Quantal analysis of excitatory postsynaptic potentials induced in hippocampal neurons by activation of granule cells

1982 ◽  
Vol 46 (2) ◽  
pp. 170-176 ◽  
Author(s):  
C. Yamamoto
1992 ◽  
Vol 67 (3) ◽  
pp. 728-737 ◽  
Author(s):  
G. G. Hwa ◽  
M. Avoli

1. Intracellular recording techniques were used to investigate the physiological and pharmacological properties of stimulus-induced excitatory postsynaptic potentials (EPSPs) recorded in regular-spiking cells located in layers II/III of rat sensorimotor cortical slices maintained in vitro. 2. Depending on the strength of the extracellular stimuli, a pure EPSP or an EPSP-inhibitory postsynaptic potential sequence was observed under perfusion with normal medium. The EPSPs displayed short latency of onset [2.4 +/- 0.7 (SD) ms] and were able to follow repetitive stimulation (tested less than or equal to 5 Hz). Variation of the membrane potential (Vm) revealed two types of voltage behavior for the short-latency EPSP. The first type decreased in amplitude with depolarization and increased in amplitude with hyperpolarization. In contrast, the second type behaved anomalously by increasing and decreasing in size after depolarization and hyperpolarization, respectively. 3. Several experimental procedures were carried out to investigate the mechanism underlying the anomalous voltage behavior of the EPSP. Results indicated that this type of Vm dependency could be mimicked by an intrinsic response evoked by a brief pulse of depolarizing current and could be abolished by N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (50 mM). Furthermore, the EPSP was not sensitive to the N-methyl-D-aspartate (NMDA) receptor antagonist 3-((+-)-2-carboxypiperazin-4-yl)-propyl-1-phosphonate (CPP, 10 microM). Thus the anomalous voltage relationship of the neuronal membrane. 4. The involvement of non-NMDA receptors in excitatory synaptic transmission was investigated with their selective antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 1-10 microM). This drug greatly reduced or completely blocked the EPSP in a dose-dependent manner (1-10 microM). The IC50 for the CNQX effect was approximately 2 microM. In the presence of CNQX (10 microM) and glycine (10 microM), synaptic stimulation failed to elicit firing of action potential. However, a CPP-sensitive EPSP was observed. 5. When synaptic inhibition was reduced by low concentration of bicuculline methiodide (BMI, 1-2 microM), extracellular stimulation revealed late EPSPs (latency to onset: 10-30 ms) that were not discernible in normal medium. Similar to the short-latency EPSP, the Vm dependency displayed by this late EPSP could be modified by inward membrane rectifications. The late EPSP appeared to be polysynaptic in origin because 1) its latency of onset was long and variable and 2) it failed to follow repetitive stimuli delivered at a frequency that did not depress the short-latency EPSP.(ABSTRACT TRUNCATED AT 400 WORDS)


1983 ◽  
Vol 218 (1210) ◽  
pp. 95-110 ◽  

(i) Following previous work on the morphological and physiological properties of the two distal joints (J2, J3) of the atenna of the rock lobster Palinurus vulgaris , the mechanical, muscular and proprioceptive organization of the two proximal joints between the antennal segments S1 and S2 (J1) and between S1 and the cephalothorax (J0) have now been studied. (ii) Articulated by two classical condyles, J1 moves in a mediolateral plane. One external rotator muscle (ER) and three internal rotator muscles (IR1, IR2, IR3) subserve its movements. J0 is articulated by two different systems: a classical ventrolateral condyle and a complex sliding system constituted by special cuticular structures on the dorsomedial side of the S1 segment and on the rostrum between the two antennae. J0 moves in the dorsoventral plane by means of a levator muscle (Lm) and a depressor muscle (Dm). A third muscle, the lateral tractor muscle (LTm), associated with J0 and lying obliquely across S1, may modulate the level of friction between the S1 segment and the rostrum. (iii) Proprioception in J1 is achieved by a muscle receptor organ AMCO-J1 (antennal myochordotonal organ for the J1 joint) associating a small accessory muscle (S1.am) located in the proximal part of the S1 segment and a chordotonal organ inserted proximally on the S1.am muscle and distally on the S2 segment. J0 proprioception is ensured by a simple chordotonal organ (CO-J0) located in the anterior part of the cephalothorax. (iv) The S1.am muscle is innervated by three motoneurons characterized by their very small diameters and inducing respectively tonic excitatory postsynaptic potentials, phasic excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Anatomical and physiological observations suggest functional correlation between S1.am and IR1 motor innervation. (v) Mechanical and muscular organization of J0 and J1 are compared with that of the other joints of the antenna. The properties of the AMCO-J1 proprioceptor are discussed in relation to the other muscle receptor organs described in crustaceans.


1980 ◽  
Vol 86 (1) ◽  
pp. 87-97
Author(s):  
PETER SIMMONS

Both of the descending contralateral movement detector (DCMD) neurones of Schistocerca americana gregaria, which respond to stimulation of the contralateral eye or to loud noises, mediate excitatory postsynaptic potentials in most ipsilateral flight motoneurones.


1996 ◽  
Vol 75 (5) ◽  
pp. 2089-2098 ◽  
Author(s):  
H. Golan ◽  
Y. Grossman

1. The cytosolic concentration of a neurotransmitter is believed to be an important factor determining its release. The effects of 3-mercaptopropionic acid (MP) and aminooxyacetic acid (AOAA), glutamate decarboxylase (GAD) blockers, on GABAergic postsynaptic and presynaptic inhibitory neurotransmission were examined in the crayfish (Procambarus clarkii) opener neuromuscular synapses. 2. Intracellular recordings of evoked excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) as well as loose macropatch clamp measurements of excitatory postsynaptic currents (EPSCs) and inhibitory postsynaptic currents (IPSCs) were used to evaluate the effects of the drugs, which were applied exclusively to the nerve bundle. 3. Under normal conditions, a stimulus train to the inhibitor preceding the excitor stimulation elicited a large reduction in EPSP amplitude in a time interval-dependent manner. This inhibition is effected by postsynaptic as well as presynaptic processes. 4. Treatment with MP or AOAA decreased the IPSP amplitude and its altered conductance but had no effect on the IPSP reversal potential or the resting potential of the cell. They did, however, slightly increase the Rin of the fiber. 5. Quantal analysis of single IPSCs revealed that GAD blockers increased the number of failures and thus reduced quantal content (m), diminished the probability of release (p), but did not affect the quantum current (q) or the statistical parameter (n), believed to be the number of available active zones. 6. Quantal analysis of EPSCs, released after interaction with the inhibitor, revealed a reduction in m without any effect on q. GAD blockers greatly reduced the efficacy of this inhibition without affecting the EPSC q. 7. GAD blockers increased the output of the excitor release sites by the following mechanisms: 1) increased EPSC, 2) increased EPSC facilitation, or 3) enhancement of spontaneous activity (miniature EPSCs). 8. Short time incubation with picrotoxin and CGP-35348 eliminated IPSCs and evoked inhibition. However, longer exposure (90 min) increased the excitor responses, similarly to the effects of GAD blockers. 9. Baclofen, a gamma-aminobutyric acid-B (GABAB) agonist, antagonized AOAA effects on evoked inhibition. 10. These results demonstrate that GAD blockers decrease postsynaptic and presynaptic inhibition by reducing both tonic and evoked release, most likely by diminishing p. 11. The reduction in GABA synthesis and release revealed a complex mechanism for GABAergic metabotropic regulation of inhibition efficacy and the release from the excitor glutamatergic terminals.


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