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PubMed1996

Presynaptic inhibition of exteroceptive afferents by proprioceptive afferents in the terminal abdominal ganglion of the crayfish.

1. Exteroceptive hairs that are sensitive to water displacement and touch are distributed over the surface of the tailfan of crayfish. We show that the sensory neurons innervating these hairs receive a primary afferent depolarization (PAD) from sensory neurons innervating a proprioceptor that monitors movements of the endopodite and protopodite of the tailfan. This PAD occurs only during high-velocity movements of the exopodite, which are similar to those that occur during swimming. The effects that the proprioceptor mediate are widespread, so that afferents in four sensory nerve roots of the terminal abdominal ganglion, innervating hairs on the protopodite, exopodite, endopodite, and telson, receive a PAD. The PAD is unlikely to be mediated through monosynaptic pathways because there is no anatomic overlap between the central projections of chordotonal afferents and many of the exteroceptive afferents. The depolarization is associated with a conductance increase and can be increased by the injection of hyperpolarizing current or reversed (approximately 10 mV above resting potential) by injection of depolarizing current. The properties of the presynaptic input are, therefore, consistent with being mediated through chemical synapses. This is supported by the observation in the electron microscope that the exteroceptive afferents receive chemical input synapses. The depolarization is mimicked by gamma-aminobutyric acid and reduced by bath application of picrotoxin or bicuculline, suggesting that it is a depolarizing inhibitory postsynaptic potential. The PAD reduces the amplitude of exteroceptive afferent spikes, an action that is thus likely to reduce transmitter release and the efficacy of synaptic transmission.

Action Potentials↗

PubMed1997

Inhibitory control of GABAergic interneurons in the hippocampus.

Hippocampal GABAergic interneurons are responsible for controlling the output and efficacy of synaptic input of large principal cell populations and, thereby, determine the oscillatory discharge patterns and synaptic plasticity in the hippocampus. Single interneurons are able to prevent repetitive firing of postsynaptic pyramidal cells (R. Miles, K. Tóth, A.I. Gulyás, N. Hájos, and T.F. Freund. Neuron, 16: 815-823, 1996), whereas on occasion a single pyramidal cell may be able to activate an interneuron under in vitro conditions (A.I. Gulyás, R. Miles, A. Sik, K. Tóth, N. Tamamaki, and T.F. Freund. Nature (London), 366: 683-687, 1993). Inhibition is therefore extremely powerful. Transient suppression of interneuronal activity allows the precise timing and synchronization of inhibitory postsynaptic potentials arriving at principal cells. A rhythmic suppression or modulation of interneuron discharge may be brought about by input from at least two major sources: (i) from other local interneurons or (ii) from subcortical centers. Of the possible local sources, in the present review particular attention will be paid to GABAergic neurons specialized to innervate other interneurons. Subcortical pathways known to modulate specific inhibitory functions in the hippocampus, i.e., the GABAergic and cholinergic septohippocampal and the serotonergic raphe hippocampal pathways, will also be reviewed. Roles of these control mechanisms may include the generation of theta and higher frequency oscillations and the selective removal of inhibition from the termination zone of specific excitatory afferents, thereby increasing their efficacy and (or) plasticity.

Acetylcholine↗

PubMed1999

Serotonergic modulation of neurotransmission in the rat basolateral amygdala.

