Nervous Tissue
    11 Introduction to the Nervous System and Nervous Tissue ou can’t turn on the television or radio, much less go online, without seeing some- 11.1 Overview of the Nervous thing to remind you of the nervous system. From advertisements for medications System 381 Yto treat depression and other psychiatric conditions to stories about celebrities and 11.2 Nervous Tissue 384 their battles with illegal drugs, information about the nervous system is everywhere in 11.3 Electrophysiology our popular culture. And there is good reason for this—the nervous system controls our of Neurons 393 perception and experience of the world. In addition, it directs voluntary movement, and 11.4 Neuronal Synapses 406 is the seat of our consciousness, personality, and learning and memory. Along with the 11.5 Neurotransmitters 413 endocrine system, the nervous system regulates many aspects of homeostasis, including 11.6 Functional Groups respiratory rate, blood pressure, body temperature, the sleep/wake cycle, and blood pH. of Neurons 417 In this chapter we introduce the multitasking nervous system and its basic functions and divisions. We then examine the structure and physiology of the main tissue of the nervous system: nervous tissue. As you read, notice that many of the same principles you discovered in the muscle tissue chapter (see Chapter 10) apply here as well. MODULE 11.1 Overview of the Nervous System Learning Outcomes 1. Describe the major functions of the nervous system. 2. Describe the structures and basic functions of each organ of the central and peripheral nervous systems. 3. Explain the major differences between the two functional divisions of the peripheral nervous system.
    [Show full text]
  • In a Sucrose Gap Apparatus to a Ca+ + -Free Ringer Solution
    Jap. J. Physiol., 23, 183-197, 1973 EFFECTS OF REDUCING THE EXTRACELLULAR CALCIUM CONCENTRATION ON THE RESTING POTENTIAL OF FROG'S SKELETAL MUSCLE FIBERS* G. B. FRANK and F. INOUE Department of Pharmacology, The University of Alberta, Edmonton, Canada Summary Exposing one end of a frog's toe muscle (ex. dig. long. IV) in a sucrose gap apparatus to a Ca+ + -free Ringer solution resulted in a depolarization of about 15 mV in about 20-25 min (or 40-45 min in a choline Ringer solution) with very little further depolarization with continued exposure (1 hr or more). As little as 0.05 mm Ca+ + was sufficient to prevent or greatly reduce the depolarization. Means and frequency histograms of membrane potentials recorded with intracellular microelectrodes were plotted for fixed time periods of exposure to 0-Ca+ + The mean depolarizations were between 12 and 35 mV when tested 15 min after exposure to 0-Ca+ + but were only about 10-15 mV when first tested after a 1-hr exposure; the maximum fall observed was about 55 mV after 90 min and 4 periods of sampling. The most consistent change produced by 0-Ca+ + was a flattening and broadening of the frequency histogram. These results suggest that the large falls (>20 mV) in frog' skeletal muscle membrane potentials in 0-Ca+ + solutions seen here and often reported by other workers are an artifact produced by the intracellular microelectrodes on the cell membranes made fragile by the reduction in membrane Ca+ + In a detailed study of the effects of changes in extracellular calcium concen- trations on the resting and action potentials of toad skeletal muscle fibers using intracellular microelectrodes, IsHIKo and SATO(1957) observed in a few experi- ments that the resting potentials were reduced and the fibers became inexcitable after about 1 hr in a calcium-free solution.
    [Show full text]
  • A Dissertation Entitled the Induction of Traumatic Brain Injury by Blood
    A Dissertation entitled The Induction of Traumatic Brain Injury by Blood Brain Barrier Disruption by Mark D. Skopin Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Engineering ________________________________________________________ Dr. Scott C. Molitor, Ph.D., Committee Chair ________________________________________________________ Dr. Ragheb Assaly, M.D., Committee Member ________________________________________________________ Dr. Ronald L. Fournier, Ph.D., Committee Member ________________________________________________________ Dr. Hermann von Grafenstein, Ph.D., Committee Member ________________________________________________________ Dr. Patricia A. Relue, Ph.D., Committee Member ________________________________________________________ Dr. Patricia R. Komuniecki, Ph.D., Dean College of Graduate Studies The University of Toledo May 2011 Copyright 2011, Mark D. Skopin This document is copyrighted material. Under copyright law, no parts of this document may be reproduced without the expressed permission of the author. An Abstract of The Induction of Traumatic Brain Injury by Blood Brain Barrier Disruption by Mark D. Skopin Submitted to the Graduate Faculty as partial fulfillment of the requirements for the Doctor of Philosophy Degree in Engineering University of Toledo May 2011 Animal models of traumatic brain injury (TBI) are utilized for the study of underlying mechanisms and for the development of potential therapeutics. Traditional TBI models apply concussive
    [Show full text]
  • Evidence for Newly Generated Interneurons in the Basolateral Amygdala of Adult Mice
    OPEN Molecular Psychiatry (2018) 23, 521–532 www.nature.com/mp ORIGINAL ARTICLE Evidence for newly generated interneurons in the basolateral amygdala of adult mice DJ Jhaveri1,2,5, A Tedoldi1,5, S Hunt1, R Sullivan1, NR Watts3, JM Power4, PF Bartlett1,6 and P Sah1,6 New neurons are continually generated from the resident populations of precursor cells in selective niches of the adult mammalian brain such as the hippocampal dentate gyrus and the olfactory bulb. However, whether such cells are present in the adult amygdala, and their neurogenic capacity, is not known. Using the neurosphere assay, we demonstrate that a small number of precursor cells, the majority of which express Achaete-scute complex homolog 1 (Ascl1), are present in the basolateral amygdala (BLA) of the adult mouse. Using neuron-specific Thy1-YFP transgenic mice, we show that YFP+ cells in BLA-derived neurospheres have a neuronal morphology, co-express the neuronal marker βIII-tubulin, and generate action potentials, confirming their neuronal phenotype. In vivo, we demonstrate the presence of newly generated BrdU-labeled cells in the adult BLA, and show that a proportion of these cells co-express the immature neuronal marker doublecortin (DCX). Furthermore, we reveal that a significant proportion of GFP+ neurons (~23%) in the BLA are newly generated (BrdU+) in DCX-GFP mice, and using whole-cell recordings in acute slices we demonstrate that the GFP+ cells display electrophysiological properties that are characteristic of interneurons. Using retrovirus-GFP labeling as well as the Ascl1CreERT2 mouse line, we further confirm that the precursor cells within the BLA give rise to mature and functional interneurons that persist in the BLA for at least 8 weeks after their birth.
    [Show full text]