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PubMed1992

Fast inhibitory postsynaptic potentials and responses to inhibitory amino acids of sympathetic preganglionic neurons in the adult cat.

Intracellular recordings were obtained from sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus (IML) in slices of upper thoracic spinal cord of the anesthetized cat. A total of 44 neurons was studied. Single shock stimulation of an area of white matter dorsolateral to the IML, close to the recording electrode (< 0.5 mm), evoked fast IPSPs with rise time of 3.8 ms and 1/2 decay time of 14.7 ms (n = 12). In 17 other cells only fast EPSPs were recorded but, after suppression of the EPSPs by the excitatory amino acid receptor antagonists CNQX (20 microM) and APV (100-250 microM), fast IPSPs were unmasked. The IPSP reversed polarity at -63 mV (-67 mV in the presence of CNQX and APV). The reversal potential shifted to a less negative value when the extracellular chloride concentration was reduced. The IPSP was reversibly abolished by the GABAA receptor antagonist bicuculline in 32% of the cells, by the glycine receptor antagonist strychnine in 47% of the cells and by the combination of the two in 21% of the cells. The IPSP was abolished by TTX (0.5 microM), had constant latency and showed no failures during high frequency stimulation. The IPSP presumably resulted from the excitation of inhibitory axons and/or inhibitory neuron somata with monosynaptic connections to the SPN. Glycine and GABA (1-3 mM) produced hyperpolarization associated with decreased membrane resistance. Sixty-nine percent of cells responded to both agonists, 19% to glycine only and 12% to GABA only. The GABAB agonist baclofen (5 microM) had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1983

Electrogenesis of the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

The ionic mechanisms of the slow surface positive (P)-potential and the slow inhibitory postsynaptic potential (IPSP), an intracellularly recorded P-potential in sympathetic ganglia, were analysed by means of sucrose-gap, intracellular microelectrode techniques, and voltage clamp technique. Both the P-potential and the slow IPSP consist of two different potential components, namely the ouabain-sensitive and the ouabain-insensitive components. The ouabain-sensitive component was enhanced by a moderate conditioning hyperpolarization. This component was most reasonably explained as a potential change generated by an activation of the electrogenic Na+ pump. The ouabain-insensitive potential component of the P-potential and the slow IPSP decreased in the amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of ouabain-insensitive component of slow IPSP and slow inhibitory postsynaptic current (IPSC) was close to the EK. The amplitude of ouabain-insensitive component of P-potential and slow IPSP was markedly decreased by an elevation of external K+ concentration. The reversal potential of ouabain-insensitive component shifted to a more positive potential level in high K+ Ringer's solution. On the other hand, it was augmented in K+-free Ringer's solution. A reduction of the membrane resistance was observed during the generation of the slow IPSP, when the membrane potential of ganglion cells was held at a membrane potential level more negative than -60 mV. The slow IPSC recorded by voltage-clamp method was associated with an increase in membrane conductance. It was concluded that the ouabain-insensitive component was generated by an activation of K+ conductance.

Animals↗
PubMed1994

Separate activation of fast and slow inhibitory postsynaptic potentials in rat neocortex in vitro.

Synaptic inhibition was investigated by stimulating inhibitory neurones with focal microapplications of glutamate, while recording from layer V pyramidal neurones of rat somatosensory cortical slices. One class of inhibitory postsynaptic potentials (IPSPs) thus elicited was characterized as a fast, chloride-mediated, GABAA IPSP in part by its fast time-to-peak (mean 2.5 ms) and brief duration, but primarily on the basis of its reversal potential at -68 mV, and its blockade by picrotoxin. The average peak amplitude for these fast IPSPs was -1.5 mV, measured at -60 mV. The peak conductance calculated for these events was about 10 nS. The conductance change associated with the maximal fast inhibitory postsynaptic potential resulting from electrical stimulation of afferent pathways ranged up to 116 nS. A second class of IPSP was encountered much less frequently. These glutamate-triggered events were characterized as slow, potassium-mediated GABAB IPSPs partly because of their longer times-to-peak (mean, 45 ms) and duration, but especially because of their extrapolated equilibrium potential at about -89 mV and blockade by 2-hydroxysaclofen. The average peak amplitude for these slow IPSPs was -2.3 mV, measured at -60 mV. The peak conductance for these events was about 8 nS. IPSPs resulting from the excitation of individual inhibitory interneurones were elicited by glutamate microapplication at particular locations relative to recording sites. Both fast and slow IPSPs were generated, but these occurred as separate events, and mixed responses were never seen. Thus, the two mechanistically distinct types of IPSPs which result from GABA interaction at GABAA and GABAB receptors on neocortical neurones may be mediated by separate classes of inhibitory neurones.

