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PubMed1984

Development of hyperpolarizing inhibitory postsynaptic potentials and hyperpolarizing response to gamma-aminobutyric acid in rabbit hippocampus studied in vitro.

The postnatal development of IPSPs and response to locally applied GABA were examined using intracellular recording techniques in region CA1 of rabbit hippocampal slices maintained in vitro. Pyramidal neurons in slices from mature rabbits demonstrated an EPSP-IPSP sequence following stimulation of stratum radiatum. In these same slices, pressure application of GABA into stratum pyramidale and stratum radiatum produced membrane hyperpolarization and depolarization, respectively. Pyramidal neurons in slices from immature rabbits (age 6 to 10 days) responded differently. Stimulation of stratum radiatum produced a prolonged depolarizing postsynaptic potential; few IPSPs were observed. Ejection of GABA into either stratum pyramidale or stratum radiatum evoked a depolarizing response. The GABA agonist, 4,5,6,7-tetrahydroisoxazolo [5,4-c] pyridine-3-ol (THIP), which has been reported to activate "hyperpolarizing" GABA receptors selectively, primarily produced membrane hyperpolarization when applied to the somata of mature neurons, but it evoked a depolarization when applied to immature neurons. Bicuculline, a GABA antagonist which may have a preferential selectivity for "depolarizing" GABA receptors, was somewhat more efficacious (at 50 microM concentration) at antagonizing GABA-evoked depolarization in immature cells than GABA-evoked hyperpolarization in mature cells. This same concentration of bicuculline partially antagonized IPSPs in mature cells, and it markedly potentiated depolarizing PSPs in immature cells. Taken together, these results suggest that the late development of synaptic inhibition in rabbit hippocampus is due, at least in part, to an immaturity in the GABAergic system.

Action Potentials↗
PubMed1992

Alterations in the properties of hippocampal pyramidal neurons in the aged rat.

The electrophysiological and pharmacological properties of CA1 hippocampal pyramidal neurons were studied in slices from young (three to four months) and aged (25-32 months) Sprague-Dawley rats having previously performed two behavioral tasks. About 20% of the aged rats were impaired in either the spontaneous alternation task or the water maze task. Electrophysiological parameters were measured and compared in young and aged animals using intracellular recordings. No age-related differences were observed in membrane potential, input resistance, amplitude of action potentials or amplitude of calcium spikes. The amplitude and duration of individual afterhyperpolarizations following a single spike were unchanged. In contrast, the neuronal excitability was significantly decreased and the spike duration significantly enhanced in aged rats as compared to young rats. The comparison of afterhyperpolarizations (which follow a burst of spikes) between young and aged rats was more complex. An increase in the amplitude and duration of afterhyperpolarizations generally occurred in aged animals. However, this increase was not consistent among animals and was dependent on the holding potential of the neuron and on the number of action potentials used to trigger the afterhyperpolarization. The depolarizing effect of bath-applied carbachol, as well as the associated increase in membrane resistance were reduced in neurons from aged rats. In contrast, the effects of carbachol on the depression of synaptic events and the blockade of the afterhyperpolarizations were similar in young and aged animals. In addition, the amplitude of the slow cholinergic excitatory postsynaptic potential induced by stimulation of cholinergic afferents in the presence of physostigmine was also decreased in aged rats. Excitatory postsynaptic potentials and inhibitory postsynaptic potentials following electrical stimulation of stratum radiatum were compared. The amplitude and duration of excitatory postsynaptic potentials were increased in aged rats. The amplitude and duration of the fast inhibitory postsynaptic potential were not significantly affected in aged animals. In contrast, the duration of the slow inhibitory postsynaptic potential was decreased in aged rats. Since the mean baclofen-induced hyperpolarization was only slightly reduced in aged rats, the most likely explanation is a decrease in the release of GABA rather than an alteration in the postsynaptic response mediated by GABAB receptors. A statistically significant correlation was found between the degree of impairment in the spontaneous alternation task and the amplitude of the carbachol-induced depolarization.

Acetylcholine↗
PubMed1988

An efferent inhibition of auditory afferents mediated by the goldfish Mauthner cell.

