The "trap"--a modification of the block of neuronal nicotinic cholinoceptors

The effect of IEM-1742, a pentaethonium derivative, on the currents induced by iontophoretic applications of acetylcholine was studied in rat superior cervical ganglion neurons using patch-clamp method in the whole-cell modification. Blocking action increased with membrane hyperpolarization and was removed by strong membrane depolarization. Apparent dissociation constant for the receptor-blocker reaction was found to be (2.9 +/- 0.6) 10(-6) M (n = 6) at -50 mV and 20-23 degrees C. IEM-1742 blocks the nicotinic acetylcholine receptor in its activated form. The dissociation of IEM-1742 from the receptor was drastically accelerated during its activation by agonist (trap-block). Trapped receptor was not released from the blocker only by membrane depolarization to the level at which any blocking effect is absent. The data obtained show that IEM-1742 in rat sympathetic ganglion neurons acts in the potential-dependent manner and displays a trap-effect.     

Ion currents through batrachotoxin-modified sodium channels of node of Ranvier membranes at high positive and negative potentials

Ionic currents through batrachotoxin-modified sodium channels in frog nerve fibres were measured over a wide range of membrane potentials. At potentials above +80 mV currents decay in time and their steady-state level decreased as potentials increased. "Instantaneous" current measurements have shown that this phenomenon was due to the decrease in net channel conductance. Scorpion toxin affected current kinetics only slightly at these potentials, which suggested that these decays were not caused by usual inactivation process. Externally applied procaine induced slow (tens of ms) potential-dependent block of batrachotoxin-modified channels at large positive potentials. At large negative potentials (above -100 mV) "instantaneus" currents decreased due to fast voltage-dependent block of the channels by calcium ions.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

Reversal potential of the EPSP of frog motoneurons

The current-chop technique has shown that I-V characteristic of the membrane are nonlinear in lumbar motoneurons of isolated perfused frog spinal cord. Input resistance of the membrane decreased with depolarization when constant current was applied during 0.1-1.0 s. However, injection of current 40-60 nA during 1-2 min led to an increase of the membrane resistance to the initial value. As a result the membrane potential could be shifted to the positive level up to +50 mV and more. Monosynaptic excitatory postsynaptic potentials evoked by stimulation of the brainstem or by microstimulation of ventrolateral tract fibres were found to reverse completely at a positive level of the membrane potential. In most cases the reversal potentials ranged between 0 mV and -10 mV.     

Enhancement of potential-dependent inactivation of calcium channels of mollusk neurons by tolbutamide]

A two-microelectrode voltage-clamp method was used to measure a potential-dependent Ca-current (ICa) on isolated snail neurons. Tolbutamide (1-5 mmol/l) and H-8 (1-30 mumol/l), inhibitors of kinase A, caused a decrease in the peak amplitude and an acceleration of the ICa decay during a depolarizing step. In the presence of tolbutamide a slow (tau 2) time constant of the ICa decay has grown 2-3 times stronger than fast (tau 1) time constant. Curves of inactivation obtained in double-pulse experiments have shown that after tolbutamide application an inactivation of the ICa enhanced when prepulses were to +30(-)+70 mV. The results suggest that dephosphorylation of Ca(2+)-channels enhances a potential-dependent component of the ICa inactivation.     

Regulation of hippocampal NMDA receptors by magnesium and glycine during development.

N-Methyl-D-aspartate (NMDA) receptors play an important role in the development of neuronal connections in the retina and visual cortex, and in synaptic plasticity in the hippocampus. The objective of this study was to determine whether the sensitivity of hippocampal NMDA receptors to magnesium, glycine or NMDA changes during development. Xenopus oocytes were injected with mRNA prepared from hippocampi from rats of different ages, and NMDA receptor properties studied under voltage clamp. Voltage-dependent block of the NMDA receptor by magnesium was studied with voltage steps of -90 mV to -30 mV, in increments of 10 mV, during application of 100 microM NMDA, 3 microM glycine and 0-1000 microM Mg2+. The IC50 of Mg2+ for blocking NMDA receptor-mediated currents varied e-fold (2.72-fold) for approximately every 15 mV of membrane potential in the middle range of membrane potential (-70 to -50 mV), but the relationship between log[IC50] for Mg2+ and membrane potential was not linear, as would be expected for simple channel block. The slopes of the curves did not change with development, indicating no change in the voltage-dependence of Mg2+ block with age. However, the IC50 of Mg2+ block did change with age at every membrane potential tested. NMDA receptors expressed from mRNA isolated from 14-15 day old rats were nearly 2-fold less sensitive to block by Mg2+ (IC50 = 33 microM at -60 mV) than those from 1-2 day old rats (IC50 = 18 microM).(ABSTRACT TRUNCATED AT 250 WORDS)     

