scholarly journals The amplitude, time course and charge of unitary excitatory post-synaptic potentials evoked in spinal motoneurone dendrites

1973 ◽  
Vol 234 (3) ◽  
pp. 665-688 ◽  
Author(s):  
R. Iansek ◽  
S. J. Redman
1992 ◽  
Vol 67 (6) ◽  
pp. 1698-1701 ◽  
Author(s):  
S. M. Thompson ◽  
B. H. Gahwiler

1. The effects of the gamma-aminobutyric acid (GABA) uptake blocker tiagabine on inhibitory synaptic potentials (IPSPs) were examined with microelectrode and whole-cell recording from CA3 pyramidal cells in rat hippocampal slice cultures. 2. Tiagabine (10-25 microM) greatly prolonged the duration of monosynaptic IPSPs elicited in the presence of excitatory amino acid antagonists but had no effect on their amplitude. Part of the prolonged time course resulted from a GABAB receptor-mediated component that was not detectable under control conditions. 3. The mean decay time constant of the underlying GABAA receptor-mediated synaptic current was increased from 16 to 250 ms. Spontaneous miniature IPSPs recorded with whole-cell clamp were unaffected by tiagabine. Pentobarbital sodium, in contrast, increased the decay time constant of both evoked and spontaneous GABAA-mediated currents. 4. Tiagabine (25 microM) inhibited spontaneous and evoked epileptiform bursting induced by increasing the extracellular potassium concentration to 8 mM. 5. We conclude that GABA uptake plays a significant role in determining the time course of evoked IPSPs and also limits the likelihood that GABAB receptors are activated.


2001 ◽  
Vol 86 (4) ◽  
pp. 1792-1802 ◽  
Author(s):  
Michael E. Hasselmo ◽  
Brian P. Fehlau

Activation of muscarinic receptors and GABABreceptors causes presynaptic inhibition of glutamatergic synaptic potentials at excitatory feedback connections in cortical structures. These effects may regulate dynamics in cortical structures, with presynaptic inhibition allowing extrinsic afferent input to dominate during encoding, while the absence of presynaptic inhibition allows stronger excitatory feedback during retrieval or consolidation. However, proposals for a functional role of such modulatory effects strongly depend on the time course of these modulatory effects; how rapidly can they turn off and on? In brain slice preparations of hippocampal region CA1, we have explored the time course of suppression of extracellularly recorded synaptic potentials after pressure pulse application of acetylcholine and GABA. Acetylcholine causes suppression of extracellular potentials with onset time constants between 1 and 2 s, and decay constants ranging between 10 and 20 s, even with very brief injection pulses. GABA causes suppression of extracellular potentials with onset time constants between 0.2 and 0.7 s, and decay time constants that decrease to values shorter than 2 s for very brief injection pulses. These techniques do not give an exact measure of the physiological time course in vivo, but they give a notion of the relative time course of the two modulators. The slow changes due to activation of muscarinic acetylcholine receptors may alter the dynamics of cortical circuits over longer intervals (e.g., between different stages of waking and sleep), setting dynamics appropriate for encoding versus consolidation processes. The faster changes in synaptic potentials caused by GABA could cause changes within each cycle of the theta rhythm, rapidly switching between encoding and retrieval dynamics during exploration.


1989 ◽  
Vol 61 (4) ◽  
pp. 681-687 ◽  
Author(s):  
B. Walmsley ◽  
R. Stuklis

1. As part of the ongoing studies on the time course of single-fiber synaptic potentials recorded in spinal neurons, a theoretical analysis of the effects of spatial and temporal dispersion of synaptic input to a neuronal cable model was undertaken. 2. Results were obtained using a simple R-C soma, equivalent dendritic cylinder cable model of a neuron. Synaptic input was represented by a current injection at various points on the dendritic cable. 3. Spatial dispersion of multiple inputs to the cable model generally produced somatic transients with smooth time courses that could be closely matched by a transient generated at a single input location, usually with a different current time course. 4. Temporal dispersion, representing nonsynchronous activation of multiple synaptic contacts at the same electrotonic location, generally resulted in somatic transients with an increased rise-time and a corresponding small increase in the half-width. The somatic transient generated by these temporally dispersed inputs could usually be well matched by a single input at a different location. 5. Addition of temporal dispersion to a spatially dispersed input produced variable results in which the rise-times and half-widths of somatically recorded transients could be either increased or decreased. 6. It is concluded that a detailed knowledge of both the spatial and temporal properties of synaptic input is essential to the interpretation of single-fiber synaptic potentials. Previous results on the amplitude and time course of single-fiber synaptic potentials recorded in spinal neurons are discussed in light of the present observations.


