Biomedical subjects

D O Carpenter

Publications and source records attributed to D O Carpenter.

At least 109 records · Page 6Linked to original sources

PubMed1992

Dynamic changes in neuronal volume resulting from osmotic and sodium transport manipulations.

Electrophysiologic parameters such as input resistance and response to microperfusion of neurotransmitters vary under circumstances where neurons from isolated ganglia of Aplysia californica are subjected to either long-term (several hours) blockade of active sodium transport or to hypo- or hyperosmotic solutions. Since one of multiple possible events under these circumstances is neuronal volume changes, we have developed a system using cultured Aplysia neurons and confocal scanning laser microscopy to directly monitor cell volume when the osmolarity of the perfusing solution is altered and when sodium transport is blocked. Volume changes of greater than 30% were observed, accompanied by changes in surface area of greater than 15%. The volume increase secondary to sodium pump inhibition and hypotonic solutions and the volume decrease secondary to hypertonic solutions were reversible. Our results demonstrate that neuronal volume may change dramatically and raise the possibility that dynamic changes in neuronal cell volume may have physiological importance.

Animals↗

PubMed1991

Pb2+ blocks calcium currents of cultured dorsal root ganglion cells.

The divalent cation lead (Pb2+) blocks sustained and transient voltage sensitive calcium channel currents of cultured rat dorsal root ganglion cells. The IC50 for inhibition of the total peak current evoked by a step depolarization from -80 to 0 mV was 0.6 microM, compared to an IC50 of 2.2 microM for Cd2+. The current activated by a depolarization from -40 to 0 mV was inhibited by 50% by 1.0 microM Pb2+. Low threshold currents activated by a step from -100 to -30 mV were blocked by Pb2+ at higher concentrations (IC50 = 6 microM). The block progressed in the absence of channel activation and showed little voltage dependence. Peak sodium current was reduced by 6.6% at 1 microM Pb2+ while at 20 microM the peak current was reduced by 40% with marked slowing of the time course of activation. The potassium rectifier current was reduced by 4.1% at 1 microM Pb2+. Thus, Pb2+ selectively blocks calcium currents at concentrations in the range of those causing toxicity in man.

Animals↗

PubMed1991

Correlation of 125I-LSD autoradiographic labeling with serotonin voltage clamp responses in Aplysia neurons.

Autoradiographic receptor binding studies using 125I-LSD (2-[125I]lysergic acid diethyamide) revealed intense labelling on the soma of a symmetrically located pair of cells in the abdominal ganglion of Aplysia californica. This binding was blocked by micromolar concentrations of serotonin and lower concentrations of the serotonergic antagonists, cyproheptadine and mianserin (Kadan and Hartig, 1988). Electrophysiological investigation of responses to serotonin of neurons in the left upper quadrant, where one of the labeled neurons is located, revealed a range of serotonin responses. Cells L3 and L6 have a K+ conductance increase in response to serotonin that is not blocked by cyproheptadine or mianserin. Cells L2 and L4 have a biphasic response to serotonin: a Na+ conductance increase, which can be blocked by cyproheptadine and mianserin, followed by a voltage dependent Ca2+ conductance which is blocked by Co2+ but not the serotonergic antagonists. Cell L1, and its symmetrical pair, R1, have in addition to the Na+ and Ca2+ responses observed in L2 and L4, a Cl- conductance increase blocked by LSD, cyproheptadine and mianserin. LSD had little effect on the other responses. We conclude that the symmetrically located cells L1 and R1 have a Cl- channel linked to a cyproheptadine- and mianserin-sensitive serotonin receptor that is selectively labelled by 125I-LSD. This receptor has many properties in common with the mammalian serotonin 1C receptor.

Acetylcholine↗

PubMed1991

Appearance of NMDA receptors triggered by anoxia independent of voltage in vivo and in vitro.