Animals↗
PubMed1986

Characterization of spontaneous and evoked inhibitory postsynaptic potentials in rat supraoptic neurosecretory neurons in vitro.

Intracellular recordings from 52 supraoptic nucleus neurosecretory neurons in perfused explants of rat hypothalamus revealed abundant spontaneous inhibitory postsynaptic potentials (sIPSPs) and a compound evoked inhibitory postsynaptic potential (eIPSP) following electrical stimulation in the diagonal band of Broca (DBB). These IPSPs were characterized in terms of the magnitude and ionic specificity of the underlying current and in terms of the transmitter responsible for their activation. sIPSPs rose rapidly to peak within 3-5 ms and decayed exponentially with a mean time constant of 20.2 +/- 1.9 ms (mean +/- SE), a value 1.6-fold greater than the mean cell time constant of 13.8 +/- 1.0 ms. The eIPSPs rose rapidly to peak within 3-10 ms and decayed exponentially over 60-100 ms with a mean time constant of 37.0 +/- 2.8 ms, which is 2.6-fold greater than the mean cell time constant. These features imply a brief persistence of the conductance underlying the IPSPs. In recordings with KAcetate-filled micropipettes, sIPSPs were hyperpolarizing at membrane potentials in the range of -50 to -70 mV and reversed polarity when the membrane was hyperpolarized beyond -80 mV. The mean reversal potential (EsIPSP) was -72.4 +/- 1.1 mV. eIPSPs were hyperpolarizing at resting membrane potential and could be reversed by membrane hyperpolarization beyond a mean reversal potential (EIPSP) of -67.4 +/- 1.4 mV. In recordings with KCl-filled micropipettes, sIPSPs were depolarizing at all membrane potentials more negative than -50 mV. Under these conditions, EsIPSP was estimated at -44 mV. sIPSPs were absent when chloride ions were removed from the perfusion medium. eIPSPs were depolarizing at all membrane potentials and often evoked action potentials; mean EeIPSP was 43.2 mV. Reversal potentials of spontaneous and evoked IPSPs were similar. At a given membrane potential, sIPSP amplitudes varied widely between 1 and 20 mV. The conductance increase underlying individual sIPSPs was estimated to vary between 0.17 and 3.0 nS (avg 0.6 nS) against a mean resting input conductance of 3.78 +/- 0.41 nS. Estimates of the conductance underlying eIPSPs varied widely between cells, from 0.8 to 22.0 nS (mean 72 nS). Accordingly, the ratio of evoked to spontaneous IPSP conductance varied from 1.6 to 43.7 (mean 13.1). The reversal potential of evoked IPSPs shifted with the extracellular concentration of Cl- ions ([Cl-]0) with a mean slope of 41 mV/log [Cl-]0.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Low-magnesium epilepsy in rat hippocampal slices: inhibitory postsynaptic potentials in the CA1 subfield.

Spontaneous, synchronous epileptiform discharges were recorded in both CA3 and CA1 subfields of rat hippocampal slices perfused with Mg2+-free medium. Surgical separation of the two areas abolished the spontaneous discharges only in the CA1 subfield. However, epileptiform responses in the isolated CA1 subfield could still be evoked by orthodromic stimulation. Intracellularly these stimulus-induced responses were characterized by a depolarization associated with a burst of action potentials. Stimulation of the alveus still evoked a hyperpolarizing potential, presumably a recurrent inhibitory postsynaptic potential (IPSP) in CA1 pyramidal cells. Both spontaneous and stimulus-induced epileptiform discharges were blocked by the selective antagonist of N-methyl-D-aspartate (NMDA) receptors DL-2-amino-phosphonovalerate (APV). APV also reduced the amplitude and duration of the IPSP induced by alveus stimulation. Thus, epileptiform discharges evoked by lowering Mg2+ in the CA1 subfield are associated with a preservation of inhibitory mechanisms. Furthermore the effects exerted by APV upon the IPSP implicate that NMDA receptors might be involved in the neuronal circuit responsible for the hyperpolarizing IPSP generated by CA1 pyramidal neurons.

