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PubMed1995

Activation of calcium-dependent chloride channels causes post-tetanic depolarization in rabbit parasympathetic neurons.

Intracellular recordings were made from neurons in rabbit and feline vesical parasympathetic ganglia in vitro. In response to cathodal current injection (0.1-1 nA for 2-20 ms) the majority of rabbit neurons (229 out of 250) exhibited a single action potential that was followed by a fast and slow after-hyperpolarization (sAHP neuron). The remainder of the cells exhibited an action potential followed by only a fast after-hyperpolarization (fAHP neuron). fAHP neurons did not exhibit anomalous rectification and a spontaneous rhythmic hyperpolarization, which were common membrane properties in sAHP neurons. In response to a train of cathodal current pulses (5-20 Hz for 0.1-10 s), fAHP neurons exhibited action potentials followed by a post-tetanic depolarization (PTD). The PTD was associated with a decrease in membrane input resistance. The amplitude and duration of the PTD were a function of the number of action potentials in the train. The amplitude of the PTD was increased by membrane hyperpolarization and its estimated reversal potential was approximately -30 mV. Low-chloride solution and intracellular injection of chloride ions augmented the amplitude and duration of the PTD, whereas low-sodium, high-potassium and low-potassium solutions did not affect them. Tetraethylammonium (5-10 mM) and barium (0.5-1 mM) increased the amplitude and duration of the PTD. Nominal calcium-free solutions and omega-conotoxin (500 nM) abolished the PTD. The data suggest that activation of chloride channels by calcium influx through omega-conotoxin-sensitive calcium channels mediates the PTD. Repetitive stimulation of the pelvic nerve evoked a train of orthodromic action potentials followed by the PTD of fAHP neurons. (+)-Tubocurarine (10 microM) and hexamethonium (200 microM), but not atropine (1 microM), abolished orthodromic action potentials and the PTD, whereas these cholinergic antagonists did not depress the PTD evoked by direct action potentials. In summary, the data suggest that the PTD may function as a slow synaptic potential in fAHP neurons. This appears likely because neither slow excitatory nor inhibitory postsynaptic potentials are present in neurons of rabbit vesical parasympathetic ganglia. In contrast, slow inhibitory and excitatory postsynaptic potentials were recorded from neurons in feline vesical parasympathetic ganglia.

Action Potentials↗
PubMed1998

Modulation of oligosynaptic cutaneous and muscle afferent reflex pathways during fictive locomotion and scratching in the cat.

We have compared state-dependent transmission through oligosynaptic (minimally disynaptic) reflex pathways from low-threshold cutaneous and muscle afferents to some flexor and extensor lumbosacral motoneurons during fictive locomotion and scratching in decerebrate unanesthetized cats. As reported in earlier work, oligosynaptic cutaneous excitatory postsynaptic potentials (EPSPs) in flexor digitorum longus (FDL) and inhibitory postsynaptic potentials (IPSPs) in extensor digitorum (EDL) longus motoneurons were enhanced markedly during the early flexion phase of fictive locomotion. We show in this paper that, in contrast, these cutaneous reflex pathways were depressed markedly during all phases of fictive scratching. On the other hand, disynaptic EPSPs produced by homonymous and synergist group I muscle afferents in flexor (tibialis anterior and EDL) motoneurons were present and strongly modulated during both fictive locomotion and scratching. During both actions, these disynaptic group I EPSPs appeared or exhibited the largest amplitude when the motoneuron membrane potential was most depolarized and the parent motor pool was active. There was an interesting exception to the simple pattern of coincident group I EPSP enhancement and motoneuron depolarization. During locomotion, disynaptic group I EPSPs in both FDL and flexor hallucis longus (FHL) motoneurons cells were facilitated during the extension phase, although FDL motoneurons were relatively hyperpolarized whereas FHL cells were depolarized. The reverse situation was found during fictive scratching; group I EPSPs were facilitated in both FDL and FHL cells during the flexion phase when FDL motoneurons were depolarized and FHL cells were relatively hyperpolarized. These observations suggest that the disynaptic EPSPs in these two motor nuclei are produced by common interneurons. Reciprocal disynaptic inhibitory pathways from group Ia muscle afferents to antagonist motoneurons were also active and subject to phase-dependent modulation during both fictive locomotion and scratching. In all but one cell tested, reciprocal disynaptic group Ia IPSPs were largest during those phases in which the motoneuron membrane potential was relatively hyperpolarized and the parent motor pool was inactive. Oligosynaptic PSPs in motoneurons produced by stimulation of the mesencephalic locomotor region (MLR) were modulated strongly during fictive locomotion but were suppressed powerfully throughout fictive scratching. Large cord dorsum potentials generated by MLR stimuli also were suppressed markedly during fictive scratching. These results allow certain inferences about the organization of interneurons in the pathways examined. They also suggest that the central pattern generators that produce fictive locomotion and scratching are organized differently.