Voltage-gated influx ion channels expressed in Xenopus oocytes after the administration of brain mRNA]

Expression of "fast", TTX-sensitive sodium and high-threshold calcium channels in the membrane of Xenopus oocytes following mRNA injection from the rat brain has been detected using two microelectrode voltage clamp technique. Barium current through expressed calcium channels was blocked by 200 mumol/l Cd2+ and was insensitive to D-600 (20 mumol/l) and nitrendipine (50 mumol/l). Expressed barium current was inhibited within 20-40 min by omega-conotoxin, a peptide neurotoxin known to block high-threshold calcium channels of the neuronal membrane, in 1 mumol/l concentration. A steady-state inactivation curve for this current could be fitted by the Boltzmann relation with V1/2 = -50 mV and k = 14 mV. Voltage-dependent and pharmacological properties of calcium channels which appeared in the oocyte membrane following mRNA injection from the mammalian brain resembled most of all those of high-threshold inactivating (HTI- or N-type) calcium channels of neurons in spite they did not demonstrate prominent time-dependent inactivation. Evidences in favour of expressed calcium channels heterogeneity were not obtained.     

Voltage-dependent nonlinearities in the membrane of locust nonspiking local interneurons, and their significance for synaptic integration

Some aspects of the electronic and active membrane properties of nonspiking local interneurons were studied in isolated locust thoracic ganglia, using the switched current- and voltage-clamp techniques in neuropilar recordings. The average transmembrane potential (Vr) of the interneurons was -58 +/- 6mV (n = 85), and the input resistance (in the linear region of the current-voltage curve) was 16.5 +/- 8 M omega (n = 19, range 8 to 32 M omega). The membrane and equalizing time constants were estimated from charging curves evoked by the injection of low density hyperpolarizing current pulses from about -80 mV, i.e., from voltages in the linear region of the I-V curve. The curves yielded 2 time constants (tau m and tau l) whose average values were 33.2 +/- 9 msec and 3.3 +/- 1 msec (n = 18), respectively. The mean specific membrane resistance is therefore about 33 k omega.cm2, assuming that the membrane capacitance is ca. 1 microF.cm-2. An outward rectification was always observed upon depolarization from potentials more negative than Vr and was accompanied by a decrease in input resistance and membrane time constant. The "resting" membrane, for example, had a time constant of 26.4 +/- 8 msec (n = 31). This outward rectification was due to at least 2 conductances with different inactivation kinetics, similar to the transient "A" and "delayed-rectifier" potassium conductances. No inward rectification was ever observed upon injection of hyperpolarizing current. In about 60% of the recordings, an active and TTX-resistant depolarizing process could be evoked by rapid depolarization around Vr. The voltage-dependent properties of the membrane of the nonspiking local interneurons had dramatic effects on the shape and time course of natural or evoked unitary PSPs. The half-width of EPSPs, for example, decreased by a factor of 7.5 if the membrane potential was shifted from -93 to -50 mV. When the membrane potential of an interneuron was altered with a triangular current waveform, the reduction of tonically occurring IPSPs depended more on the sign and rate of the induced voltage change than on the absolute transmembrane potential. For 2 identical instantaneous values of membrane potential, for example, the reduction of the PSPs was greater during the depolarizing phase than during the hyperpolarizing phase of the current waveform. The possible nature of the active membrane conductances underlying the nonlinear electrical behavior of the membrane is discussed, together with their functional significance for local circuit synaptic integration.     