Using rat hippocampus we have studied the pattern of neuronal death, abnormal discharge and loss of electrical excitability in slices prepared from animals subjected to bilateral, four-vessel cerebral anoxia and in slices prepared from normal animals that are subjected to anoxia in the recording chamber. As others have reported, pyramidal neurons in area CA1 are lost first after anoxia, while CA3 neurons have an intermediate sensitivity, and those in dentate are relatively anoxia-resistant. After anoxic damage to the intact animal, neurons in both CA1 and CA3 show abnormal bursting discharges in response to synaptic activation for several days, and then the response in CA1 decreases in amplitude and finally the area become unexcitable. While antagonists for N-methyl-D-aspartate (NMDA) receptors have essentially no effect on synaptic responses in control animals, they reduce the bursting responses and greatly depress the small responses in CA1 as neurons are becoming unexcitable after anoxia. With intracellular recording CA1 neurons from animals made transiently anoxic, in contrast to controls, show prolonged synaptic responses, the later components of which are blocked by NMDA antagonists. When slices from normal animals are subjected to anoxia such that excitability is totally lost over a period of about 10 min, there is no significant membrane depolarization during the anoxic episode and recovery of excitability occurs with reoxygenation. However, a period of hyperexcitability and bursting follows and electrical excitability is lost in CA1 but not CA3 neurons after about 90 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Lead and zinc block a voltage-activated calcium channel of Aplysia neurons.

1. The effects of Pb2+ and Zn2+ on the peak of the voltage-activated calcium current of Aplysia neurons were examined. Calcium currents were reversibly blocked by Pb2+ at concentrations that did not significantly affect potassium and sodium currents and by Zn2+ at concentrations associated with a delay and reduction of peak sodium and potassium currents. 2. The block by both was concentration dependent, and percentage blockade was reduced in elevated Ca2+. The threshold Pb2+ concentration for blockade in 20 mM Ca artificial sea water (ASW) was approximately 1 microM, whereas for Zn2+ it was 2 mM. The Hill coefficient for Pb2+ action was near 1.0 under all conditions, whereas for Zn2+ it was 1.4-1.6. 3. With addition of Pb2+, the voltage at which peak calcium current was generated shifted to hyperpolarized voltages, an effect similar to that caused by reduction of Ca2+ concentration in the absence of Pb2+. Zn2+ shifted the voltage at which peak current was generated in a depolarizing direction. 4. Pb2+ did not significantly change inactivation but shifted the voltage dependence of activation to hyperpolarized voltages in a dose-dependent manner. Zn2+ shifted both activation and inactivation in a depolarizing direction in a dose-dependent fashion. 5. The blockade of calcium currents by Pb2+ but not Zn2+ was highly voltage dependent and increased with depolarization. 6. Our results suggest that Pb2+ is a specific, potent, competitive, and reversible blocker of calcium currents. These observations are consistent with a competition by Pb2+ with Ca2+ at a binding site within the calcium channel. In contrast, the blockade of calcium currents by Zn2+ is probably through actions at fixed charge sites external to the channel.

Animals↗

PubMed1991

Effects of inorganic and triethyl lead and inorganic mercury on the voltage activated calcium channel of Aplysia neurons.

Using conventional two electrode voltage clamp techniques we have studied the effects of Pb2+, triethyl lead (TEL) and Hg2+ on voltage-activated calcium channels of Aplysia neurons and found that all three metals are potent inhibitors at micromolar concentrations. However, the time course of current reduction or block and its reversibility vary when comparing Pb2+ to TEL and Hg2+. With application of Pb2+ the calcium current decreases immediately and a steady state is reached within three to seven minutes, depending upon the concentration of Pb2+ (IC50 = 61 microM). The block was easily reversed upon wash out of Pb2+ with a time course similar to that of onset. Perfusion with either TEL (5 to 50 microM) or Hg2+ (5 to 200 microM) resulted only in a small reduction of current when the substances reached the cell membrane but with clear reduction within 2 min. The decrease continued at about the same speed for the total duration of the application. Upon washing there was no recovery of the response. At the onset of washing the rate of current decline stopped for several minutes, but then the current continued to decline at a slower rate in the absence of toxicant. Our data suggest that Pb2+ acts by a direct and reversible blockade of the calcium channel. In contrast TEL and Hg2+ act slowly and irreversibly to block calcium channels at concentrations which do not greatly affect membrane potential or resistance. In spite of the slow time course these substances are probably acting directly on the calcium channel.

Animals↗

PubMed1990

Zn2+ blocks the voltage activated calcium current of Aplysia neurons.

