PubMed Health⌕ Search

Biomedical subjects

S Roper

Publications and source records attributed to S Roper.

29 records · Page 2Linked to original sources
PubMed1976

Synaptic organization and acetylcholine sensitivity of multiply innervated autonomic ganglion cells.

The principal cells of the mudpuppy cardiac ganglion receive synapses from three sources: vagal axons, interneurons and axon collaterals from other principal cells. The simplicity of the structural organization and the visual clarity in the living preparation provide favorable conditions for examining the function of these synapses and how different classes of synapses on the same cell influence its function. We have studied the sensitivity of the principal cells to iontophoretically applied acetylcholine--the transmitter at synapses made by the vagal axons and by postganglionic axon collaterals from other principal cells. In normal ganglia, the ACh sensitivity on the cell surface is highest at the region of synapses. Partial denervation, produced by severing the vagus nerves, results in an increased ACh sensitivity in nonsynaptic areas but does not appear to affect synaptic transmission at the remaining synapses.

Acetylcholine↗
PubMed1976

An electrophysiological study of chemical and electrical synapses on neurones in the parasympathetic cardiac ganglion of the mudpuppy, Necturus maculosus: evidence for intrinsic ganglionic innervation.

1. The cardiac ganglion of the mudpuppy is situated on a thin sheet of tissue. Two nerve cell types can be distinguished readily in the living preparation - principal cells and smaller interneurones which synapse with the principal cells. The purpose of this study was to investigate synaptic transmission and the functional organization of neuronal connections of ganglion cells with intracellular micro-electrodes. 2. Stimulation of the preganglionic, vagus, nerves evoked a large excitatory response in principal cells. About three quarters of these neurones were innervated by a single vagal axon. The remaining cells received two or more preganglionic nerve fibres. 3. The quantum content of vagal excitatory post-synaptic potentials (e.p.s.p.s) was measured. Normally, the e.p.s.p. was suprathreshold and consisted of about twenty-two quanta, whereas only about nine quanta were required to reach threshold and initiate an action potential. 4. Intracellular stimulation of principal cells evoked e.p.s.p.s in neighbouring principal cells. The responses were blocked by cholinergic antagonists. These potentials were caused by excitation of principal cell axon collateral synapses. 5. Principal cells also formed electrical junctions with each other. These electrical junctions were very weak. Although they transmitted slow potential changes, only a small response was recorded in one cell when an electrically coupled neighbouring cell fired an impulse. The resistance of the electrical junction between principal cells was calculated to be about 5-8 X 10(8) omega. 6. Stable penetrations of interneurones were only rarely achieved, making it difficult to study their functional relationship to principal cells. Action potentials were recorded from interneurones in a few instances. 7. These data demonstrate that parasympathetic ganglion cells in the heart of the mudpuppy receive innervation from more than one source involving both chemical and electrical synapses, and that some of the synapses are intrinsic to the ganglion.

Action Potentials↗
PubMed1976

The acetylcholine sensitivity of the surface membrane of multiply-innervated parasympathetic ganglion cells in the mudpuppy before and after partial denervation.

1. The surface chemosensitivity to iontophoretically applied acetylcholine (ACh) of single nerve cells in the cardiac ganglion of the mudpuppy was examined. 2. Some synapses on the neurones can be recognized in the living preparation with differential interference contrast optics. Identified synaptic regions of the ganglion cells were more sensitive to ACh than were other areas. The mean sensitivity of synaptic areas was 509 mV/nC, but that of random spots on the cell surface (which were mainly non-synaptic) was only 190 mV/nC. The mean rise time of ACh responses at synapses was 23 msec and at random spots was 36 msec. These data suggest that the density of ACh receptors is highest under the synapses on the post-synaptic membrane. 3. When some, but not all, of the presynaptic terminals on the ganglion cells are destroyed by cutting the vagus nerve, the sensitivity of the entire surface membrane to applied ACh increases. This increase in sensitivity reaches a maximum about 4-6 weeks after the operation. 4. Synaptic transmission at excitatory collateral synapses which remain after vagal degeneration is not altered by this hypersensitivity. 5. Neurones from ganglia which have been isolated and maintained in organ culture also become hypersensitive to applied ACh. this heightened chemosensitivity deveoops much faster in vitro; hypersensitivity in cultured ganglia becomes manifest within 4-5 days, in contrast with 4-6 weeks after vagus degeneration in vivo.