Evidence for voltage-activated outward currents in the neuropilar membrane of locust nonspiking local interneurons

Outward currents activated by depolarization were studied in the neuropilar membrane of locust nonspiking local interneurons, using the single-electrode voltage-clamp technique in situ. Preliminary observation of these currents in 272 neurons revealed two families. The first and most commonly observed (85% of recordings) showed a large transient current followed by a slowly decaying/late current. The second (15% of recordings) showed an additional outward current with a slow rate of activation, a peak within 100-150 msec, and a slow rate of inactivation. Only neurons of the first type were studied further. The transient current was activated by depolarization around -60 mV, with a time to peak of approximately 11 msec at -50 mV and less than 3 msec at -20 mV. This current decayed exponentially, with a time constant of 8.1 +/- 1.6 msec (n = 8 interneurons) at -30 mV. This time constant of inactivation did not appear to depend strongly on membrane voltage, in the range in which it was studied. A second and longer time constant of inactivation of 50-400 msec could not be assigned to either of the transient and late components of the outward current. The ratio of transient-to-late current varied between 1.6 and 5.4, with a mean of about 2.5. The reversal potential for the transient current could, on average, be shifted by 14 mV by a threefold increase in the bath K+ concentration, indicating that K+ is a charge carrier for the current. The transient current became inactivated with maintained depolarization and appeared half-inactivated at about -60 mV (slope factor k1/2 = 8 mV). This current was thus not fully inactivated at "resting" potential (average, -58 mV). Recovery from inactivation followed a single exponential time course, with a time constant of approximately 100 msec at -80 mV. The time course of recovery from inactivation of the transient current was well correlated with that of the recovery of transient outward rectification, as measured in current-clamp recording. Tetraethylammonium, at a bath concentration of 10 mM reduced the transient current by 70% and the delayed current by 60%. 4-Aminopyridine, at a bath concentration of 5 mM, had a significant effect in only two of five interneurons, reducing the transient current by approximately 85% and the late current by approximately 15%. Quinidine at a bath concentration of 100 microM was ineffective. Although these blockers did not allow a clear pharmacological separation of the currents, they were effective in reducing the outward rectification observed in current clamp during step depolarization.(ABSTRACT TRUNCATED AT 400 WORDS)     

Characteristics of IA currents in adult rabbit cerebellar Purkinje cells

Classical conditioning the rabbit nictitating membrane involves changes in synaptic and intrinsic membrane properties of cerebellar Purkinje cell dendrites, and a 4-aminopyridine (4-AP)-sensitive potassium channel underlies these membrane properties. We characterized I(A) currents in adult, rabbit Purkinje cells to determine whether I(A) is the target channel involved in learning. Whole-cell recordings of Purkinje cell somas and dendrites revealed a fast activating and inactivating current with half maximal activation at -27.08 +/- 3.48 mV and -25.51 +/- 1.15 mV in somas and dendrites, respectively; half maximal inactivation at -58.91 +/- 2.34 mV and -49.90 +/- 2.58 mV; and a recovery time constant of 22.81 +/- 1.92 ms and 16.60 +/- 4.26 ms. Outside-out patch recordings from cerebellar Purkinje cell somas confirmed these 4-AP-sensitive currents with half maximal activation at -13.85 +/- 1.17 mV and half maximal inactivation at -55.07 +/- 5.54 mV. More importantly, there was an overlap of activation and incomplete inactivation at potentials from -60 to -40 mV, suggesting a "window" current that was responsible for subthreshold variations of membrane potential and might underlie conditioning-specific increases in Purkinje cell excitability. The potassium current was inhibited by 4-AP and by Heteropodatoxin, a specific blocker of Kv4.2 and Kv4.3 channels, but not by Stromatoxin, a blocker of Kv4.2 channels. Mouse monoclonal antibody labeling identified both Kv4.3 and Kv4.2 subunits in the granule cell layer but only Kv4.3 subunits in the molecular layer. This is the first demonstration of A-type currents in adult, rabbit Purkinje cells that may play a role in regulating membrane potential and firing frequency and comprise the target channel mediating conditioning-specific changes of excitability in rabbit Purkinje cell dendrites.     