We have investigated the effect of Zn2+ on voltage-activated calcium currents of Aplysia neurons, using conventional two-electrode voltage-clamp techniques. The peak of these currents was reversibly reduced by Zn2+ (50% reduction at 3.75 mM; total block at 20 mM), while the current-voltage relation and the activation and inactivation curves were shifted to depolarized voltages. The effects of Zn2+ were concentration-dependent. The Hill coefficient was 1.62. The high concentrations required, the shift of the current-voltage relation and the effects on activation and inactivation are best explained by a charge-screening effect combined with a specific binding site for Zn2+ near the entrance of the channel.

Animals↗

PubMed1990

Differential effects of baclofen and gamma-aminobutyric acid (GABA) on rat piriform cortex pyramidal neurons in vitro.

1. The effects of baclofen and GABA on rat piriform cortex neurons were investigated electrophysiologically using a brain slice preparation. 2. At resting potential GABA depolarized and baclofen hyperpolarized the cell, probably through activation of Cl and K conductances acting at GABAA and GABAB receptors, respectively. 3. The GABAA receptors were concentrated on the apical and basal dendrites near the cell body, while the baclofen-sensitive GABA receptors were concentrated particularly on the basal dendrites. 4. The different distributions of receptor localization must have functional consequences which remain to be elucidated.

Animals↗

PubMed1990

Influences of trypsin and collagenase on acetylcholine responses of physically isolated single neurons of Aplysia californica.

1. The influences of enzyme treatments (trypsin and collagenase) on responses to perfused acetylcholine were examined on physically isolated single Aplysia neurons, using the voltage-clamp, internal perfusion, and rapid external perfusion technique. 2. During treatment with trypsin (0.025 to 0.1%) for 10 to 30 min at room temperature (22 to 25 degrees C), the peak amplitude of the Na current induced by acetylcholine increased in a time- and dose-dependent manner, and the decay in the continued presence of acetylcholine was slowed. This effect of trypsin treatment was irreversible after washing for 60 min without enzyme. 3. Edrophonium, a cholinesterase inhibitor, has previously been shown to augment the Na acetylcholine response in this preparation by inhibition of acetylcholinesterase. After treatment of the neuron with trypsin, the augmentation after edrophonium was abolished. Furthermore, in the presence of edrophonium, trypsin also failed to increase the response. The dose-response curve for acetylcholine after treatment of trypsin was similar to that in the presence of edrophonium. These results suggest that the modification of the current response by trypsin is a result of removal of cholinesterase activity from the membrane. 4. In contrast to the effects of trypsin, collagenase (0.03 to 0.1%) for 10 to 60 min did not change the current amplitude of the acetylcholine response. However, collagenase treatment did alter the kinetics of the acetylcholine response in a dose-dependent manner, in that the rate of decay was accelerated. A similar acceleration was seen in the acetylcholine responses on other neurons which were due to Cl or K currents, suggesting that the effect was independent on the type of channel. This effect of collagenase was reversible after 30 to 60 min of washing of the neuron. 5. In the presence of edrophonium or after the treatment with trypsin, collagenase still accelerated the current kinetics of the acetylcholine response, indicating that cholinesterase activity is not related to this effect. Furthermore, heated collagenase (presumably inactivated) had a similar action, suggesting that the enzymatic activity of collagenase is not related to the modification of the response. 6. These results suggest that Aplysia acetylcholinesterase is sensitive to trypsin but not to collagenase. However, the preparation of a collagenase used in these studies contains some factor which alters the response to acetylcholine, but this effect is reversible and unrelated to enzymatic activity.

Acetylcholine↗

PubMed1990

Lead inhibits the voltage-activated calcium current of Aplysia neurons.

Lead is a potent and reversible inhibitor of the voltage-dependent calcium current of Aplysia neurons in a concentration range (1-1000 microM) similar to that which elicits toxic effects in man. The threshold for inhibition is 1 microM and the dissociation constant about 90 microM. The inhibition is due to reduction of the peak current amplitude, and not due to alteration of the voltage dependence of the activation or inactivation. The effect of lead is specific to the calcium current as the delayed rectifier potassium and the sodium currents are not affected by concentrations of lead (200 microM) which give near-maximal inhibition. The calcium current of Aplysia neurons appears similar to the current flowing through the mammalian L-type calcium channel. This suggests that inhibition of the investigated calcium channel may contribute to the toxic effects of lead in mammals.

