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P A Getting

Publications and source records attributed to P A Getting.

At least 37 records · Page 2Linked to original sources
PubMed1985

Thyrotropin-releasing hormone induces rhythmic bursting in neurons of the nucleus tractus solitarius.

The nucleus tractus solitarius (NTS) contains neurons that are part of the central neuronal network controlling rhythmic breathing movements in mammals. Nerve terminals within the NTS show immunoreactivity to thyrotropin-releasing hormone (TRH), a neuropeptide that has potent stimulatory effects on respiration. By means of a brainstem slice preparation in vitro, TRH induced rhythmic bursting in neurons in the respiratory division of the NTS. The frequency of bursting was voltage-dependent and could be reset by short depolarizing current pulses. In the presence of tetrodotoxin, TRH produced rhythmic oscillations in membrane potential whose frequency was also voltage-dependent. These observations suggest that TRH modulates the membrane excitability of NTS neurons and allows them to express endogenous bursting activity.

Action Potentials↗
PubMed1985

Mechanisms of pattern generation underlying swimming in Tritonia. IV. Gating of central pattern generator.

Swimming behavior in the marine mollusc Tritonia diomedea is episodic, consisting of a series of alternating dorsal and ventral flexions initiated by a brief sensory stimulus. The swim motor pattern is generated by a network formed of four groups of premotor interneurons: cerebral cell 2 (C2), dorsal swim interneurons (DSIs), and two types of ventral swim interneurons (VSI-A and VSI-B). The initiation and maintenance of swimming depends on the establishment of a long-lasting ramp depolarization in both the premotor, pattern-generating interneurons, and the motor neurons (i.e., flexion neurons). Voltage clamp was used to measure the membrane current responsible for the ramp depolarization. In all cell classes the current had two components: a tonic inward current, which decayed as the swim progressed, and phasic inward current waves, which provided the synaptic drive during each swim burst. The ramp current in the flexion neurons and in C2 was generated largely by activity within the interneuronal pattern-generating network (PGN). The ramp current could be mimicked by driving activity in the pattern-generating interneurons. In VSI-B, the tonic component of the ramp current was independent of activity within the PGN and appeared to be derived from the long-lasting effect of an extrinsic input. The phasic components of the ramp, however, were dependent on PGN activity. The phasic inward current waves were blocked when pattern generation was prevented. In addition, phasic inward currents similar to those occurring during swimming could be produced by driving the C2. The tonic component of the ramp current in a DSI was dependent both on extrinsic inputs and PGN activity. Extrinsic inputs appeared to control the first 10-15 s of the tonic current. At longer times, activity within the DSI population itself maintained the ramp current. When one DSI was driven in a quiescent preparation, all other DSIs were inhibited, yet the DSIs are known to be coupled by monosynaptic, reciprocal excitatory synapses. This effect could be explained by the action of an unidentified inhibitory interneuron (I-neuron), which was excited by DSIs and in turn inhibited all other DSIs. The DSIs were therefore coupled reciprocally by both monosynaptic excitation and polysynaptic inhibition. Activity in C2 switched the DSI-DSI interaction from inhibition to excitation by inhibiting the I-neuron.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1984

Firing pattern of neurons in the nucleus tractus solitarius: modulation by membrane hyperpolarization.

Neurons in the ventral region of the nucleus tractus solitarius (NTS) of guinea pigs were studied using an in vitro brainstem slice preparation. One group of neurons was characterized electrophysiologically by a delay between the onset of a depolarizing stimulus and the first spike. This delay could be as large as 760 ms and was modulated by the membrane potential level preceding the stimulus. The firing rate during the depolarizing stimulus was also modulated by the preceding membrane potential level. A fast transient outward current, similar to A-current in molluscan neurons, appeared to be responsible for the delay in firing while a slower calcium-activated potassium current affected the firing rate. These data suggest that intrinsic membrane properties may play an important role in determining the firing pattern of NTS neurons. In vivo, inhibitory synaptic inputs could modulate the expression of these intrinsic properties during subsequent excitation.

Action Potentials↗
PubMed1980

Ionic basis of presynaptic inhibitory potentials at crayfish claw opener.

