The non-impulsive stretch-receptor complex of the crab: a study of depolarization-release coupling at a tonic sensorimotor synapse

A new preparation for the study of synaptic transmission is described from the thoracic ganglion of the crab Callinectes sapidus . The central anatomy of the nonimpulsive stretch-receptor neurons of the thoracic-coxal joint and that of the promotor motoneurons with which they form synaptic junctions was studied with intracellular cobalt staining and light and electron microscopy. Attention was centred on the interaction of the stretch-receptor T-fibre and the four large motoneurons supplying the promotor muscle which have their cell-bodies on the dorsal surface of the ganglion. The presynaptic terminal region of the T-fibre appeared to be a simple cylinder in form with a diameter of 40-60 μm and containing large stores of synaptic vesicles at its periphery, opposite the complex of motoneuron dendrites. The transmission characteristics of the junctions between receptor cell and motoneurons were studied by transmembrane current injection into the isolated T-fibre by means of a sucrose gap and simultaneous intracellular recording with microelectrodes from the presynaptic terminal and the somata of postsynaptic cells. It was shown that depolarization-release coupling in the T-fibre has similar properties to those that have been demonstrated in the squid giant synapse, with the same values for ‘threshold’, peak release and ‘suppression potential’. The crab synapses differ from that of the squid in that they normally transmit prolonged, graded depolarizations (i.e. receptor potentials) which are decrementally conducted from the periphery. Consistent with this role, the junctions were found to be capable of continuous tonic transmission over many seconds without the strong depletion seen in more phasic synapses. In a study of the relation between the synaptic properties and the stretch reflex it was shown that some of the time- and amplitude-dependent behaviour of the overall reflex can be encoded at the level of the synaptic transmission, largely through the parameter of transmitter availability. Conduction of electrical signals in the proximal and presynaptic part of the sensory fibre was also investigated. Transient responses to step depolarizing currents in the fibre indicate the existence of a mechanism for the partial compensation of capacitative distortion in the decrementally conducted receptor potential. This is the first example of intracellular recording from presynaptic terminals of nonimpulsive neurons with simultaneous monitoring of postsynaptic potential changes, allowing for a direct analysis of depolarization-release coupling characteristics. The use of the preparation for further study of synaptic physiology and sensorimotor systems is discussed.

2010 ◽  
Vol 34 (2) ◽  
pp. 115-116 ◽  
Author(s):  
Erik Montagna ◽  
Adriana M. S. de Azevedo ◽  
Camilla Romano ◽  
Ronald Ranvaud

Even students that obtain a high grade in neurophysiology often carry away a serious misconception concerning the final result of the complex set of events that follows the arrival of an action potential at the presynaptic terminal. The misconception consists in considering that “at a synapse, information is passed on from one neuron to the next” is equivalent to (and often expressed explicitly as) “the action potential passes from one neuron to the next.” More than half of four groups of students who were asked to comment on an excerpt from a recent physiology textbook that openly stated the misconception had no clear objection to the text presented. We propose that the first culprit in generating this misconception is the term “synaptic transmission,” which promotes the notion of transferring something or passing something along (implicitly unchanged). To avoid establishing this misconception, the first simple suggestion is to use words like “synaptic integration” rather than “synaptic transmission” right from the start. More generally, it would be important to focus on the function of synaptic events rather than on rote listing of all the numerous steps that are known to occur, which are so complex as to saturate the mind of the student.


Physiology ◽  
1994 ◽  
Vol 9 (2) ◽  
pp. 59-64 ◽  
Author(s):  
J Vautrin

When quantal synaptic transmission was discovered four decades ago, elementary transmitter releases initially were assigned to individual activity of presynaptic terminal units. Soon after an alternative hypothesis was proposed: elementary transmitter packets are preformed in specialized vesicles and released by exocytosis. Although the latter representation largely prevails, data are not conclusive.