Whole cell patch-clamp recordings were obtained from projection neurons and interneurons of the rat basolateral amygdala (BLA) to understand local network interactions in morphologically identified neurons and their modulation by serotonin. Projection neurons and interneurons were characterized morphologically and electrophysiologically according to their intrinsic membrane properties and synaptic characteristics. Synaptic activity in projection neurons was dominated by spontaneous inhibitory postsynaptic currents (IPSCs) that were multiphasic, reached 181 +/- 38 pA in amplitude, lasted 296 +/- 27 mS, and were blocked by the GABAA receptor antagonist, bicuculline methiodide (30 microM). In interneurons, spontaneous synaptic activity was characterized by a burst-firing discharge patterns (200 +/- 40 Hz) that correlated with the occurrence of 6-cyano-7-nitroquinoxaline-2,3-dione-sensitive, high-amplitude (260 +/- 42 pA), long-duration (139 +/- 19 mS) inward excitatory postsynaptic currents (EPSCs). The interevent interval of 831 +/- 344 mS for compound inhibitory postsynaptic potentials (IPSPs), and 916 +/- 270 mS for EPSC bursts, suggested that spontaneous IPSP/Cs in projection neurons are driven by burst of action potentials in interneurons. Hence, BLA interneurons may regulate the excitability of projection neurons and thus determine the degree of synchrony within ensembles of BLA neurons. In interneurons 5-hydroxytryptamine oxalate (5-HT) evoked a direct, dose-dependent, membrane depolarization mediated by a 45 +/- 6.9 pA inward current, which had a reversal potential of -90 mV. The effect of 5-HT was mimicked by the 5-HT2 receptor agonist, alpha-methyl-5-hydroxytryptamine (alpha-methyl-5-HT), but not by the 5-HT1A receptor agonist, (+/-) 8-hydroxydipropylaminotetralin hydrobromide (8-OH-DPAT), or the 5-HT1B agonist, CGS 12066A. In projection neurons, 5-HT evoked an indirect membrane hyperpolarization ( approximately 2 mV) that was associated with a 75 +/- 42 pA outward current and had a reversal potential of -70 mV. The response was independent of 5-HT concentration, blocked by TTX, mimicked by alpha-methyl-5-HT but not by 8-OH-DPAT. In interneurons, 5-HT reduced the amplitude of the evoked EPSC and in the presence of TTX (0.6 microM) reduced the frequency of miniature EPSCs but not their quantal content. In projection neurons, 5-HT also caused a dose-dependent reduction in the amplitude of stimulus evoked EPSCs and IPSCs. These results suggest that acute serotonin release would directly activate GABAergic interneurons of the BLA, via an activation of 5-HT2 receptors, and increase the frequency of inhibitory synaptic events in projection neurons. Chronic serotonin release, or high levels of serotonin, would reduce the excitatory drive onto interneurons and may act as a feedback mechanism to prevent excess inhibition within the nucleus.

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

PubMed1997

Noradrenaline-mediated lateral inhibition in the sympathetic ganglion.

Intracellular recordings were made from neurons of denervated superior cervical ganglion (SCG) of the rat. Focal electrical stimulation near the recording site evoked a monosynaptic inhibitory postsynaptic potential (IPSP) in about 15% of SCG neurons. The IPSP was reversibly abolished by alpha2-adrenoceptor antagonist, yohimbine. The ionic mechanism of the IPSP appeared to be due to an increase of potassium conductance following the activation of alpha2-adrenoceptor. Electron microscopic observations confirmed that these cells received synapses of intrinsic type. It was concluded that some SCG neurons were under an inhibitory control from neighboring neurons via noradrenergic synapses.

Animals↗

PubMed2000

Anticonvulsant A(1) receptor-mediated adenosine action on neuronal networks in the brainstem-spinal cord of newborn rats.

Membrane potential of ventral respiratory group neurons as well as inspiratory-related cranial (hypoglossal) and spinal (C(1)-Th(4)) nerve activities were analysed in brainstem-spinal cord preparations from neonatal rats. Block of Cl(-)-mediated inhibition with bicuculline (plus strychnine) affected neither rhythmic depolarizations nor spike discharge in 23 of 30 ventral respiratory group cells. In the other seven neurons, block of inhibitory postsynaptic potentials evoked pronounced depolarizations and spike discharge that was synchronous with seizure-like spinal nerve activity. Respiratory hypoglossal nerve activity persisted after transection at the spinomedullary junction, whereas spinal rhythm was blocked. After transection, the moderate bicuculline-evoked seizure-like perturbation of hypoglossal nerve activity was abolished and rhythmic ventral respiratory group neuron activity was not disturbed, whereas epileptiform discharge persisted in spinal nerves. The seizure-like nerve activity and depolarization of the minor subpopulation of perturbed ventral respiratory group neurons were reversed by either adenosine or the A(1) adenosine receptor agonist 2-chloro-N(6)-cyclopentyladenosine. The A(2) receptor agonist CGS 21860 had no effect. In control preparations, inspiratory nerve activity and membrane potential fluctuations (29 of 35 cells) were not changed by adenosine, 2-chloro-N(6)-cyclopentyladenosine or CGS 21860. In the other six cells, adenosine evoked a hyperpolarization (<10 mV) with no major change in input resistance. The anticonvulsant effects of adenosine and 2-chloro-N(6)-cyclopentyladenosine were antagonized by the A(1) adenosine receptor blocker 8-cyclopentyl-1,3-dipropylxanthine. After pre-incubation with 8-cyclopentyl-1,3-dipropylxanthine, bicuculline also evoked seizure-like discharge in the hypoglossal nerve. The results indicate that seizure-like spinal motor output of the respiratory network upon block of Cl(-)-mediated inhibition is caused by disinhibition of spinal neuronal networks with afferent connections to the ventral respiratory group. Presynaptic A(1) adenosine receptors exert an anticonvulsant action on the disinhibited spinal motor network, but have no depressing effect per se on the isolated medullary respiratory network.