1. Intracellular recordings from the claw opener excitor axon of the crayfish, Procambarus clarkii, were obtained near the terminal arborizations of the axon on the surface of the opener muscle. Rest potential in the excitor axon averaged --80 mV over 20 cells. Action-potential amplitude and duration averaged 100 mV and 2 ms, respectively. 2. A single action potential in the opener inhibitor axon produces a hyperpolarizing synaptic potential (average amplitude 0.3 mV) in the excitor axon. The apparent reversal potential of this inhibitory synaptic potential is approximately 5 mV more negative than rest in control saline. No excitor axons were observed to have depolarizing synaptic potentials at rest. 3. A decrease in external chloride concentration from 240 to 24 mM causes the apparent reversal potential to depolarize an average of 12 mV, with no change in rest potential. In low-chloride saline, the synaptic potential evoked by stimulation of the inhibitor axon becomes depolarizing. 4. An increase in external potassium concentration from 5 to 10 mM causes the apparent reversal potential to depolarize by 16 mV; however, rest potential depolarizes by 10 mV. Low external potassium has the opposite effects, causing both rest potential and the apparent reversal potential to hyperpolarize. 5. Presynaptic inhibition at the Procambarus claw opener neuromuscular junction appears to be mediated by a hyperpolarizing synaptic potential. The results of these experiments suggest that chloride serves as the charge for the presynaptic potential. The evidence for a direct involvement of potassium as a charge carrier is equivocal due to Donnan equilibrium effects involving Cl.

Animals↗
PubMed1979

Inactivation of delayed outward current in molluscan neurone somata.

1. Inactivation of delayed outward current was studied by voltage clamp of isolated neurone somata of the molluscs Archidoris and Anisodoris. During prolonged voltage clamp steps in normal artificial sea water delayed outward current rises to a peak and then declines to a non-zero steady-state. During repetitive clamp pulses at repetition rates slower than 2/sec, the amplitude of peak outward current in the second pulse is commonly less than the amplitude at the end of the preceding pulse, giving the impression of continued inactivation during the repolarized interval. We have termed this property cumulative inactivation. 2. Two components of delayed outward current were separated using tetraethyl ammonium ions (TEA) and cobalt ions (Co). External TEA blocks 90% of a voltage and time dependent outward current termed K current (IK). External Co blocks 85% of a Ca activated delayed outward current termed Ca current (ICa does not inactivate during prolonged or repetitive voltage clamp pulses. IK, however, inactivates during prolonged voltage clamp steps and shows cumulative inactivation during repetitive voltage clamp pulses. 3. Inactivation of IK is voltage and time dependent and does not require influx of Ca ions. 4. As measured by a prepulse method, the onset of inactivation is characterized by a two time constant process. Fast inactivation occurs with a time course comparable to the rate of rise of outward current and can account for 90% of total inactivation. 5. Recovery from inactivation is slow with a time constant approximately an order of magnitude slower than the onset of inactivation. 6. The current-voltage (I-V) curve for peak IK can be N-shaped, with a region of negative slope resistance in the range of +30 to +80 mV. The I-V curve for steady-state IK, however, shows little or no tendency to form a local maximum. 7. The pattern of delayed outward current varies considerably between cells. A major contributing factor to this variability appears to be the relative contributions of ICa and IK to delayed outward current.

Animals↗
PubMed1979

Mechanism of frequency-dependent broadening of molluscan neurone soma spikes.

1. Action potentials recorded from isolated dorid neurone somata increase in duration, i.e. broaden, during low frequency repetitive firing. Spike broadening is substantially reduced by external Co ions and implicates an inward Ca current. 2. During repetitive voltage clamp steps at frequencies slower than 1 Hz, in 100 mM-tetraethyl ammonium ions (TEA) inward Ca currents do not increase in amplitude. 3. Repetitive action potentials result in inactivation of delayed outward current. Likewise, repetitive voltage clamp steps which cause inactivation of delayed outward current also result in longer duration action potentials. 4. The frequency dependence of spike broadening and inactivation of the voltage dependent component (IK) of delayed outward current are similar. 5. Inactivation of IK is observed in all cells, however, only cells with relative large inward Ca currents show significant spike broadening. Spike broadening apparently results from the frequency dependent inactivation of IK which increases the expression of inward Ca current as a prominent shoulder on the repolarizing phase of the action potential. In addition, the presence of a prolonged Ca current increases the duration of the first action potential thereby allowing sufficient time for inactivation of IK.

Action Potentials↗