2-Amino-5-phosphonovalerate↗
PubMed1993

Somatostatin-mediated inhibitory postsynaptic potential in sympathetically denervated guinea-pig submucosal neurones.

1. Intracellular recordings were made from submucosal neurones in guinea-pig ileum. In some animals, the extrinsic (sympathetic) nerves to the submucosal plexus were severed 5-7 days previously. The actions of somatostatin and somatostatin analogues on membrane potential, membrane current and inhibitory postsynaptic potentials (IPSPs) were examined. 2. Somatostatin, somatostatin(1-28), [D-Trp8]somatostatin and the somatostatin analogue CGP 23996 all produced equivalent maximum hyperpolarizations or outward currents; half-maximal concentrations (EC50 values) were 9-11 nM. The somatostatin analogue MK 678 had an EC50 of 0.9 nM. Extrinsic sympathectomy did not alter concentration-response relations for somatostatin or its analogues. 3. Somatostatin (> 100 nM) produced hyperpolarization or outward current that declined almost completely during superfusion for 2-4 min; decline of the somatostatin current was exponential with a time constant of 30 s in the presence of 2 microM somatostatin. Desensitization was not altered by extrinsic denervation. 4. Recovery from desensitization was rapid and followed the time course of agonist wash-out. Forskolin, phorbol esters, dithiothreitol, hydrogen peroxide, concanavalin A, or reducing temperature from 35 to 29 degrees C did not alter the time course, degree of, or recovery from desensitization. 5. The somatostatin-induced desensitization was of the homologous type; no cross-desensitization to opiate or alpha 2-adrenoceptor agonists (which activate the same potassium conductance) occurred. 6. Somatostatin desensitization did not alter the adrenergic IPSP seen in sympathetically innervated preparations but abolished the non-adrenergic IPSP recorded from normal preparations and from preparations in which the extrinsic sympathetic nerve supply had been surgically removed. 7. The selective blockade of the non-adrenergic IPSP by the homologous-type somatostatin desensitization characterized in the present study provides strong support for the hypothesis that somatostatin is the neurotransmitter underlying the non-adrenergic IPSP in both normal and extrinsically denervated submucosal neurones.

Animals↗
PubMed1995

Reduction of GABA-mediated inhibitory postsynaptic potentials in hippocampal CA1 pyramidal neurons following oral flurazepam administration.

Oral administration of the benzodiazepine, flurazepam, for one week results in tolerance in vivo and in vitro and in a reduction in recurrent and feedforward inhibition in vitro in the CA1 pyramidal cell region of hippocampus. In the present study CA1 pyramidal cells were examined intracellularly in vitro in rat hippocampal slices (500 microns) from rats sacrificed two or seven days after cessation of oral flurazepam treatment. Following drug treatment, the membrane characteristics of CA1 pyramidal cells were not significantly different from control neurons. GABAA-mediated, early inhibitory postsynaptic potentials were significantly reduced in amplitude (60%) in pyramidal neurons from rats killed two days, but not in those killed seven days, after the end of drug administration. The decrease in early inhibitory postsynaptic potential amplitude was observed using just-subthreshold, threshold and supramaximal orthodromic stimulation as well as following antidromic activation. The magnitude of the decrease in the early inhibitory postsynaptic potential amplitude was similar in the presence of the GABAB antagonist, CGP 35348, and could not be attributed to differences in the strength of afferent stimulation between flurazepam-treated and control groups. The size of the GABAB-mediated, late inhibitory postsynaptic potentials was also significantly decreased (45%) in comparison to control cells. Reversal potentials for both the early (-72 mV) and late (-92 mV) hyperpolarizations were not significantly different between groups. Following high intensity orthodromic stimulation, in the presence of an intracellular sodium channel blocker (QX-314) which also blocks the GABAB-mediated late hyperpolarization, a bicuculline-sensitive late depolarizing potential was unmasked in neurons from FZP-treated rats, but never from control cells. Excitatory postsynaptic potential amplitude was significantly increased in flurazepam-treated neurons and the threshold for the synaptically-evoked action potential was significantly increased. Following depolarizing current injection, the duration and frequency of pyramidal cell discharges and the action potential threshold were not altered by oral flurazepam treatment. The amplitude of the fast afterhyperpolarization was also not changed. Overall, the findings indicate an impairment of transmission at GABAergic synapses onto hippocampal CA1 pyramidal cell neurons after chronic benzodiazepine treatment at a time when rats are tolerant to the anticonvulsant effects of the benzodiazepines in vivo.