Adenosine↗

PubMed2004

Convergence of forelimb afferent actions on C7-Th1 propriospinal neurones bilaterally projecting to sacral segments of the cat spinal cord.

Propriospinal neurones located in the cervical enlargement and projecting bilaterally to sacral segments of the spinal cord were investigated electrophysiologically in eleven deeply anaesthetized cats. Excitatory or inhibitory postsynaptic potentials from forelimb afferents were recorded following stimulation of deep radial (DR), superficial radial (SR), median (Med) and ulnar (Uln) nerves. 26 cells were recorded from C7, 22 from C8 and 3 from Th1 segments. The majority of the cells were located in the Rexed's laminae VIII and the medial part of the lamina VII. In 10 cases no afferent input from the forelimb afferents was found. In the remaining neurones effects were evoked mostly from DR (88%) and Med (63%), less often from SR (46%) and Uln (46%). Inhibitory actions were more frequent than excitatory. The highest number of IPSPs was evoked from high threshold flexor reflex afferents (FRA)--all connections were polysynaptic. However, inhibitory actions were often evoked from group I or II muscle afferents (polysynaptic or disynaptic) and, less frequently, from cutaneous afferents (mostly polysynaptic). Di- or polysynaptic IPSPs often accompanied monosynaptic EPSPs from group I or II muscle afferents. Disynaptic or polysynaptic EPSPs from muscle and cutaneous afferents were also recorded in many neurones, while polysynaptic EPSPs from FRA were observed only exceptionally. Various patterns of convergence in individual neuronal subpopulations indicate that they integrate different types of the afferent input from various muscle and cutaneous receptors of the distal forelimb. They transmit this information to motor centers controlling hind limb muscles, forming a part of the system contributing to the process of coordination of movements of fore--and hind--limbs.

Afferent Pathways↗

PubMed1983

Postsynaptic inhibition of invertebrate neuromuscular transmission by avermectin B1a.

The avermectins are a family of novel macrocyclic lactones which paralyze nematodes and insects. One highly potent member of this family, avermectin B1a, has been shown to block neuromuscular transmission in the lobster opener and stretcher muscles. Continuous superfusion of these muscles with the drug (6 microM) resulted in a rapid loss of intracellularly recorded inhibitory postsynaptic potentials. Amplitudes of excitatory potentials and membrane input resistance declined at a slower rate, with a similar time course (25-30 min). These effects were not reversed by prolonged washing. A 3-5 mV hyperpolarization was also observed, which was reversed to depolarization in low chloride lobster saline. Picrotoxin (20 microM) blocked the effects of avermectin B1a on excitatory postsynaptic potentials. Both gamma-aminobutyric acid (GABA) and avermectin B1a decreased the slope of current voltage curves in the stretcher muscle, reflecting an increase in membrane conductance. These changes were greatly reduced by application of bicuculline (50 microM) or picrotoxin (20 microM) Avermectin B1a had no effect on the "fast" axon excitatory electrical responses (glutaminergic) of the cockroach extensor tibiae muscle fibers which lack an inhibitory (GABAergic) input. It is concluded that at the lobster neuromuscular junction, avermectin B1a acts on the GABAergic synapse and lowers input resistance of the muscle membranes by causing an increase in chloride ion permeability.

Animals↗

PubMed1992

Monitoring the excitability of neocortical efferent neurons to direct activation by extracellular current pulses.