Kinetics of sodium current decay during normal axon membrane repolarization and in the presence of scorpion toxin

Decay of sodium currents in repolarization ("tail current") was studied in from axonal membrane. The decay in the membrane repolarization to -40 divided by -60 mV has two exponential components: fast and slow. The fraction of the slow component in the total "tail current" (theta M) decreases as the repolarization potential (Vp) becomes more negative; at Vp more negative than -80 mV "tail" follows practically one-exponential time course. When lengthening the test pulse (at the given Vp) the fraction of the fast component in the "tail" decreases quicker than that of the slow component, following approximately the kinetics of inactivation during the tests pulse. Scorpion toxin treatment results in slowing down "tail" kinetics mainly at the expense of increasing the fraction of the slow component. A kinetic diagram assuming two open state for the channel is suggested. A hypothesis is advanced that scorpion toxin, DDT and trinitrophenol have a common "site" to interact with the gating mechanism of the sodium channel.     

Characterization of excitatory amino acid receptors expressed by embryonic chick motoneurons in vitro

We have examined the effect of L-glutamate and other excitatory amino acids on embryonic chick motoneurons maintained in cell culture along with other types of spinal cord cells. When the motoneuron membrane is clamped at -50 mV, glutamate induces a dose-dependent inward current. Although the dose-response curve is hyperbolic with an ED50 of 78 microM, glutamate apparently activates 2 types of receptors on motoneurons. The first, G1, is activated by N-methyl-D-aspartate (NMDA) and aspartate and inhibited by 2-amino-5-phosphonovaleric acid (2-APV). The second, G2, is activated by kainate and quisqualate and is not inhibited by 2-APV. At -50 mV, 38% of the glutamate current is due to activation of G1 receptors and the remaining 62% to G2 activation. In contrast to motoneurons grown with other spinal cord cells, sorted motoneurons grown in isolation apparently exhibit only G2 receptor-mediated currents. Both G1 and G2 currents reverse polarity between -10 and -5 mV. However, they could be distinguished when the membrane was hyperpolarized. G2 currents increased but G1 currents decreased when the membrane potential was increased beyond -50 mV. Consistent with the mixed agonist action of glutamate, glutamate currents remained nearly constant on hyperpolarization. No evidence was obtained that the G2 class of receptors on motoneurons could be subdivided: Quisqualate and kainate apparently compete for the same sites; gamma-glutamylglycine blocked quisqualate as effectively as it blocked kainate currents when the different potencies of the 2 agonists were taken into account.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ionic basis of the resting membrane potential in cultured rat sympathetic neurons

The conductances which determine the resting membrane potential of rat superior cervical ganglia (SCG) neurons were investigated using perforated voltage- and current-clamp whole-cell techniques. The resting potential of SCG cells varied from -47 to -80 mV (-58.3 +/- 0.8 mV, n = 55). Blockade of M and h currents induced a depolarisation (7.4 +/- 0.7 mV, n = 22) and a hyperpolarisation (7.2 +/- 0.7 mV, n = 20) respectively; however, no correlation between the amplitude of these currents and the resting potential was found. The inhibition of the Na/K pump also induced membrane depolarisation (3.2 +/- 0.2 mV, n = 8). Inhibition of voltage-gated currents unmasked a voltage-independent resting conductance reversing at -50 mV. The reversal potential of the voltage-independent conductance, which included the electrogenic contribution of the Na/K pump, was strongly correlated with the resting potential (R = 0.87, p < 0.0001, n = 30). Ionic substitution experiments confirmed the existence of a voltage-independent conductance (leakage) with four components, a main potassium conductance, two minor sodium and chloride conductances and a small contribution of the Na/K pump. It is concluded that the resting potential of SCG cells strongly depends on the reversal potential of the voltage-independent conductance, with voltage-activated M and h currents playing a prominent stabilising role.     