Afferent Pathways↗
PubMed1997

In vitro investigation of synaptic relations between interneurons surrounding the trigeminal motor nucleus and masseteric motoneurons.

Because of their many inputs and bilateral projections, interneurons surrounding the trigeminal motor nucleus (MotV) are thought to be very important in control of jaw movements and reflexes. However, their interactions with the trigeminal motoneurons are almost unknown. In the present study an in vitro slice preparation was used to investigate this relationship in rat. The zone bordering MotV has been subdivided into four regions: the supra-, juxta-, and intertrigeminal areas (SupV, JuxtV, and IntV, respectively) and the parvocellular reticular formation ventral and caudal to MotV. Stimulation of all areas evoked short-latency excitatory postsynaptic potentials (EPSPs) in masseteric motoneurons. Frequently the EPSPs masked inhibitory postsynaptic potentials (IPSPs) or were followed by long-lasting inhibitory potentials. Only responses obtained from stimulation of JuxtV and IntV seemed devoid of inhibitory components. The EPSPs were mediated through kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, whereas the IPSPs appear to be due to gamma-aminobutyric acid and glycine. EPSPs and IPSPs were also recorded in SupV premotor interneurons after stimulation of IntV and MotV, respectively, thus suggesting that reciprocal connections exist between premotor areas and also between premotor interneurons of SupV and inhibitory interneurons located within MotV. It is concluded that the preparation used here will doubtless prove useful for further investigation of the circuitry involved in the bilateral coordination of the jaw.

Animals↗
PubMed1994

Spatial and temporal features of recurrent facilitation among motoneurons innervating synergistic muscles of the cat.

1. The temporal features and strength of recurrent facilitatory potentials were examined in pairs of lumbosacral motoneurons that were separated by a known distance and were identified by antidromic stimulation of muscle nerves. One motoneuron was stimulated by injecting depolarizing current pulses, and responses were recorded in the second motoneuron. The distance between motoneurons in pairs was also measured to assess the spatial distribution in strength of recurrent facilitation in motor pools. All motoneurons in these pairs innervated muscles that act as hip or ankle extensors. 2. Recurrent facilitatory potentials were found frequently among motoneurons innervating the hindlimb extensor muscles examined. Several categories of recurrent facilitatory responses were identified. One category was composed of facilitation responses that followed an inhibition response. A second category was composed of facilitation responses that were not preceded by a significant inhibition and consisted of a monophasic response. There was a considerable range of latencies in this category. 3. Responses in which recurrent facilitatory potentials were preceded by recurrent inhibitory postsynaptic potentials (RIPSPs) among close motoneuron pairs demonstrated an inverse correlation between the durations of the facilitatory and the inhibitory phases. In addition, the duration of inhibition responses without facilitation was longer on average, than the duration of inhibitory responses that were followed by facilitation. It was suggested that recurrent facilitation may restrict the time course of RIPSPs. 4. In contrast to the topographic distribution of RIPSPs described in the previous report, amplitudes of monophasic facilitations were directly correlated with the distance separating motoneurons in pairs, rather than inversely correlated as was the case for RIPSP amplitudes.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed2004

Reticulospinal neurons receive direct spinobulbar inputs during locomotor activity in lamprey.

Reticulospinal neurons of the lamprey brain stem receive rhythmic input from the spinal cord during locomotor activity. The goal of the present study was to determine whether such spinal input has a direct component to reticulospinal neurons or depends on brain stem interneurons. To answer this question, an in vitro lamprey brain stem-spinal cord preparation was used with a diffusion barrier placed caudal to the obex, separating the experimental chamber into two baths. Locomotor activity was induced in the spinal cord by perfusion of d-glutamate or N-methyl-dl-aspartate into the spinal cord bath. The brain stem bath was first perfused with normal Ringer solution followed by a high-Ca(2+), -Mg(2+) solution, which reduced polysynaptic transmission. The amplitudes of membrane potential oscillations of reticulospinal neurons in the posterior and middle rhombencephalic reticular nuclei (PRRN and MRRN, respectively) recorded with sharp intracellular microelectrodes did not significantly change from normal to high-divalent solution. This finding suggests a large part of the spinal input creating the oscillations is direct to the reticulospinal neurons. Application of strychnine to the high-Ca(2+), -Mg(2+) solution decreased membrane potential oscillation amplitude, and injection of Cl(-) reversed presumed inhibitory postsynaptic potentials, indicating a role for direct spinal inhibitory inputs. Although reduced, the persistence of oscillations in strychnine suggests that spinal excitatory inputs also contribute to the oscillations. Thus it was concluded that both excitatory and inhibitory spinal neurons provide direct rhythmic inputs to reticulospinal cells of the PRRN and MRRN during locomotor activity. These inputs provide reticulospinal cells with information regarding the activity of the spinal locomotor networks.