Intracellular recordings from goldfish auditory afferents revealed a hyperpolarization triggered by a single impulse in the Mauthner cell. The firing of either one of the two Mauthner cells alone was sufficient to evoke this potential change. The all or none hyperpolarization, which could only be recorded in some auditory fibers, presumably was an inhibitory postsynaptic potential. The inhibitory postsynaptic potential typically had a latency of 6 ms, an amplitude of 1 mV and a half-decay time of 6.8 ms; it could block or delay impulses evoked by direct current injection and could attenuate the amplitude of excitatory postsynaptic potentials evoked by sound pulses. However, this inhibitory postsynaptic potential did not reduce the amplitudes of electrotonic coupling potentials produced by antidromic impulses in the Mauthner cell. We propose that the inhibitory postsynaptic potential is generated at the dendrites of the auditory fibers, i.e. in the ear, rather than at the central terminals of the afferent, where the antidromic coupling potentials originate. The possibility that the inhibitory postsynaptic potential actually represented dis-facilitation due to an efferent inhibition of the hair cells, which tonically depolarize the saccular fibers, was ruled out because depolarization of these fibers increased the inhibitory postsynaptic potential amplitude. Possible morphological substrates for the efferent inhibition and the behavioral significance of this inhibition are discussed.

Animals↗
PubMed1985

The ionic mechanism of postsynaptic inhibition in motoneurones of the frog spinal cord.

The ionic mechanism of postsynaptic inhibition in frog spinal motoneurones was studied with conventional and with ion-sensitive microelectrodes. In these neurones the inhibitory postsynaptic potential was depolarizing, its reversal potential being 15 mV less negative than the resting membrane potential. During the inhibitory postsynaptic potential the input resistance of the motoneurones was reduced to 20% of the resting value, indicating a strong increase of membrane conductance. The Cl- equilibrium potential calculated from intra- and extracellular Cl- activity measurements coincided with the reversal potential of the inhibitory postsynaptic potential to within a few millivolts. During repetitive inhibitory postsynaptic activity the intracellular Cl- activity decreased markedly, while the extracellular Cl- activity increased slightly. These changes of intra- and extracellular Cl- activities were no longer found after suppression of the inhibitory postsynaptic potential by strychnine. Blockade of an active, inward-going Cl- transport system in motoneurones by NH+4 led to a shift of the Cl- equilibrium potential and the reversal potential of the inhibitory postsynaptic potential towards the resting membrane potential. After prolonged action of NH+4, the Cl- equilibrium potential approached the membrane potential to within 5 mV, while the reversal potential of the inhibitory postsynaptic potential and resting membrane potential coincided. The difference between Cl- equilibrium potential and membrane potential after blockade of the Cl- pump is traced back to interfering intracellular ions, such as HCO-3 or SO42-, leading to an overestimation of intracellular Cl- activity and to the calculation of an erroneous Cl- equilibrium potential. Inhibitory amino acids like gamma-aminobutyrate or beta-alanine evoked depolarizations with reversal potentials similar to that of the inhibitory postsynaptic potential. These depolarizations were associated with a marked decrease of neuronal input resistance during inhibition. During the actions of these compounds a decrease of intracellular and a small increase of extracellular Cl- activity were found. The activities of other ions (K+, Ca2+ and Na+) did not change significantly, with the exception of extracellular K+ activity, which was slightly increased. Evidence is presented that the inhibitory postsynaptic potential, as well as the depolarizing action of inhibitory amino acids in motoneurones, is the result of an increase in membrane Cl- permeability and an efflux of Cl- from these cells, while other ions do not seem to be involved.

Amino Acids↗
PubMed1985

Slow postsynaptic potentials in neurones of submucous plexus of guinea-pig caecum and their mimicry by noradrenaline and various peptides.