1. Extracellular action potentials were recorded from antidromically activated efferent neurons in visual, somatosensory, and motor cortex of the awake rabbit using low-impedance metal microelectrodes. Efferent neurons were also activated by current pulses delivered near the soma [juxtasomal current pulses (JSCPs)] through the recording microelectrode. Action potentials generated by JSCPs were not directly observed (because of the stimulus artifact), but were inferred with the use of a collision paradigm. Efferent populations studied include callosal neurons [CC (n = 80)], ipsilateral corticocortical neurons [C-IC (n = 21)], corticothalamic neurons of layer 6 [CF-6 (n = 57)], and descending corticofugal neurons of layer 5 [CF-5, corticotectal neurons of the visual cortex (n = 48)]. 2. Most CC neurons (45/46) and all C-IC (8/8) and CF-6 neurons (39/39) were directly activated by JSCPs at near-threshold intensities. Some CF-5 neurons (9/38), however, showed evidence of indirect activation. All efferent classes had similar current thresholds (means 1.85-2.10 microA) to direct activation by JSCPs, and thresholds were inversely related to extracellular spike amplitude. For each neuron, the range of JSCP intensities that generated response probabilities of between 0.2 and 0.8 was measured, and this "range of uncertainty" was significantly greater in CF-5 neurons (mean 32.7% of threshold) than in CC (mean 19.0%) or CF-6 (mean 20.4%) neurons. 3. Several factors indicate that the threshold of efferent neurons to JSCPs is very sensitive to excitatory and inhibitory synaptic inputs. Iontophoretic applications of gamma-aminobutyric acid (GABA) increased the threshold to JSCPs, and glutamate reduced the threshold. Electrical stimulation of afferent pathways at intensities just below threshold for eliciting action potentials resulted in a dramatic decrease in JSCP threshold. This initial short-latency threshold decrease was specific to stimulation of particular afferent pathways and is thought to reflect excitability changes associated with EPSPs. Examination of such subliminal responses revealed subthreshold synaptic inputs that were not revealed by examination of all-or-none action potentials. In contrast to the specificity of the short-latency threshold decrease, a long-lasting increase in JSCP threshold was seen in virtually all neurons after stimulation of each of the afferent pathways tested. This increase in threshold usually began 20-40 ms after stimulation, lasted for 100-200 ms, and is thought to reflect excitability changes associated with a long-lasting inhibitory postsynaptic potential (IPSP) seen in many cortical neurons. 4. Many neurons in primary somatosensory cortex of rat, cat, and rabbit have no demonstrable receptive fields.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1995

Ischaemia-induced long-term hyperexcitability in rat neocortex.

The long-term structural and functional consequences of transient forebrain ischaemia were studied with morphological, immunohistochemical and in vitro electrophysiological techniques in the primary somatosensory cortex of Wistar rats. After survival times of 10-17 months postischaemia, neocortical slices obtained from ischaemic animals were characterized by a pronounced neuronal hyperexcitability in comparison with untreated age-matched controls. Extra- and intracellular recordings in supragranular layers revealed all-or-none long-latency recurrent responses to orthodromic synaptic stimulation of the afferent pathway. These responses were characterized by durations up to 1.7 s, by multiple components and by repetitive synaptic burst discharges. The reversible blockade of this late activity by DL-amino-phosphonovaleric acid (APV) suggested that this activity was mediated by N-methyl-D-aspartate (NMDA) receptors. The peak conductance of inhibitory postsynaptic potentials was significantly smaller in neurons recorded in neocortical slices obtained from ischaemic animals than those from the controls. However, the average number of parvalbumin (PV)-labelled neurons per mm3, indicative of a subpopulation of GABAergic interneurons, and the average number and length of dendritic processes arising from PV-containing cells was not significantly different between ischaemic and control cortex. The prominent dysfunction of the inhibitory system in ischaemic animals occurred without obvious structural alterations in PV-labelled cells, indicating that this subpopulation of GABAergic interneurons is not principally affected by ischaemia. Our data suggest a long-term down-regulation of inhibitory function and a concurrent NMDA receptor-mediated hyperexcitability in ischaemic neocortex. These alterations may result from structural and/or functional properties of inhibitory non-PV-positive neurons or permanent functional modifications on the subcellular molecular level, i.e. alterations in the phosphorylation status of GABA and/or NMDA receptors. The net result of these long-term changes is an imbalance between the excitatory and inhibitory systems in the ischaemic cortex with the subsequent expression and manifestation of intracortical hyperexcitability.