Animals↗
PubMed1982

Inhibitory postsynaptic currents at Aplysia cholinergic synapses: effects of permeant anions and depressant drugs.

Inhibitory postsynaptic potentials (i.p.s.ps) and, under voltage-clamp conditions, inhibitory postsynaptic currents (i.p.s.cs) were recorded in neurons in buccal ganglia of Aplysia juliana. The decay of i.p.s.cs was exponential with a single time constant, tau, which decreased with membrane depolarization. In external solutions containing iodide or bromide ions instead of chloride ions, tau varied according to the sequence tau (I) greater than tau (Br) greater than tau (Cl), and the voltage sensitivity of tau was altered. In iodide solution, the voltage sensitivity of tau was reversed. Furthermore, the foreign halides depressed the peak current amplitude and shifted the reversal (zero-current) potential to more positive membrane potentials. In low concentrations of sodium pentobarbitone (100-200 microns), the decay of i.p.s.cs became biphasic. Increasing drug concentration and membrane hyperpolarization had differential effects on the rates and relative amplitudes of the two components of i.p.s.c. decay. Octanol (0.5-1 mM) reduced the amplitude of i.p.s.ps and increased the rate of decay of i.p.s.cs without changing the voltage sensitivity of tau. The effect of foreign halides and barbiturates on i.p.s.c. decay were interpreted in terms of a reaction between the anion and an ion-binding site(s) associated with the anion-selective channel, which affects the probability of anions entering the channel and normal channel closure.

Acetylcholine↗
PubMed1992

The actions of 3-aminopropanephosphinic acid at GABAB receptors in rat hippocampus.

The actions of 3-aminopropanephosphinic acid (APPA) were examined using whole-cell patch-clamp recording in rat hippocampal slice. In recordings from neurons in subfield CA1 of slices from young (2-4 weeks) and adult (greater than 2 month) rats, APPA (0.5-50 microM) produced membrane hyperpolarization and outward current under voltage-clamp. APPA also inhibited excitatory postsynaptic potentials with an IC50 of 2.3 microM, and reduced inhibitory postsynaptic potentials at concentrations from 0.1 to 1 microM. The hyperpolarizing and synaptic depressant effects of APPA were reduced by 2-OH-saclofen an antagonist at the B-type receptor for the neurotransmitter gamma-aminobutyric acid (GABA). In this preparation APPA exhibited potencies similar to those previously reported for the GABAB receptor agonist baclofen. APPA was much less effective in inhibiting synaptic transmission measured using field potential recordings. The observations made with whole-cell patch-clamp recording indicate that in hippocampus APPA acts as a potent agonist at presynaptic GABAB receptors associated with both excitatory and inhibitory synapses, and also activates postsynaptic GABAB receptors.

Action Potentials↗
PubMed1988

Control of feeding movements in the freshwater snail Planorbis corneus. I. Rhythmical neurons of buccal ganglia.