Intracellular recordings of membrane potential and membrane currents were made from neurones in the submucous plexus of the guinea-pig caecum in vitro. Fast and slow excitatory postsynaptic potentials and slow inhibitory postsynaptic potentials were recorded from the majority of neurones following focal stimulation of presynaptic fibres in the plexus. The slow inhibitory postsynaptic potential was associated with an increase in membrane conductance and reversed its polarity at -90 mV; it was reversibly blocked by yohimbine. The slow excitatory postsynaptic potential and its underlying current was associated with a decrease in membrane conductance. Two kinds of voltage-dependence both of the slow excitatory postsynaptic potential and current were observed; in 80% of cells, the excitatory postsynaptic potential and current became smaller with membrane hyperpolarization and reversed polarity at -90 mV (reversing type) but in 20% of cells both the excitatory postsynaptic potential and current simply disappeared when the membrane potential reached -70 mV (non-reversing type). The effects of acetylcholine, adenosine 5'-triphosphate, bombesin, 5-hydroxytryptamine, neurotensin, noradrenaline, substance P and vasoactive intestinal polypeptide were examined. The only substance which mimicked the slow inhibitory postsynaptic potential was noradrenaline; brief applications of noradrenaline caused hyperpolarizations which had the same time-course, reversal potential and sensitivity to yohimbine as the slow inhibitory postsynaptic potential. The non-reversing type of slow excitatory postsynaptic potential was mimicked only by adenosine 5'-triphosphate. The reversing type of slow excitatory postsynaptic potential was mimicked by bombesin, neurotensin, substance P and vasoactive intestinal polypeptide. 5-Hydroxytryptamine and vasoactive intestinal polypeptide (in some neurones) caused a depolarization with an increase in membrane conductance. All three synaptic potentials were reversibly depressed by superfusion of noradrenaline but noradrenaline did not affect the potential changes evoked by brief application of exogenous acetylcholine or substance P. It is concluded that, in guinea-pig submucous plexus neurones, the slow inhibitory postsynaptic potential is mediated by noradrenaline and results from a potassium conductance increase.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed2002

Presynaptic modulation of GABAergic inhibition by GABA(B) receptors in the rat's inferior colliculus.

Whole-cell patch clamp recordings were made from neurons in a brain slice preparation of the inferior colliculus in 11-15-day-old rat pups. Synaptic responses were elicited by applying a current pulse to the lateral lemniscus just below the central nucleus of the inferior colliculus. To examine GABAergic inhibition in the inferior colliculus all excitatory postsynaptic potentials and glycinergic inhibitory postsynaptic potentials were blocked by bath application of their respective antagonists and the contribution of GABA(B) receptors was determined for the remaining inhibitory postsynaptic potentials. For most cells the isolated inhibitory postsynaptic potential was completely blocked by the GABA(A) receptor antagonist, bicuculline, but was unaffected by the GABA(B) receptor antagonist, phaclofen. The GABA(B) receptor agonist, baclofen (10-20 microM), decreased the amplitude of the inhibitory postsynaptic potentials. This effect was completely blocked by phaclofen. Baclofen did not increase the cell membrane conductance or alter the rate of firing produced by depolarization of the cell membrane. In contrast, muscimol, a GABA(A) receptor agonist, greatly increased membrane conductance and lowered the firing rate produced by depolarization. Our results indicate that GABAergic inhibition in the auditory midbrain can be reduced by the activation of GABA(B) receptors and suggest that the effects are presynaptic.

Animals↗
PubMed1989

Selective antagonism of muscarinic potentials on the superior cervical ganglion of the rat.

Selective antagonists have been used to classify the muscarinic receptors involved in the slow excitatory postsynaptic potential and slow inhibitory postsynaptic potential of the superior cervical ganglia of the rat, as recorded in 1 microM neostigmine, using a grease-gap method. Cardioselective M2 antagonists, e.g. AF-DX 116, depressed the slow inhibitory postsynaptic potential and enhanced the slow excitatory postsynaptic potential. The M1 selective antagonist pirenzepine depressed both potentials equally. The high potency of pirenzepine against the slow excitatory postsynaptic potential, however, indicates that it is mediated by M1 receptors. The slow excitatory and inhibitory postsynaptic potentials were found to be pharmacologically similar to the muscarinic agonist-induced depolarisation and hyperpolarisation of this preparation, respectively. The actions of two muscarinic agonists on the postsynaptic potentials were also studied. It is concluded that the slow excitatory postsynaptic potential is mediated by M1 receptors and the slow inhibitory postsynaptic potential by cardiac-like M2 receptors.

Animals↗
PubMed1988

Non-cholinergic synaptic potentials mediated by lumbar colonic nerve in the guinea-pig inferior mesenteric ganglion in vitro.