Asymmetry in voltage-dependent movements of isolated outer hair cells from the organ of Corti

The electrically induced movements of outer hair cells (OHC) were studied using the whole-cell voltage-clamp technique and video analysis. Cell shortening occurs during depolarization and elongation occurs during hyperpolarization from holding potentials near -70 mV. However, a marked asymmetry in response magnitude exists such that depolarization produces larger cell length changes than do comparable levels of hyperpolarization. The response is such that at normal resting potentials in vivo, displacements are about 2 nm/mV, but increase to about 15 nm/mV as the cell is depolarized. This mechanical rectification in the depolarizing direction manifests itself during symmetrical sinusoidal voltage stimulation as a "DC" reduction in cell length superimposed upon "AC" length changes. The observed OHC mechanical rectification may be involved in the reported production of "DC" basilar membrane displacements during suprathreshold acoustic stimulation (LePage, 1987). Estimates of the magnitude of OHC movements at acoustic threshold levels induced by receptor potentials in the high-frequency region of the cochlea indicate a disparity between basilar membrane and OHC movements on the order of 21 dB. Thus, it appears questionable whether OHC mechanical movements solely underlie the "active process" thought to be responsible for the high degree of neural tuning at sound pressures near 0 dB.     

Sodium conductance in cultured myenteric AH-type neurons from guinea-pig small intestine

Whole-cell patch clamp methods were used to investigate sodium conductance in after-hyperpolarization-type (AH) enteric neurons in culture after dissociation from the myenteric plexus of guinea-pig small intestine. Inward current carried by Na+ (I(Na)) was identified and its current-voltage characteristics were compared with those for inward Ca2+ current (I(Ca)). The I(Na) current was a rapidly inactivating current relative to I(Ca). Application of tetrodotoxin (TTX) blocked I(Na) with an EC50 of 10.7 nM. Activation curves for I(Na) showed a rapid decrease in time to peak for test potentials from holding potentials of -80 mV to between -40 and -10 mV. Voltage-dependence of steady-state inactivation curves for I(Na) was fit to the Boltzmann equation with potential for half-inactivation (V(1/2)) = -55.6 mV and slope factor (k) = 6.4 mV. Steady-state inactivation for I(Ca) fit the Boltzmann equation with a V(1/2) = -38.9 mV and k= 14.4 mV. Kinetics for inactivation of I(Na) were voltage dependent at potentials between -70 and -30 mV and accelerated and became less voltage-dependent at more positive potentials. The time constant (tau) for inactivation at -70 mV was tau = 161 +/- 23 ms and decreased to tau = 2.3 +/- 0.2 ms at -30 mV. Rapid acceleration of inactivation occurred between -50 and -40 mV. This was also the range where activation began. Recovery from inactivation with the membrane potential clamped at -100 or -80 mV was rapid and fit by a single exponential with tau = 7.3 +/- 1.1 ms for -100 mV and 21.5 +/- 5.1 ms for -80 mV. The results suggest that AH-type enteric neurons have only one type of Na+ channel that behaves like the "classical" voltage-gated tetrodotoxin-sensitive fast channel. The findings support the hypothesis that I(Na) current is an important factor in determination of excitability and firing behavior in AH neurons. I(Na) and I(Ca) together determine the properties of the rising phase of the spike and thereby contribute to global determinants of excitability as the neurons are exposed to multiple depolarizing and hyperpolarizing stimuli from synaptic inputs and mediators released from enteroparacrine cells.     

Effect of tetrodotoxin in low concentrations on the ion currents of trigeminal ganglion neurons in the rat

Isolated neurons from trigeminal ganglia of one-month-old rats were studied under conditions of intracellular perfusion and voltage clamp. Increase of the inward current amplitude and deceleration of current decay due to the action of low external concentrations of tetrodotoxin (10(-12)-10(-10) M) were observed in a number of the cells tested. Such changes were absent in chloride-free extracellular solution. The existence of a transient potential-dependent current carried by chloride anions through tetrodotoxin-sensitive chloride channels in the membrane of trigeminal ganglion neurons is postulated.     

Different Types of Potassium Outward Current in Relay Neurons Acutely Isolated from the Rat Lateral Geniculate Nucleus