Animals↗

PubMed1990

Neural mechanisms of emesis.

Emesis is a reflex, developed to different degrees in different species, that allows an animal to rid itself of ingested toxins or poisons. The reflex can be elicited either by direct neuronal connections from visceral afferent fibers, especially those from the gastrointestinal tract, or from humoral factors. Emesis from humoral factors depends on the integrity of the area postrema; neurons in the area postrema have excitatory receptors for emetic agents. Emesis from gastrointestinal afferents does not depend on the area postrema, but probably the reflex is triggered by projections to some part of the nucleus tractus solitarius. As with a variety of other complex motor functions regulated by the brain stem, it is likely that the sequence of muscle excitation and inhibition is controlled by a central pattern generator located in the nucleus tractus solitarius, and that information from humoral factors via the area postrema and visceral afferents via the vagus nerve converge at this point. This central pattern generator, like those for motor functions such as swallowing, presumably projects to the various motor nuclei, perhaps through interneuronal pathways, to elicit the sequential excitation and inhibition that controls the reflex.

Animals↗

PubMed1989

Desensitization kinetics of a K+ acetylcholine response in Aplysia.

We have studied the process of acetylcholine receptor desensitization on Aplysia medial pleural neurons under voltage clamp conditions. Acetylcholine, applied by microperfusion, elicits a biphasic response on these neurons, a rapid component which reverses polarity at about -60 mV and is Cl-dependent, and a slower component which reverses at about -85 mV and is K-dependent. Both components show desensitization, and the present study focuses on the K-dependent component, which could be isolated by maintaining membrane potential at the Cl equilibrium potential or by blocking the Cl component pharmacologically. K-dependent acetylcholine responses on these neurons varied in regard to time to peak of response and rate of desensitization. While the rising phase of the response was always fitted by a single exponential process, times to peak were divided somewhat arbitrarily into three broad groups of fast (less than 3 s), medium (3-6 s) and slow (greater than 6 s). Desensitization of fast responses was best described by two exponential processes plus a constant, medium responses by a double exponential, and slow responses by single exponential plus a constant. The apparent dissociation constant of acetylcholine was 17.3 +/- 1.6 microM. The best fit of responses for a given cell remained constant over a range of acetylcholine doses, but the kinetics of both fast and slow components accelerated with dose and depolarization. The fast component of desensitization was very temperature dependent. In neurons where it was present it was abolished by cooling, while in neurons with no fast component at room temperature it would appear with warming. The time constant of the fast component varied inversely with temperature. The time constant of the slow component was maximal at 22-24 degrees C, and fell on either side of this temperature. These results suggest that receptor desensitization for acetylcholine K responses is, like Na-dependent responses, composed of two independent processes. When responses to the acetylcholine agonists, carbachol and arecoline, were compared to those of acetylcholine on fast-type neurons, the times to peak varied in the order acetylcholine less than carbachol less than arecoline. The carbachol response was best fitted by two exponential functions, while arecoline was best fitted by a single exponential plus a constant.

Acetylcholine↗

PubMed1989

Desensitization kinetics of a chloride acetylcholine response in Aplysia.

The kinetics of desensitization of acetylcholine-evoked Cl conductance increased response of Aplysia RC neurons of the abdominal ganglion were studied under voltage-clamp conditions for comparison with results of similar studies on acetylcholine Na and K responses. The response evoked by acetylcholine on RC neurons was an outward current at resting potential (about -45 mV) that reversed at about -65 mV and was blocked by D-tubocurarine and strychnine but not hexamethonium and was not activated by arecoline. From the current-voltage relation this response can be ascribed to a pure conductance increase to Cl. The apparent KD was 40.6 microM. Upon prolonged exposure to acetylcholine the response peaked within 200-400 ms, and then decayed to a plateau current in the continued presence of the agonist. The peak and plateau currents reversed at the same potential, indicating that there had not been significant redistribution of Cl. The current decay in every cell was best fit by a double exponential function plus a constant, and the average time constants were tau fast = 1.8 +/- 0.2 s and tau slow = 16.2 +/- 1.0 s. Both components were slowed by cooling. While tau fast did not change with dose, tau slow increased with dose. Both components accelerated with hyperpolarization and upon application of trifluoperazine (2 microM). These results are consistent with the interpretation that desensitization of the acetylcholine Cl response is composed of two independent processes. This conclusion is the same as that derived from studies of the acetylcholine Na and K responses, and is in general consistent with desensitization being a property of a common acetylcholine receptor, and independent of the ionic selectivity of the associated channel. There are, however, significant differences in voltage, temperature and trifluoperazine dependence of the two components of the three ionic responses which may reflect influence of the different ion channels and/or transduction mechanisms.