Acetates↗
PubMed1981

Comparison of the receptors mediating the catecholamine hyperpolarization and slow inhibitory postsynaptic potential in sympathetic ganglia.

We investigated the proposed catecholamine receptor in the superior cervical ganglion of the rabbit with the sucrose-gap technique to characterize the receptor pharmacologically. It has been suggested that this receptor is involved in the slow inhibitory postsynaptic potential in sympathetic ganglia. Epinephrine, norepinephrine and dopamine consistently hyperpolarized the ganglion membrane (N = 60). The order of potency was epinephrine greater than or equal to norepinephrine much greater than dopamine. Clonidine (10(-5) M), phenylephrine (10(-4) M) and isoproterenol (10(-3) M) also hyperpolarized the ganglion. However, apomorphine, even at millimolar concentration, did not hyperpolarize the membrane. The alpha antagonists phentolamine (10(-6) M) and yohimbine (10(-6) M) depressed the response to all catecholamines and shifted the catecholamine concentration-response curve to the right; dopamine and beta antagonists and the alpha-1 antagonist prazosin had no effect on the catecholamine hyperpolarizations. In contrast, the nerve-evoked slow inhibitory postsynaptic potential was selectively depressed only by atropine (10(-7) M). In conclusion, we characterized an alpha-2 adrenergic receptor in the rabbit superior cervical ganglion responsible for the catecholamine hyperpolarization and found that the slow inhibitory postsynaptic potential does not appear to be mediated by the same receptor.

Adrenergic alpha-Antagonists↗
PubMed1992

Diverse actions of 5-hydroxytryptamine on frog spinal dorsal horn neurons in vitro.

The effects of 5-hydroxytryptamine on the membrane potential and input resistance of 86 dorsal horn neurons were studied using intracellular recordings in isolated, hemisected spinal cords of adult frogs (Rana pipiens). Bath application of serotonin (5-100 microM) caused membrane depolarizations in 58 (67%) neurons, hyperpolarizations in 12 (14%) cells, biphasic responses in nine (11%) neurons, and no detectable change in seven (8%) cells. In some neurons depolarized by serotonin, the amine's responses could be mimicked by the selective 5-HT2 agonist (+/-)-1(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride and the 5-HT1C/2 agonist alpha-methyl-5-hydroxytryptamine, and blocked by the 5-HT1C/2 antagonists ketanserin and mianserin. In other neurons depolarized by serotonin, the 5-HT3 agonist 2-methyl-5-hydroxytryptamine mimicked, and the 5-HT3 antagonist, 3-tropanyl-3,5-dichlorobenzoate, blocked the serotonin-induced responses. Depolarizing responses due to activation of 5-HT1C/2 receptors were generally accompanied by increases in the membrane input resistance, whereas depolarizations mediated by 5-HT3 receptors were associated with a decreased membrane input resistance. Superfusion with tetrodotoxin or low-Ca2+/high-Mg(2+)-containing media abolished about half of the depolarizing responses. Hyperpolarizations caused by serotonin were associated with a decrease in membrane input resistance, and might have been due to activation of a potassium conductance. These responses persisted in bathing solutions containing tetrodotoxin or low-Ca2+/high-Mg2+. The 5-HT1A agonist 8-hydroxy-2-(di-N-propylamine)tetralin hydrobromide mimicked, whereas the 5-HT1A antagonist spiroxatrine blocked, these hyperpolarizing responses. Other antagonists selective for 5-HT1C/2 or 5-HT3 receptors were without effect. Serotonin-produced biphasic responses consisted of either an initial depolarization followed by a hyperpolarization or the reverse. The selective 5-HT2 agonist (+/-)-1(2,5-dimethyoxy-4-iodophenyl)-2-aminopropane hydrochloride could only mimic the depolarizations, whereas the 5-HT1A agonist 8-hydroxy-2-(di-N-propylamine)tetralin hydrobromide produced only the hyperpolarizations. Spiroxatrine, a 5-HT1A antagonist, blocked only the hyperpolarizations without affecting the depolarizations, and methysergide, a non-specific 5-HT receptor antagonist, depressed both the depolarizations and hyperpolarizations. Serotonin also appeared to affect spinal dorsal horn neurons indirectly because it produced excitatory postsynaptic potentials, inhibitory postsynaptic potentials, and a mixture of both.(ABSTRACT TRUNCATED AT 400 WORDS)