(1) The buccal mass of the freshwater snail Planorbis corneus, dissected together with the buccal ganglia, performs rhythmic feeding movements. Radula movements and the electrical activity in various nerves of buccal ganglia were recorded in such a preparation. The cycle of radula movements consisted of three phases: quiescence (Q), protraction (P) and retraction (R). The activity in the radular nerve was observed mainly in the P-phase and that in the dorsobuccal nerve, largely in the R-phase. (2) Isolated buccal ganglia were capable of generating a feeding rhythm, the activity in buccal nerves being similar to that observed in the buccal mass-buccal ganglion preparation, i.e., a burst in the radular nerve preceded a burst in the dorsobuccal nerve. The activity of neurons in isolated buccal ganglia during generation of the feeding rhythm has been studied with intracellular microelectrodes. About 10% of ganglion neurons exhibited periodic activity related to the feeding rhythm ("rhythmic" neurons). (3) Rhythmic neurons have been divided into 7 groups according to the phase of their activity and to the characteristics of slow oscillations of the membrane potential during the feeding cycle. Group 1 neurons revealed a gradual increase of depolarization during the Q- and P-phases. In subgroup 1e neurons, spike discharges began in the Q-phase, while in subgroup 1d neurons activity started in the P-phase. During the R-phase, group 1 neurons were strongly hyperpolarized, and their discharges terminated. In group 2 neurons, small depolarization gradually increased during the Q- and P-phases. Then, in the R-phase, a large (20-50 mV) rectangular wave of depolarization arose with superimposed high-frequency oscillations. Group 3 neurons exhibited an excitatory postsynaptic potential (EPSP) in the P-phase and inhibitory postsynaptic potential (IPSP) in the R-phase. The neurons of group 4 revealed two EPSPs: a small one in the P-phase and a larger one in the R-phase. Group 5 neurons exhibited an EPSP in the P-phase, those of group 7 - an IPSP in the R-phase, and those of group 9 - IPSPs in the P- and R-phases. Neurons within each of the groups 1, 2 and 4 were electrically coupled, and in addition, there were also electrical connections between neurons of groups 2 and 4. (4) Data are presented showing that neurons of groups 1 and 2 are the main source of postsynaptic potentials in rhythmic neurons in the P-phase and in the R-phase of the cycle, respectively.

Action Potentials↗
PubMed1983

Effects of delta 9-tetrahydrocannabinol on cat spinal motoneurons.

The influence of delta 9-tetrahydrocannabinol (delta 9-THC) on cat spinal motoneurons was investigated with intracellular recording techniques in order to identify possible mechanisms of action of the drug's central excitatory and depressant properties. delta 9-THC increased the amplitude of the excitatory postsynaptic potentials (EPSPs) and decreased the amplitude of the inhibitory postsynaptic potentials (IPSPs); these excitatory effects do not appear to be the result of changes in the afferent input. However, an observed increase in membrane resistance may account for, or contribute to, the enhanced EPSPs. The cannabinoid also concomitantly caused depression, as evidenced by a rise in the firing threshold for the motoneuron action potential. The responses of the motoneuron to the drug suggest synaptic sites and mechanisms of action.

Action Potentials↗
PubMed1987

Properties of stereotyped series of postsynaptic potentials in hypoglossal motoneurons.

A stereotyped series of postsynaptic potentials produced in cat hypoglossal motoneurons by stimulation of the cerebral cortex, the inferior alveolar nerve or the lingual nerve was studied. These include an excitatory postsynaptic potentials (EPSP) and subsequently 3 different types of inhibitory postsynaptic potentials (IPSPs). The first is a short-lasting IPSP which was blocked by strychnine administration. The second is a gamma-aminobutyric acid (GABA) IPSP which was blocked by picrotoxin administration. This IPSP was sensitive to membrane polarization and dependent on a conductance increase. The third is a long-duration hyperpolarizing potential which was enhanced by the injection of picrotoxin and insensitive to membrane polarization. Moreover, we have demonstrated that the amplitude of cortically induced EPSPs decreased greatly with depolarization.

Animals↗
PubMed1999

A new cellular mechanism for coupling inputs arriving at different cortical layers.

Pyramidal neurons in layer 5 of the neocortex of the brain extend their axons and dendrites into all layers. They are also unusual in having both an axonal and a dendritic zone for the initiation of action potentials. Distal dendritic inputs, which normally appear greatly attenuated at the axon, must cross a high threshold at the dendritic initiation zone to evoke calcium action potentials but can then generate bursts of axonal action potentials. Here we show that a single back-propagating sodium action potential generated in the axon facilitates the initiation of these calcium action potentials when it coincides with distal dendritic input within a time window of several milliseconds. Inhibitory dendritic input can selectively block the initiation of dendritic calcium action potentials, preventing bursts of axonal action potentials. Thus, excitatory and inhibitory postsynaptic potentials arising in the distal dendrites can exert significantly greater control over action potential initiation in the axon than would be expected from their electrotonically isolated locations. The coincidence of a single back-propagating action potential with a subthreshold distal excitatory postsynaptic potential to evoke a burst of axonal action potentials represents a new mechanism by which the main cortical output neurons can associate inputs arriving at different cortical layers.

Action Potentials↗
PubMed1999

Glutamate modulates neurotransmission in the submucosal plexus of guinea-pig small intestine.