Animals↗

PubMed1986

Opioid peptides and epileptogenesis in the limbic system: cellular mechanisms.

The localization of opioid peptides in the rat hippocampal formation and the epileptogenic action of beta-endorphin and certain enkephalin analogues have led to speculations that opioids may play a role in limbic seizures. These immunochemical and electroencephalographic data are compatible with single-unit electrophysiological studies showing predominant excitations of hippocampal pyramidal neurons in CA1 and CA3 fields produced by iontophoresis of endorphins or enkephalins. These excitations are naloxone sensitive and appear to arise from a disinhibitory mechanism due to inhibition of inhibitory interneurons. Thus, intracellular recordings in in vitro preparations of hippocampus usually show opioid-induced reduction of inhibitory postsynaptic potentials. However, more recent studies suggest that a major opioid-containing pathway in the hippocampus, the mossy fiber projection from the dentate gyrus to CA3 pyramidal neurons, contains more pro-dynorphin-derived peptides than pro-enkephalin. Intracerebroventricular dynorphin does not induce epileptiform activity in the rat, and single-unit and field-potential studies show mixed effects on CA3 neuronal excitability, with more inhibitory responses than are seen with the enkephalins. Selective inactivation of mu opioid receptors reveals that dynorphin, which was previously shown to express specificity for kappa receptors, can act on delta receptors in CA1. Furthermore, a specific kappa agonist, U50,488H, has inhibitory actions when applied directly to CA3 neurons. These data suggest the presence of multiple opioid receptor types in the hippocampus. These multiple receptors may point to heterogeneous functions of the different families of opioid peptides in various regions of the hippocampus, and could explain the divergent effects reported for the various opioids and naloxone to promote or prevent paroxysmal activity.

Animals↗

PubMed1989

Neural mechanism generating firing patterns in jaw motoneurons during the food-induced response in Aplysia kurodai. I. Identification and characterization of premotor neurons.

1. In each right and left buccal ganglia of Aplysia kurodai, we identified 4 premotor neurons impinging on the ipsilateral jaw-closing and -opening motoneurons. Three of them (MA1 neurons) had features of multifunctional neurons. Current-induced spikes in the MA1 neurons produced excitatory junction potentials (EJPs) in the buccal muscle fibers. In addition, tactile stimulation of the buccal muscle surface produced a train of spikes in the MA1 neurons without synaptic input. The other neuron (MA2) had only a premotor function. 2. The MA1 and MA2 neurons had similar synaptic effects on the jaw-closing and -opening motoneurons. Current-induced spikes in the premotor neurons gave rise to monosynaptic inhibitory postsynaptic potentials (IPSPs) in the ipsilateral jaw-closing motoneurons. Simultaneously, spikes in one of the MA1 neurons and the MA2 also gave rise to monosynaptic excitatory postsynaptic potentials (EPSPs) in the ipsilateral jaw-opening motoneuron. 3. The IPSPs and the EPSPs induced by spikes in the premotor neurons were reversibly blocked by d-tubocurarine and hexamethonium, respectively, suggesting that the MA1 and MA2 neurons are cholinergic. 4. When depolarizing and hyperpolarizing current pulses were passed into one premotor neuron, attenuated but similar potential changes were produced in another randomly selected premotor neuron in the same ganglion, suggesting that they are electronically coupled.

Animals↗

PubMed1984

Direct evidence for postsynaptic inhibition in the embryonic chick spinal cord.

Motoneurons were recorded intracellularly in the isolated perfused spinal cord of 10 - 16-day chick embryos. Inhibitory postsynaptic potentials (IPSPs) were present in motoneurones of all ages studied and could be evoked by both ventral white column and dorsal root stimulation. IPSPs produced by orthodromic stimulation displayed many features of mature vertebrate motoneuronal IPSPs including the chloride dependence and sensitivity to currents passed through the cell membrane. Strychnine and chloride-free solution produced marked disinhibitory effects in the spinal cord indicating the presence of inhibitory synapses in interneuronal circuits of at least 11-day and older embryos. Possible sources of descending inhibitory influences on motoneurones and some functional aspects are discussed. The results support the hypothesis that the inhibition starts in the embryonic chick spinal cord rather early, before the 10th day of development.