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1986

The pathway for the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

Intracellular and sucrose gap recording techniques were used to examine synaptically evoked potentials and the response of neurons in bullfrog paravertebral sympathetic ganglia to muscarinic agonists. These neurons were defined as either B or C cells on the basis of the conduction velocity of antidromically evoked action potentials. Following stimulation of preganglionic C-fibers in the rostral portion of the VIIIth spinal nerve, a fast nicotinic excitatory postsynaptic potential (EPSP) and a slow atropine-sensitive inhibitory postsynaptic potential (IPSP) could be recorded intracellularly in C cells of the IXth and Xth paravertebral ganglia treated with 70 microM d-tubocurarine chloride (dTC). Under these conditions, local iontophoretic application of acetylcholine (ACh) could produce a slow hyperpolarization of C cell membrane potential. ACh hyperpolarizations or slow IPSPs were not detected in ganglionic B cells. Stimulation of the preganglionic B-fibers in the sympathetic chain produced a fast nicotinic EPSP and a slow muscarinic EPSP in ganglionic B cells. A small population of C cells also received cholinergic B-fiber innervation from the sympathetic chain and exhibited a slow IPSP upon tetanic stimulation of this pathway. When curarized ganglia were examined by means of sucrose gap recording, superfusion of the muscarinic agonist, methacholine (MCh), produced an initial hyperpolarization (MChH) followed by a depolarization (MChD). Both responses were blocked by atropine and therefore presumably reflect the activation of muscarinic receptors involved in the generation of the slow IPSP and the slow EPSP, respectively. Although synaptic transmission was blocked by Ringer solution containing 4 mM Co2+, neither this solution nor 10 microM tetrodotoxin reduced the amplitude of the MChH. The MChH was slightly reduced by Ringer solution containing 0.1 mM Ca2+, however, the response could be restored by the addition of 6 mM Mg2+. These results indicate that the MChH in curarized bullfrog sympathetic ganglia results from a direct muscarinic action on ganglionic cells. This suggests that the slow IPSP is mediated by ACh released from cholinergic preganglionic fibers that make synaptic contact with ganglionic C cells.

Acetylcholine↗
PubMed1992

Long-term potentiation and sprouting of mossy fibers produced by brief episodes of hyperactivity.

A brief application of high K+ or excitatory amino acids (i.e. kainic acid) generated repetitive synchronized burst that persisted for the duration of the application, in the CA3 field. Once excitability has been enhanced, further stimulation of various inputs evoked burst instead the typical excitatory postsynaptic potential--inhibitory postsynaptic potential sequence evoked in control conditions. These long-lasting changes in synaptic efficacy involved the activation of glutamate receptors of N-methyl-D-aspartate (NMDA) subtype. A brief period of hyperactivity (i.e. kindling of limbic pathways or administration of kainic acid) also resulted in a more delayed synaptic remodeling, notably of hippocampal mossy fibers (i.e. the axons of granule cells that mostly contact the apical dendrites of CA3 pyramidal neurons). Thus mossy fibers sprouted and made multiple ectopic asymmetrical synapses with spines of both granule cells dendrites and basilar dendrites of CA3 pyramidal cells. Finally, sprouting of mossy fibers was associated with a significant rise in the density of kainic acid binding sites (fmol/mg tissue) in the aberrantly innervated zones: the inner third of molecular layer and the stratum oriens of CA3. Saturation studies revealed that this rise did not significantly affect the affinity (Kd values) but the Bmax. In conclusion, brief seizure episodes produced in the hippocampus remarkably long-lasting changes in synaptic efficacy; synaptic density and the mean density of excitatory amino acid receptors of non-NMDA subtype. The role that such plastic changes may play in the permanence of the epilepsy is finally discussed.

Afferent Pathways↗
PubMedDate not supplied

Epileptogenic effects of radiographic contrast agents: experimental study.