Different classes of potassium (K+) outward current activated by depolarization were characterized in relay neurons acutely isolated from the rat lateral geniculate nucleus (LGN), using the whole-cell version of the patch-clamp technique. A fast-transient current (IA), activated at around - 70 mV, declined rapidly with a voltage-dependent time constant (tau=6 ms at + 45 mV), was 50% steady-state inactivated at - 70 mV, and rapidly recovered from inactivation with a monoexponential time course (tau=21 ms). IA was blocked by 4-aminopyridine (4-AP, 2 - 8 mM) and was relatively insensitive to tetraethylammonium (TEA, 2 - 10 mM). After elimination of IA by a conditioning prepulse (30 ms to - 50 mV), a slow-transient K+ current could be studied in isolation, and was separated into three components, IKm, IKs and a calcium (Ca2+)-dependent current, IK[Ca]. The slow-transient current was not consistently affected by 4-AP (up to 8 mM), while TEA (2 - 10 mM) predominantly blocked IKs and IK[Ca]. The component IKm persisted in a solution containing TEA and 4-AP, activated at around - 55 mV, declined monoexponentially during maintained depolarization (tau=98 ms at + 45 mV), was 50% inactivated at - 39 mV, and recovered with tau=128 ms from inactivation. IKs activated at a similar threshold, but declined much slower with tau=2662 ms at + 45 mV. Steady-state inactivation of IKs was half-maximal at - 49 mV, and recovery from inactivation occurred relatively fast with tau=116 ms. From these data and additional current-clamp recordings it is concluded that the K+ currents, due to their wide range of kinetics and dependence on membrane voltage or internal Ca2+ concentration, are capable of cooperatively controlling the firing threshold and of shaping the different states of electrophysiological behaviour in LGN relay cells.     

Modelling the oscillatory electrical activity of mollusk neurons

A model is suggested describing slow membrane potential oscillations in moluscan neurons. It is based on the assumptions that the depolarization phase of oscillations is induced by slow calcium current and the hyperpolarization phase--by potassium current activated by intracellular Ca ions. It is stated that three types of neuronal electrical activity are possible depending on the values of the model parameters: stable membrane hyperpolarization down to the resting potential (-49 divided by -53 mV); slow oscillations of the membrane potential in a range of -30 divided by -60 mV with the period of 12-17 s; stable membrane depolarization up to -40 divided by -30 mV, which may lead to a repetitive firing behaviour of these neurons. Calculated dependence of the amplitude of membrane potential oscillations upon extracellular concentration of Ca, K and Na ions is in quantitative agreement with experimental data obtained by Barker and Gainer [4].     

Ionic conductances underlying the activity of interneurons that control heartbeat in the medicinal leech

Electrical properties of interneurons that control heartbeat in the leech (HN cells) were studied using intracellular recording and stimulation in isolated ganglia bathed by salines of various ionic compositions. Substitution of Na+ ions in the bath by Tris stopped the spontaneous firing of HN cells and led to their gradual hyperpolarization by 15-20 mV. In the absence of Na+, HN neurons produced long-lasting regenerative plateau potentials with thresholds near -55 mV and peaks near -30 mV that were accompanied by an increase in membrane conductance. Elevation of Ca2+ concentration enhanced plateaus, as did replacement of Ca2+ by Ba2+. Plateaus were formed when Sr2+ replaced Ca2+, but were blocked by addition of Mg2+ or Co2+ to the bath, Co2+ being effective at lower concentrations than Mg2+. Hyperpolarization of HN neurons with injected currents revealed a time-dependent change in membrane potential, whereby initial maximum hyperpolarization was followed by a "sag" in potential towards more depolarized values. The sag showed dual voltage dependence, being diminished when HN neurons were hyperpolarized or depolarized outside the normal range of oscillation. The sag was found to depend on the presence of Na+ ions and to be blocked by Cs+ but not by Ba2+. This time-dependent change in membrane potential counters hyperpolarizations of HN neuron membrane potential and may contribute to the escape of these neurons from synaptic inhibition.     

The relationship of afterhyperpolarizations of extraocular motoneurons to membrane potential.

The effect of membrane potential displacements caused by external current injection on the amplitudes of two antidromically evoked afterhyperpolarizations (AHP1 and AHP2) was measured in extraocular motoneurons. AHP1 had a reversal potential of-70mV and an average compensation for displacements from the reversal potential ("compensation gain") of -0.36. AHP2 had a reversal potential of-80mV and a compensation gain of -0.08. Measurements of input resistance of these motoneurons demonstrate a 30-50% decrease at depolarized membrane potentials. This rectification could account for the apparent lack of summation of AHP2. The functional role of AHP1 and AHP2 in the regulation of discharge frequencies of extraocular motoneurons during nromal eye movements is discussed.