Animals↗

PubMed1996

Physiological properties of rat ventral pallidal neurons recorded intracellularly in vivo.

1. The physiology of ventral pallidal (VP) cells was investigated using in vivo intracellular recording and staining techniques in adult rats. Based on electrophysiological criteria, three different types of cells were found: type A cells, which fired phasic spikes that did not exhibit a substantial afterhyperpolarization (AHP), type B cells, which exhibited a slow ramplike depolarization that preceded the short-duration action potential; the spike was followed by a prominent AHP, and type C cells, which were the only cells that fired spikes in couplets or bursts, with the spikes in a burst exhibiting a progressive increase in duration and a decrease in amplitude. These cells also exhibited a rebound low threshold spikelike event. Furthermore, 18% of the VP cells recorded exhibited a slow subthreshold oscillation of the membrane potential (< 1 Hz). 2. The response of VP cells to stimulation of fibers arising from the prefrontal cortex, nucleus accumbens, and mediodorsal thalamic nucleus (MD) was examined. In contrast to our initial predictions, all cells responded to nucleus accumbens stimulation with excitation. Type A and B cells responded to nucleus accumbens stimulation with excitation and to MD stimulation with antidromic-like responses, orthodromic excitation, or evoked inhibitory postsynaptic potentials. Only type A cells responded to prefrontal cortical stimulation. Type C cells only responded to stimulation of the nucleus accumbens, which resulted in evoked excitatory postsynaptic potentials. 3. The cells in the VP therefore can be segregated into three physiologically defined groups according to action potential discharge patterns and their response to afferent fiber stimulation.

Action Potentials↗

PubMed2006

Dopamine presynaptically depresses fast inhibitory synaptic transmission via D4 receptor-protein kinase A pathway in the rat dorsolateral septal nucleus.

The lateral septal nucleus receives a diffuse dopaminergic input originating from the ventral tegmental area of the brain stem. We examined whether dopamine (DA) modulates synaptic transmission in the slice preparation of the rat dorsolateral septal nucleus (DLSN). Bath application (10-15 min) of DA (30 muM) markedly depressed the amplitude of fast and slow inhibitory postsynaptic potentials (IPSPs) in DLSN neurons, while it produced only a minor depression of the amplitude of excitatory postsynaptic potentials (EPSPs) obtained in the presence of bicuculline. DA (30 muM) depressed the monosynaptic fast IPSP to approximately 50% of control, but did not depress the inward current (I(GABA)) induced by exogenous gamma-aminobutyric acid (GABA). DA decreased the frequency of miniature fast IPSPs (m-fIPSPs) without significantly changing their amplitude. PD 168077, a selective D4 receptor agonist, depressed the fast and slow IPSPs but not the EPSP and decreased the frequency of m-fIPSPs. Both DA and PD 168077 increased the paired-pulse ratio of the monosynaptic fast IPSP. The inhibitory effect of DA on the fast IPSP was significantly attenuated by L-741,742, an antagonist at D4 receptors, but not by SCH 23390 and sulpiride, a D1-like and a D2-like receptor antagonist, respectively. N-ethylmaleimide, a blocker of pertussis toxin (PTX)-sensitive G protein (G(i/o)), attenuated the DA-induced depression of the fast IPSP. N-[2-((p-bromocinnamyl) amino)ethyl]-5-isoquinoline sulfonamide, a protein kinase A (PKA) inhibitor, attenuated the DA-induced depression of the fast IPSP. These results suggest that DA inhibits spontaneous and evoked release of GABA via the D4 receptor-G(i)-protein-PKA system in DLSN neurons.

Animals↗

PubMed2000

Long-term potentiation in the inferior colliculus studied in rat brain slice.