Effects of glutamate on synaptic transmission in the submucosal plexus of guinea-pig small intestine were studied with intracellular electrophysiological recording methods. Glutamate suppressed stimulus-evoked slow excitatory postsynaptic potentials (EPSPs) and increased the amplitude of slow inhibitory postsynaptic potentials (IPSPs) in submucosal neurons. The actions of glutamate were mimicked by the group I metabotropic glutamate receptor (mGluRs) agonist DHPG, but not by the group II agonist S-4C3HPG, the group III agonist L-AP4, or selective agonists for ionotropic glutamate receptors (iGluRs). Glutamate actions were suppressed by the selective group I mGluRs antagonist S-4CPG, but not by group II and III mGluRs antagonist CPPG or iGluRs antagonists. Glutamate suppressed substance P- and 5-HT-evoked slow EPSP-like responses and potentiated norepinephrine-induced slow IPSP-like responses. The results suggest that group I mGluRs mediate glutamate-induced suppression of slow EPSPs and potentiation of slow IPSPs in S-type uniaxonal submucosal neurons.

Animals↗
PubMed1988

The dependence of motoneurone membrane potential on extracellular ion concentrations studied in isolated rat spinal cord.

1. Intracellular recordings from ninety-nine motoneurones have been made in an in vitro hemisected spinal cord preparation. Their mean resting membrane potential in normal artificial cerebrospinal fluid (CSF) was -71 +/- 0.5 mV (+/- S.E.M.). The mean amplitude of the action potential was 84.0 +/- 1.4 mV (n = 50), and the mean input conductance was 101 +/- 7 nS (n = 49). 2. Both membrane potential and input conductance were sensitive to changes in [K+]o, [Na+]o, [Cl-]o and [Ca2+]o. 3. Replacement of extracellular Ca2+ by Mn2+ resulted in less than 1 mV hyperpolarization and a decrease in input conductance from 102 +/- 7 to 93 +/- 6 nS (n = 15). 4. At high [K+]o (greater than 10 mM) the membrane potential followed the potential predicted by the Nernst equation for K+ ions with a slope of 58 mV per 10-fold change in [K+]o. At low [K+]o (less than 10 mM) there was significant deviation from K+ equilibrium potential (EK). 5. [K+]i was found to be 106 mM when estimated from the reversal potential of the after-hyperpolarization of the antidromic action potential. 6. The reversal potential of the recurrent inhibitory postsynaptic potential (IPSP) in normal CSF was used to calculate [Cl-]i. This was 6.6 mM, which is less than would be expected if Cl- was passively distributed, indicating the presence of an outwardly directed Cl- pump. 7. Decreasing [Cl-]o from control (134 mM) to 4 mM resulted in a depolarization of 6.9 +/- 0.9 mV and a decrease in input conductance from 102 +/- 5 to 90 +/- 5 nS (n = 14) in 3 mM [K+]o. 8. Decreasing [Na+]o from 156 to 26 mM by substitution with choline resulted in a 6.2 +/- 0.5 mV hyperpolarization and a decrease in input conductance from from 102 +/- 4 to 76 +/- 4 nS (n = 5) in 3 mM [K+]o. 9. The input conductances for Na+, Cl- and K+ at the resting potential were calculated. After allowing for a microelectrode leak conductance, the relative input conductances were gNa/gK = 0.13 and gCl/gK = 0.25.

Action Potentials↗
PubMed1990

Phencyclidine actions measured intracellularly in hippocampal CA1 neurons.

The electrophysiological effects of phencyclidine (PCP) were measured intracellularly in guinea pig hippocampal CA1 neurons in vitro. At all doses tested (0.2 microM - 10 mM), PCP increased the width of action potentials (APs). Doses of 10 microM and higher were associated with decreased action potential amplitude. PCP decreased inhibitory postsynaptic potentials and excitatory postsynaptic potentials but did not alter responses to focally applied GABA. At the lowest dose (0.2 microM), PCP decreased the input resistance (Rin), while at all other doses Rin was increased. PCP decreased post-spike train afterhyperpolarizations at low and medium doses. PCP effects persisted in low calcium medium and also in medium containing 10(-6) M tetrodotoxin. It is concluded that in these central neurons, PCP primarily blocks potassium conductances at all doses and, at anesthetic doses, depresses sodium-dependent spikes.

Action Potentials↗
PubMed1993

Physiological and morphological properties of neurons in sphincter of Oddi region of the guinea pig.