Acetylcholine↗

PubMed1989

Electrophysiological estimation of the actions of acetylcholinesterase inhibitors on acetylcholine receptor and cholinesterase in physically isolated Aplysia neurones.

1. The actions of representative cholinesterase inhibitors on the acetylcholine responses of physically isolated single neurones from the pedal ganglion of Aplysia californica were studied, using electrophysiological techniques and rapid agonist application to analyse both the inhibitory actions on the acetylcholine receptor-channel complex and the degree of inhibition of acetylcholinesterase activity on the same neurone. The inhibitors used were physostigmine, edrophonium and diisopropylfluorophosphate (DFP). 2. When selected neurones were suddenly exposed to 50 microM acetylcholine by a 'concentration clamp' technique a large Na-dependent inward current was initiated, and decayed in the continued presence of acetylcholine without external perfusion. However, if perfusion of the acetylcholine solution was reinitiated the current increased somewhat, indicating that the decay of current was due to some combination of receptor desensitization and local depletion of acetylcholine at the membrane by acetylcholinesterase. 3. With simultaneous application of acetylcholine (50 microM) and physostigmine (0.1 to 100 microM) there was a dose-dependent reduction of peak amplitude of the acetylcholine response. However, physostigmine at low concentrations (0.1 to 10 microM) caused a time-dependent increase in the current amplitude alone with a time- and dose-dependent inhibition of acetylcholinesterase activity. At the highest concentration of physostigmine (100 microM) acetylcholinesterase activity was abolished but the current peak was very depressed. After removal of physostigmine from the bathing solution, the current amplitude decreased toward the control at the two lower concentrations as the inhibitory actions on acetylcholinesterase activity were almost reversible, while at the two higher concentrations (10 and 100 microM) the current increased and the inhibition of acethylcholinesterase remained. 4. When acetylcholine (50 microM) and edrophonium (0.1 to 10 microM) were applied simultaneously, edrophonium caused a dose-dependent increase in the peak amplitude that was correlated with a dose-dependent inhibition of acetylcholinesterase activity. Prolonged exposure to edrophonium did not change the peak amplitude and there was no time-dependent change in the inhibition of acetylcholinesterase activity. At the highest concentration of edrophonium used (100 microM), simultaneous application with acetylcholine augmented the peak amplitude relative to control, but to a lesser extent than 10 microM. Prolonged exposure to the highest concentration of edrophonium caused a time-dependent reduction in the peak amplitude. The effects of edrophonium were quickly reversible after the removal of the drug from the bathing solution. 5. DFP (1 and 10mM), similar to 1OO microM physostigmine, caused a dramatic reduction of the peak current on simultaneous application with ftetylcholine. During exposure to DFP the current amplitude and acetylcholinesterase activity were very depressed. After removing DFP from the bathing solution the current amplitude increased to more than the control level after 1 mm DFP, while it did not recover to the control level after 10mM DFP. The inhibition of acetylcholinesterase activity remained at both concentrations. 6. These results indicate that all three cholinesterase inhibitors have dose-dependent actions both at the acetylcholine receptor-channel complex and at acetylcholinesterase. The methods we have developed may be useful in the evaluation of various cholinesterase inhibitors.

Animals↗

PubMed1989

Voltage-clamp characterization of Cl- conductance gated by GABA and L-glutamate in single neurons of Aplysia.