1997 ◽  
Vol 78 (5) ◽  
pp. 2772-2789 ◽  
Author(s):  
Bharathi Jagadeesh ◽  
Heidi Sue Wheat ◽  
Leonid L. Kontsevich ◽  
Christopher W. Tyler ◽  
David Ferster

Jagadeesh, Bharathi, Heidi Sue Wheat, Leonid L. Kontsevich, Christopher W. Tyler, and David Ferster. Direction selectivity of synaptic potentials in simple cells of the cat visual cortex. J. Neurophysiol. 78: 2772–2789, 1997. The direction selectivity of simple cells in the visual cortex is generated at least in part by nonlinear mechanisms. If a neuron were spatially linear, its responses to moving stimuli could be predicted accurately from linear combinations of its responses to stationary stimuli presented at different positions within the receptive field. In extracellular recordings, this has not been found to be the case. Although the extracellular experiments demonstrate the presence of a nonlinearity, the cellular process underlying the nonlinearity, whether an early synaptic mechanism such as a shunting inhibition or simply the spike threshold at the output, is not known. To differentiate between these possibilities, we have recorded intracellularly from simple cells of the intact cat with the whole cell patch technique. A linear model of direction selectivity was used to analyze the synaptic potentials evoked by stationary sine-wave gratings. The model predicted the responses of cells to moving gratings with considerable accuracy. The degree of direction selectivity and the time course of the responses to moving gratings were both well matched by the model. The direction selectivity of the synaptic potentials was considerably smaller than that of the intracellularly recorded action potential, indicating that a nonlinear mechanism such as threshold enhances the direction selectivity of the cell's output over that of its synaptic inputs. At the input stage, however, the cells apparently sum their synaptic inputs in a highly linear fashion. A more constrained test of linearity of synaptic summation based on principal component analysis was applied to the responses of direction-selective cells to stationary gratings. The analysis confirms that the summation in these cells is highly linear. The principal component analysis is consistent with a model in which direction selectivity in cortical simple cells is generated by only two subunits, each with a different receptive-field position and response time course. The response time course for each of the two subunits is derived for four analyzed cells. Each derived subunit is linear in spatial summation, suggesting that the neurons that comprise each subunit are either geniculate X-cells or receive their primary synaptic input from X-cells. The amplitude of the response of each subunit is linearly related to the contrast of the stimulus. The subunits are nonlinear in the time domain, however: the response to a stationary stimulus whose contrast is modulated sinusoidally in time is nonsinusoidal. The principal component analysis does not exclude models of direction selectivity based on more than two subunits, but such higher-order models would have to include the constraint that the extra subunits form a smooth continuum of interpolation between the properties derived from the two subunit solution.


Author(s):  
K.W. Lee ◽  
R.H. Meints ◽  
D. Kuczmarski ◽  
J.L. Van Etten

The physiological, biochemical, and ultrastructural aspects of the symbiotic relationship between the Chlorella-like algae and the hydra have been intensively investigated. Reciprocal cross-transfer of the Chlorellalike algae between different strains of green hydra provide a system for the study of cell recognition. However, our attempts to culture the algae free of the host hydra of the Florida strain, Hydra viridis, have been consistently unsuccessful. We were, therefore, prompted to examine the isolated algae at the ultrastructural level on a time course.


Author(s):  
P. Maupin-Szamier ◽  
T. D. Pollard

We have studied the destruction of rabbit muscle actin filaments by osmium tetroxide (OSO4) to develop methods which will preserve the structure of actin filaments during preparation for transmission electron microscopy.Negatively stained F-actin, which appears as smooth, gently curved filaments in control samples (Fig. 1a), acquire an angular, distorted profile and break into progressively shorter pieces after exposure to OSO4 (Fig. 1b,c). We followed the time course of the reaction with viscometry since it is a simple, quantitative method to assess filament integrity. The difference in rates of decay in viscosity of polymerized actin solutions after the addition of four concentrations of OSO4 is illustrated in Fig. 2. Viscometry indicated that the rate of actin filament destruction is also dependent upon temperature, buffer type, buffer concentration, and pH, and requires the continued presence of OSO4. The conditions most favorable to filament preservation are fixation in a low concentration of OSO4 for a short time at 0°C in 100mM sodium phosphate buffer, pH 6.0.


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