Intracellular recordings and dye injections were used to investigate neurons located in ganglia of the sphincter of Oddi (SO) region in guinea pigs. Four types of neurons were encountered based on physiological properties. The two most abundant types, tonic and phasic, had similar membrane characteristics and morphologies but yet could be differentiated by their spiking characteristics. Tonic cells spiked throughout a depolarizing current pulse and were sometimes spontaneously active. Phasic cells fired only a single action potential at the onset of a current pulse regardless of stimulus amplitude or duration. Both tonic and phasic cells had Dogiel type I morphologies. They typically had a single long process and several very short processes emanating from the soma. NADPH diaphorase activity was demonstrated in cells with similar morphologies, indicating that nitric oxide may be an intrinsic transmitter in some of these cells. Cells with a prolonged afterhyperpolarization (AH cells), similar to the type 1/AH cells of the gut, were rarely encountered. This finding was consistent with the observation that very few calbindin D-immunoreactive neurons exist in this region. Action potentials could not be generated in the fourth type of neuron, called nonspiking neurons, even though they did receive synaptic input. Most tonic and phasic cells received at least one nicotinic fast excitatory postsynaptic potential (EPSP). In addition, both slow EPSPs and inhibitory postsynaptic potentials were observed. Most AH cells received only slow excitatory synaptic input.

Action Potentials↗
PubMed2003

The mormyromast region of the mormyrid electrosensory lobe. II. Responses to input from central sources.

This is the second in a series of two papers on the mormyromast regions of the electrosensory lobe (ELL) of mormyrid electric fish. In this study, we examined the effects of artificial stimulation of two of the three major central inputs to ELL on different morphologically identified cell types of ELL. The three major central inputs to ELL are the eminentia granularis posterior, the juxtalobar nucleus, and the preeminential nucleus. We stimulated the juxtalobar and preeminential nuclei. We compared the effects of such stimulation with effects of the electric organ corollary discharge (EOCD) on the same cells to understand the origins of EOCD effects in ELL. Responses to juxtalobar stimulation were different in different cell types and remarkably similar to corollary discharge responses in the same cells. In addition, responses to juxtalobar stimulation were consistently depressed when the stimulus was delivered immediately after the naturally occurring EOCD response. These findings indicate that the juxtalobar nucleus is a major source of the EOCD responses of ELL cells. In contrast, preeminential stimulation evoked similar responses in medium ganglionic cells, and the two types of efferent cells that were quite different from the EOCD responses of these cells, suggesting that the preeminential nucleus is less important than the juxtalobar nucleus in determining the EOCD responses of ELL cells. Preeminential responses of medium ganglionic and efferent cells consisted of a short-latency excitatory postsynaptic potential (EPSP) followed by a long-lasting inhibitory postsynaptic potential (IPSP). Both the EPSPs and IPSPs were facilitated when brief bursts of closely spaced stimuli were delivered.

Action Potentials↗
PubMed2007

Granular cells of the mormyrid electrosensory lobe and postsynaptic control over presynaptic spike occurrence and amplitude through an electrical synapse.

Primary afferent fibers from the electroreceptors of mormyrid electric fish use a latency code to signal the intensity of electrical current evoked by the fish's own electric organ discharge (EOD). The afferent fibers terminate centrally in the deep and superficial granular layers of the electrosensory lobe with morphologically mixed chemical-electrical synapses. The granular cells in these layers seem to decode afferent latency through an interaction between primary afferent input and a corollary discharge input associated with the EOD motor command. We studied the physiology of deep and superficial granular cells in a slice preparation with whole cell patch recording and electrical stimulation of afferent fibers. Afferent stimulation evoked large all-or-none electrical excitatory postsynaptic potentials (EPSPs) and large all or none GABAergic inhibitory postsynaptic potentials (IPSPs) in both superficial and deep granular cells. The amplitudes of the electrical EPSPs depended on postsynaptic membrane potential, with maximum amplitudes at membrane potentials between -65 and -110 mV. Hyperpolarization beyond this level resulted in either the abrupt disappearance of EPSPs, a step-like reduction to a smaller EPSP, or a graded reduction in EPSP amplitude. Depolarization to membrane potentials lower than that yielding a maximum caused a linear decrease in EPSP amplitude, with EPSP amplitude reaching 0 mV at potentials between -55 and -40 mV. We suggest that the dependence of EPSP size on postsynaptic membrane potential is caused by close linkage of pre- and postsynaptic membrane potentials through a high-conductance gap junction. We also suggest that this dependence may result in functionally important nonlinear interactions between synaptic inputs.

Action Potentials↗