1. Cl- conductance gated by gamma-aminobutyric acid (GABA) and L-glutamate in the medial pleural neurons of Aplysia was studied using conventional two-electrode voltage-clamp techniques and a continuous microperfusion system that allowed rapid and uniform agonist application. 2. Both GABA and glutamate elicited current responses that rapidly activated and then decayed (desensitized) during maintained presence of agonist. 3. Recovery from desensitization was rapid for both agonists. For intermediate concentrations of each agonist, recovery was approximately 90% complete within 1 min. 4. Dose-response experiments at a holding potential of -45 mV showed that 1) maximal peak responses to glutamate were on the average approximately 40% of those to GABA, 2) the dose-peak response curve for glutamate was steeper than that for GABA, and 3) time-to-peak (risetime) and desensitization half-time decreased monotonically with dose for GABA but were relatively insensitive to dose and more variable for glutamate. 5. Peak conductances elicited by GABA were voltage dependent, increasing with depolarization, whereas the Cl- conductance elicited by glutamate was voltage independent. Risetime and desensitization kinetics were insensitive to voltage for both agonists. 6. Lowering the temperature of the perfusion medium by 10 degrees C slowed activation and desensitization for both 0.1 mM GABA and 2 mM glutamate. The responses to the two agonists differed, however, in that the peak response to glutamate increased, whereas that to GABA decreased in amplitude.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Effects of exogenous ganglioside and cholesterol application on excitability of Aplysia neurons.

The effects of pressure-ejected gangliosides GM1 and GMix ("Cronassial") and cholesterol dissolved in sea water on the electrophysiological characteristics of Aplysia neurons were studied using voltage-clamp recording techniques. Two types of electrophysiological effects were found. In about 5% of neurons brief pulses (0.1-0.2 sec) of GM1 or GMix elicited fast and large currents associated with an increase in membrane conductance and clear reversal potentials. These currents were similar to those elicited by common neuro-transmitters. Thus it appears that gangliosides may activate a membrane-bound receptor on at least some neurons. Most (about 85%) of the 121 neurons studied showed responses to longer pulses (1.0-2.5 sec) of gangliosides. These responses were much smaller, usually had a relatively slow component, and could be mimicked by application of cholesterol. The currents elicited were either inward or outward and were often biphasic, with an small initial outward component followed by a larger slow inward current. The responses often became larger upon repeated application at short intervals, and long periods of wash were required for recovery. This type of response appears to reflect changes in the electrical properties of the cell induced by incorporation of small amounts of gangliosides or cholesterol into the membrane.

Animals↗

PubMed1988

Characterization of an inward current elicited by edrophonium in physically isolated and internally perfused Aplysia neurons.

We have studied the ionic and pharmacological properties of an inward current elicited by edrophonium, a cholinesterase inhibitor, on physically isolated and internally perfused Aplysia neurons using the voltage clamp, internal perfusion and rapid external perfusion techniques. The current amplitude was dependent on the external Na concentration [(Na)o] in an almost linear manner. However, complete replacement of (Na)o with Tris or sucrose failed to abolish the current. Internal application of Na [increased (Na)i] reduced the current amplitude. In normal (Na)o, changing (Ca)o (both increases and decreases in (Ca)o) reduced the current amplitude. In the sucrose-substituted (Na)o-free condition, edrophonium still could cause a small current (less than 5% of the control). However, an increased (Ca)o did not augment this residual current. Cs and Li carried the edrophonium-activated current when substituted for (Na)o. With sucrose-substituted Na-free sea water outside, edrophonium elicited an outward current when the neuron was internally perfused with Cs, but not when the neuron was internally perfused with K. Therefore, it is unlikely that K is permeant. External application of tetrodotoxin, a blocker of voltage-dependent Na channels, external application of Cd and internal application of F did not affect the current. The edrophonium response was most sensitive to strychnine, which was about 10 times more potent than D-tubocurarine. Hexamethonium, however, had no effect. The local anesthetics, lidocaine and procaine, inhibited the response over the same concentration range as D-tubocurarine. We conclude that edrophonium opens a monocationic channel (presumably a type of Na channel) which is sensitive to (Ca)o.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1988

N-methyl-D-aspartate (NMDA) receptors are inactivated by trypsin.

Acute isolation of hippocampal CA3 pyramidal cells using trypsin produces neurons which respond to kainate and quisqualate but not N-methyl-D-aspartate (NMDA). Incubation of 6- to 12-day-old cultured hippocampal neurons or slices of pyriform cortex with trypsin irreversibly removes the NMDA responses normally present without significant effect on responses to kainate or quisqualate. These data indicate that the NMDA receptor has a trypsin-sensitive component which is necessary for agonist recognition or ion channel activation.

Action Potentials↗