Acetylcholine↗
PubMed1973

The membrane effects, and sensitivity to strychnine, of neural inhibition of the Mauthner cell, and its inhibition by glycine and GABA.

1. Anionic conductance changes in Mauthner neurones of goldfish were measured during synaptically evoked inhibition and inhibition caused by iontophoretic application of the putative inhibitory transmitters glycine and gamma-aminobutyric acid (GABA).2. The effects of either amino acid were indistinguishable from those of the neural inhibitory transmitter(s). The membrane permeability during the neural or drug response was increased to Br(-), Cl(-), I(-), SCN(-), NO(3) (-), ClO(3) (-), and formate (HCOO(-)), but not to HCO(3) (-), BrO(3) (-), IO(3) (-), SO(4) (-), HPO(4) (-), H(2)PO(4) (-), acetate and citrate.3. Strychnine was injected intramuscularly, iontophoretically, or applied topically to the exposed brain in order to compare quantitatively its ability to prevent inhibition evoked by synaptic activation and by pharmacological means. Inhibitions were measured by the increase in membrane conductance.4. Strychnine, at concentrations just adequate to block completely the late collateral inhibition (LCI) and crossed VIII nerve inhibition, had little effect on the pharmacological inhibition caused by glycine, and sometimes there was no detectable effect at all. In one experiment even a local iontophoretic application of strychnine in a sufficient dose to diffuse over the cell and block the LCI almost completely, merely halved the effect of a small dose of glycine applied to the same localized region of the membrane.5. Higher concentrations of strychnine than those necessary to block synaptically evoked inhibition would reduce the effect of glycine but not that of GABA. The evidence indicated that any apparent effect of strychnine upon GABA could be explained by displacement of the GABA-containing iontophoretic pipette.6. The glycine-blocking action of iontophoretic pulses of strychnine was of relatively very slow onset and long duration compared to the effects of pulses of glycine and GABA.7. These findings can be interpreted as either (1) strychnine has a presynaptic action, preventing the release of inhibitory neurotransmitter, in addition to its less potent post-synaptic one in blocking pharmacological inhibition, or (2) strychnine acts entirely post-synaptically, but the physiological transmitter action differs from that of glycine and GABA in being considerably more sensitive to strychnine antagonism. In either case, the use of strychnine as evidence for the claim that glycine is an inhibitory neurotransmitter at the Mauthner cell is questionable.

Aminobutyrates↗
PubMed1973

Analysis of Mauthner cell responses to iontophoretically delivered pulses of GABA, glycine and L-glutamate.

1. The intracellularly recorded responses of goldfish Mauthner neurones to iontophoretically applied pulses of amino acids have been analysed: their time courses have been compared with each other, and with those predicted from diffusion theory.2. The rise time of the response to GABA is slower than that to glycine or L-glutamate. The response curves of the latter substances were very similar, and unlike that of GABA were markedly affected by increasing the distance of pipette-tip from the membrane. The results suggest that the time course of the responses to glycine and L-glutamate are determined mainly by free diffusion in the brain tissue (at least within about 200 mum of the cell), while that to GABA must be rate-limited by other factors, e.g. drug-receptor activation time.3. The possibility that the responses are influenced by some desensitizing process was investigated by applying a second (test) drug pulse during the response to a prior conditioning one. In the case of glycine and of L-glutamate there was no attenuation of the response to a second pulse at any time. With GABA, however, the second response was reduced during the period of the conditioning response; the reduction was progressively less marked the later the test pulse occurred. A similar effect with GABA was seen when glycine was used as the test pulse. The responses to long-maintained drug pulses also indicated that for GABA, but not for glycine or glutamate, there seems to be some desensitizing process present.4. Calculated time courses of responses to brief pulses of glycine and of L-glutamate (based upon diffusion theory) differed somewhat from the observed curves, largely during the falling phase. However, when the calculations were based upon second-order reactions (two molecules of drug per receptor) the diffusion model gave results very like the observed ones.5. Possible implications of these results for the role these three amino acids may have as neuro-transmitters are mentioned.

Aminobutyrates↗