Electrical activity in cells directly exposed to water-soluble radiographic contrast agents was investigated by intracellular recordings from neurons of the abdominal ganglia of Aplysia. Measurements of membrane resting potential, membrane conductance, synaptic and action potential configuration, and spontaneous electrical activity were performed. Test solutions included sodium diatrizoate, meglumine iothalamate, metrizamide, and control solutions. Solutions (100 and 200 mOsm) of these agents did not significantly alter resting membrane potential, membrane conductance, action potential frequency or configuration, or excitatory postsynaptic potentials. Inhibitory postsynaptic potentials were suppressed by contrast agents. These results suggest that contrast agents affect at least some neurons by disinhibition.

Action Potentials↗
PubMed1997

Strychnine blocks inhibitory postsynaptic potentials elicited in masseter motoneurons by sensory stimuli during carbachol-induced motor atonia.

In previous studies we reported that large-amplitude inhibitory potentials were elicited in masseter motoneurons by auditory stimuli (95-dB clicks) and stimulation of the sciatic nerve in alpha-chloralose-anesthetized cats [Kohlmeier K. A. et al. (1994) Soc. Neurosci. Abstr. 20, 1218; Kohlmeier K. A. et al. (1995) Sleep Res. 24, 9]. These potentials were always elicited during motor atonia induced by the pontine injection of carbachol into the nucleus pontis oralis and were never elicited prior to atonia. In the present report, the hyperpolarizing potentials that arose in response to clicks and stimulation of the sciatic nerve were blocked following the juxtacellular application of strychnine, a glycinergic antagonist. In contrast, bicuculline, a GABA(A) receptor antagonist, did not suppress the carbachol-dependent hyperpolarizing potentials elicited by these stimuli. In some motoneurons, blockade of the inhibitory potential by strychnine revealed a depolarizing potential. These data suggest that clicks and stimulation of the sciatic nerve not only elicit inhibition of motoneurons but also activate an excitatory drive which is masked by elicited inhibitory postsynaptic potentials. These findings suggest that glycine is likely to be the neurotransmitter that is responsible for the inhibitory postsynaptic potentials elicited in masseter motoneurons following the presentation of auditory and somatosensory stimuli during carbachol-induced motor atonia. We suggest that the same system that mediates glycinergically-dependent motor atonia during naturally occurring active sleep [Chase M. H. et al. (1989) J. Neurosci. 9, 743-751] also mediates the carbachol-dependent response of motoneurons to sensory stimuli.

Animals↗
PubMed1994

Topography of recurrent inhibitory postsynaptic potentials between individual motoneurons in the cat.

1. The amplitude of recurrent inhibitory postsynaptic potentials (RIPSPs) was 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 postsynaptic responses were recorded and averaged in the second motoneuron. Input resistance, rheobase, and conduction velocity were determined for many motoneurons. Most motoneurons innervated extensor muscles. 2. RIPSP values as large as -283 microV were recorded, but most were between -10 and -40 microV. RIPSPs from individual motoneurons of a pool are distributed to several heteronymous motor nuclei and have a range of amplitudes comparable with homonymous RIPSPs. 3. A specific spatial distribution of RIPSP amplitudes was found whereby the largest RIPSP amplitudes (> 40 microV) occurred in motoneurons located within +/- 1.4 mm of the stimulated motoneuron. A significant correlation was found between RIPSP amplitude and the distance between motoneurons for all motoneuron pairs. This correlation was also found within individual groups of motoneuron pairs that innervate the lateral gastrocnemius, medial gastrocnemius, anterior-middle biceps femoris, or soleus muscles. 4. The dependency of RIPSP amplitude on the motoneuron species, which is the particular muscle a motoneuron innervates, is less distinct than the dependency of RIPSP amplitude on topography. Pooling all motoneuron species of close motoneuron pairs indicated that RIPSPs measured in homonymous motoneuron pairs were greater in amplitude than RIPSPs measured in heteronymous pairs. In addition, homonymous RIPSPs of anterior middle biceps femoris or lateral gastrocnemius motoneurons were greater than heteronymous RIPSPs of those motoneurons in all heteronymous combinations. However, homonymous and heteronymous RIPSPs were not significantly different when heteronymous pairs were restricted to individual combinations of species. These findings indicate that RIPSP amplitudes within a set of motor nuclei interconnected by recurrent inhibition are dependent in some cases on the species of motoneurons, but this effect is less important than the effect of topography on RIPSP amplitude. 5. These results indicate that recurrent inhibition in motoneuron pools that innervate hindlimb extensor muscles has a strong topographic organization, such that the strongest recurrent inhibition is produced by each motoneuron in a restricted rostrocaudal zone that includes both homonymous and heteronymous motor nuclei. This suggests that recurrent inhibition is organized for the control of several motor nuclei engaged in common motor activity as well as regulation of activity within individual motor pools.