2019 ◽  
Vol 121 (3) ◽  
pp. 881-892 ◽  
Author(s):  
David D. Kline ◽  
Sheng Wang ◽  
Diana L. Kunze

Chronic intermittent hypoxia (CIH) reduces afferent-evoked excitatory postsynaptic currents (EPSCs) but enhances basal spontaneous (s) and asynchronous (a) EPSCs in second-order neurons of nucleus tractus solitarii (nTS), a major area for cardiorespiratory control. The net result is an increase in synaptic transmission. The mechanisms by which this occurs are unknown. The N-type calcium channel and transient receptor potential cation channel TRPV1 play prominent roles in nTS sEPSCs and aEPSCs. The functional role of these channels in CIH-mediated afferent-evoked EPSC, sEPSC, and aEPSC was tested in rat nTS slices following antagonist inhibition and in mouse nTS slices that lack TRPV1. Block of N-type channels decreased aEPSCs in normoxic and, to a lesser extent, CIH-exposed rats. sEPSCs examined in the presence of TTX (miniature EPSCs) were also decreased by N-type block in normoxic but not CIH-exposed rats. Antagonist inhibition of TRPV1 reduced the normoxic and the CIH-mediated increase in sEPSCs, aEPSCs, and mEPSCs. As in rats, in TRPV1+/+ control mice, aEPSCs, sEPSCs, and mEPSCs were enhanced following CIH. However, none were enhanced in TRPV1−/− null mice. Normoxic tractus solitarii (TS)-evoked EPSC amplitude, and the decrease after CIH, were comparable in control and null mice. In rats, TRPV1 was localized in the nodose-petrosal ganglia (NPG) and their central branches. CIH did not alter TRPV1 mRNA but increased its protein in NPG consistent with an increased contribution of TRPV1. Together, our studies indicate TRPV1 contributes to the CIH increase in aEPSCs and mEPSCs, but the CIH reduction in TS-EPSC amplitude occurs via an alternative mechanism. NEW & NOTEWORTHY This study provides information on the underlying mechanisms responsible for the chronic intermittent hypoxia (CIH) increase in synaptic transmission that leads to exaggerated sympathetic nervous and respiratory activity at baseline and in response to low oxygen. We demonstrate that the CIH increase in asynchronous and spontaneous excitatory postsynaptic currents (EPSCs) and miniature EPSCs, but not decrease in afferent-driven EPSCs, is dependent on transient receptor potential vanilloid type 1 (TRPV1). Thus TRPV1 is important in controlling nucleus tractus solitarii synaptic activity during CIH.


1973 ◽  
Vol 62 (1) ◽  
pp. 77-86 ◽  
Author(s):  
Peter Hillman ◽  
F. A. Dodge ◽  
S. Hochstein ◽  
B. W. Knight ◽  
B. Minke

The recovery in the dark of the early receptor potential, as a direct manifestation of the state of the visual pigments, has been studied by intracellular recording in the ventral photoreceptors of Limulus and lateral photoreceptors of Balanus. The recovery is exponential with 1/e time constants of about 80 ms at 24°C for both preparations and 1800 ms at 4°C for Balanus. The 24°C rate extrapolates to total recovery of the pigment within 2 s. The later part of the dark adaptation of the late receptor potential, which may take from seconds to minutes in these preparations, appears thus to be unrelated to the state of the pigment.


1972 ◽  
Vol 60 (2) ◽  
pp. 121-147 ◽  
Author(s):  
Richard L. Chappell ◽  
John E. Dowling

Intracellular responses from receptors and postsynaptic units have been recorded in the median ocellus of the dragonfly. The receptors respond to light with a graded, depolarizing potential and a single, tetrodotoxin-sensitive impulse at "on." The postsynaptic units (ocellar nerve dendrites) hyperpolarize during illumination and show a transient, depolarizing response at "off." The light-evoked slow potential responses of the postsynaptic units are not altered by the application of tetrodotoxin to the ocellus. It appears, therefore, that the graded receptor potential, which survives the application of tetrodotoxin, is responsible for mediating synaptic transmission in the ocellus. Comparison of pre- and postsynaptic slow potential activity shows (a) longer latencies in postsynaptic units by 5–20 msec, (b) enhanced photosensitivity in postsynaptic units by 1–2 log units, and (c) more transient responses in postsynaptic units. It is suggested that enhanced photosensitivity of postsynaptic activity is a result of summation of many receptors onto the postsynaptic elements, and that transients in the postsynaptic responses are related to the complex synaptic arrangements in the ocellar plexus to be described in the following paper.


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