Non-cholinergic slow synaptic potentials mediated by the lumbar colonic nerve have been investigated using an in vitro preparation of the guinea-pig inferior mesenteric ganglion attached to a distal colonic segment. Non-cholinergic potential responses to colonic nerve stimulation, colonic distension and chemical activation of sensory afferents were recorded intracellularly from neurons in the inferior mesenteric ganglion. Electrical stimulation of the lumbar colonic nerve produced either a slow excitatory postsynaptic potential, or a slow inhibitory postsynaptic potential followed by a slow excitatory postsynaptic potential. The extrapolated reversal potential of the slow excitatory postsynaptic potential was in the range of 0 to -20 mV and that of the slow inhibitory postsynaptic potential was -90 to 110 mV. The slow excitatory postsynaptic potential and the slow inhibitory postsynaptic potential were reversibly abolished by perfusion of the ganglion with tetrodotoxin (1 microM), or perfusion with low calcium (200 microM), high magnesium (12 mM) containing solution. Capsaicin (1 microM) evoked a reversible depolarization of inferior mesenteric ganglion cells after which desensitization occurred and the slow excitatory postsynaptic potential was abolished but the slow inhibitory postsynaptic potential was enhanced in amplitude and prolonged in duration. Bath application of substance P (2 microM) evoked a prolonged depolarization of inferior mesenteric ganglion neurons, during which the slow excitatory postsynaptic potential but not the slow inhibitory postsynaptic potential was abolished. Distensions of the colon to pressures in the range of 2-25 cm of water produced a stimulus graded non-cholinergic slow depolarization which was occasionally followed by a late slow hyperpolarization. Both types of response were abolished by tetrodotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

Neuronal pathways from low-threshold muscle and cutaneous afferents innervating tail to trunk muscle motoneurons in the cat.

We studied neuronal pathways from low-threshold muscle (group I, II) and cutaneous afferents (group A(alpha)beta) innervating the tail to motoneurons innervating trunk muscles (m. iliocostalis lumborum and m. obliquus externus abdominus) in 18 spinalized cats. Stimulation of group I muscle afferents produced excitatory postsynaptic potentials or excitatory postsynaptic potentials followed by inhibitory postsynaptic potentials in all motoneurons innervating the m. iliocostalis lumborum which showed effects (32%), and predominantly inhibitory postsynaptic potentials in motoneurons innervating the m. obliquus externus abdominus (47%). Stimulation of group I+II afferents produced significant increases of the incidence of motoneurons showing postsynaptic potentials (the notoneurons innervating the m. iliocostalis lumborum, 87%; the motoneurons innervating the m. obliquus externus abdominus, 82%). The effects of low threshold cutaneous afferents were bilateral, predominantly producing inhibitory postsynaptic potentials in motoneurons innervating both muscles. These results suggest that neuronal pathways from muscle afferents to back muscle motoneurons mainly increase the stiffness of the trunk to maintain its stability, while those to abdominal muscles help to extend the dorsal column by decreasing their activities. The results also indicate that neuronal pathways from cutaneous afferents to trunk motoneurons functionallY disconnect the tail from the trunk.

Action Potentials↗
PubMed1999

Differential channeling of sensory stimuli onto a motor neuron in the leech.

We studied a specific sensory-motor pathway in the isolated leech ganglia. Pressure-sensitive mechanosensory neurons were stimulated with trains of action potentials at 5-20 Hz while recording the responses of the annulus erector motorneurons that control annuli erection. The response of the annulus erector neurons was a succession of excitatory postsynaptic potentials followed by inhibitory postsynaptic potentials. The excitatory postsynaptic potentials had a brief time-course while the inhibitory postsynaptic potentials had a prolonged time-course that enabled their temporal summation. Thus, the net effect of pressure-sensitive neuron stimulation on the annulus erector neurons was inhibitory. Both phases of the response were mediated by chemical transmission; the excitatory postsynaptic potentials were transmitted via a monosynaptic pathway, and the inhibitory postsynaptic potentials via a polysynaptic one. The pattern of expression of this dual response depended on the field of innervation of the sensory neuron and it was under the influence of cell 151, a non-spiking interneuron, that could regulate the expression of the hyperpolarization. The interaction between pressure-sensitive neurons and annulus erector neuron reveals how sensory specificity, connectivity pattern and regulatory elements interplay in a specific sensory-motor network.

Animals↗