Animals↗
PubMed1978

Involvement of an interneuron in the generation of the slow inhibitory postsynaptic potential in mammalian sympathetic ganglia.

Acetylcholine (AcCho) was applied electrophoretically to cells of isolated rabbit superior cervical ganglia, and the response was recorded by means of intracellular recording techniques. In the presence of d-tubocurarine (5 micron), AcCho applied by tetanic current pulses elicited three distinct membrane potential changes: a slow depolarization, a slow hyperpolarization, and a biphasic response consisting of an initial hyperpolarization followed by a depolarization. Atropine (1 micron) abolished all the membrane potential changes elicited by AcCho. On the other hand, superfusion with a low-Ca/high-Mg solution, tetrodotoxin (0.1 micron), or haloperidol (0.1 micron) selectively and reversibly blocked AcCho-induced hyperpolarization without appreciably affecting the depolarization. The membrane resistance remained relatively constant during the course of hyperpolarization. Application of steady depolarizing and hyperpolarizing currents decreased and increased, respectively, the amplitude of hyperpolarization. These results demonstrate that the hyperpolarization elicited by AcCho is electrophysiologically and pharmacologically similar to the slow inhibitory postsynaptic potential induced by nerve stimulation; furthermore, they support the view that the slow inhibitory postsynaptic potential elicited by presynaptic stimulation is a disynaptic phenomenon involving the release of a second transmitter, possibly dopamine, from an interneuron.

Acetylcholine↗
PubMed1987

Characteristics of long-duration inhibitory postsynaptic potentials in rat neocortical neurons in vitro.

The characteristics of long-duration inhibitory postsynaptic potentials (1-IPSPs) which are evoked in rat frontal neocortical neurons by local electrical stimulation were investigated with intracellular recordings from an in vitro slice preparation. Stimulation with suprathreshold intensities evoked 1-IPSPs with typical durations of 600-900 msec at resting membrane potential. Conductance increases of 15-60% were measured at the peak amplitude of 1-IPSPs (150-250 msec poststimulus). The duration of the conductance increases during 1-IPSPs displayed a significant voltage dependence, decreasing as the membrane potential was depolarized and increasing with hyperpolarization. The reversal potential of 1-IPSPs is significantly altered by reductions in the extracellular potassium concentration. Therefore it is concluded that 1-IPSPs in rat neocortical neurons are generated by the activation of a potassium conductance. 1-IPSPs exhibit stimulation fatigue. Stimulation with a frequency of 1 Hz produces a complete fatigue of the conductance increases during 1-IPSPs after approximately 20 consecutive stimuli. Recovery from this fatigue requires minutes. 1-IPSPs are not blocked by bicuculline but are blocked by baclofen.

Animals↗
PubMed1997

[Electrophysiological and pharmacological properties of inhibitory postsynaptic potentials evoked in laryngeal motoneurons in decerebrate cats].

Electrophysiological and pharmacological properties of inhibitory postsynaptic potentials (IPSPs) induced in respiratory laryngeal motoneurons (LMNs) by electrical stimulation of the superior laryngeal nerve were investigated in decerebrate, paralyzed, vagotomized and artificially ventilated cats. In the inspiratory phase, a single pulse stimulation caused a short latency excitation followed by long-lasting inhibition of phrenic nerve discharge. A long latency wave of IPSPs occurred in inspiratory LMNs. In the expiratory phase, the same stimulation provoked a transient excitation in the phrenic nerve. An IPSP wave of long-latency was induced in post-inspiratory LMNs. The time course of each long-latency IPSP wave corresponded to that of either inspiratory inhibition or expiratory excitation of the phrenic discharge. These IPSP waves induced in both types of LMNs were decreased in amplitude by iontophoresed bicuculline but not by strychnine. These results suggest that laryngeally evoked IPSP waves in inspiratory and post-inspiratory LMNs are mediated through poly-synaptic pathways within the central respiratory network and that GABAA-receptors are involved in their final pathway.

Animals↗