The purpose of this study is to determine whether long-term potentiation (LTP) can be induced in the central nucleus of the inferior colliculus (ICC) by electrical stimulation of the lateral lemniscus. If LTP can be induced, is it mediated by N-methyl-D-aspartate (NMDA) and/or other receptors? Brain slices of the ICC were obtained from 14-35 day old Wistar rats. The field potentials were recorded from the ICC after GABAergic and glycinergic inhibition was suppressed. Following tetanic stimulation (50 Hz, 20 s), the amplitude of the response was increased to about 146% of control response for at least 30 min. LTP was observed in about 78% of the cases tested. Induction of LTP in the ICC required activation of both NMDA and gamma-aminobutyric acid (GABA)(B) receptors. GABAergic inhibitory postsynaptic potentials (IPSPs) were blocked by the GABA(A) receptor antagonist, but not by the GABA(B) receptor antagonist. The IPSPs were decreased by the GABA(B) receptor agonist, baclofen. The intrinsic postsynaptic membrane properties were not affected by baclofen. These results suggest that GABAergic inhibition in the ICC is mediated only by GABA(A) receptors, but that it is modulated by presynaptic GABA(B) receptors. The GABA(B) receptors in the ICC may suppress GABAergic inhibition and promote induction of LTP.

Animals↗

PubMed2005

Elevated voltage gated Cl- channel expression enhances fast paired-pulse inhibition in the dentate gyrus of seizure sensitive gerbil.

The present study was performed to determine whether the voltage gated Cl- channel (CLC) expression is altered in the hippocampus of seizure sensitive (SS) gerbils, and to identify the strong fast paired-pulse inhibition in the dentate gyrus of SS gerbils is associated with altered CLC expression. In the hippocampal proper and the granule cell layer of the dentate gyrus of the SS gerbils, strong CLC-2 immunoreactivity was detected, as compared with seizure resistant (SR) gerbils. In addition, CLC-3 immunoreactivity was observed in the CA1-3 pyramidal cells, and the granule cell and the molecular layer of the dentate gyrus in the SS gerbils, whereas its immunoreactivity was rarely detected in the SR gerbils. However, CLC-3 immunoreactivity in the mossy fiber was reduced, as compared with SR gerbils. Moreover, infusion of the potential CLC inhibitor (4,4'-diisothiocyanostibene-2,2'-disulfanic acid, DIDS) reduced fast paired-pulse inhibition in the dentate gyrus of SS gerbils, although evoked responses in the dentate gyrus between SR and SS gerbils were similarly detected. These findings suggest that enhancement of CLC expression in the dentate gyrus of SS gerbils may be one of the compensatory responses for reduced GABA(A) receptor-mediated fast postsynaptic inhibitory potentials.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1996

Spindle oscillation in cats: the role of corticothalamic feedback in a thalamically generated rhythm.

1. Spindles represent an oscillatory activity (7-14 Hz) of the electroencephalogram (EEG) originating in the thalamus and appearing during early stages of sleep. We investigated: (i) the phase relations between thalamic and cortical neurons during this rhythm; (ii) the patterns of spindles under different anaesthetics and their modifications at various levels of the membrane potential (Vm); and (iii) the potentiating role of the corticothalamic feedback in the genesis of spindles. Intra- and extracellular recordings were performed in cats from reticular and dorsal thalamic nuclei, as well as from various cortical areas. 2. In thalamic reticular neurons, spindles were sequences of waves at 7-14 Hz, riding on a prolonged depolarizing plateau and occurring in phase with depth-negative cortical EEG waves. In thalamocortical cells, spindles consisted of inhibitory postsynaptic potentials (IPSPs) in phase with depth-positive cortical EEG waves and occasionally leading to rebound spike bursts. In cortical cells, spindle waves were rhythmic (7-14 Hz) excitatory postsynaptic potentials (EPSPs) that sometimes gave rise to action potentials. Spindles occurred in phase among thalamic reticular, thalamocortical and neocortical neurons. 3. In thalamic reticular neurons, spindle waves and their depolarizing plateaux increased in amplitude with slight cellular hyperpolarization, but at a Vm more negative than -80 or -85 mV they decreased in amplitude. No frequency alterations were observed with these Vm changes. 4. The waxing-and-waning pattern of spontaneous spindles under barbiturate anaesthesia was distinct from the waning pattern under ketamine-xylazine anaesthesia. Under all anaesthetics, spindles had a waning pattern when elicited by cortical stimuli. The amplitude of cortical-evoked spindle waves diminished with the decrease in stimulation intensity. 5. Under urethane or ketamine-xylazine anaesthesia, spindle sequences were grouped by a cortically generated slow oscillation (< 1 Hz) and were preceded by a depth-positive EEG wave that corresponded to a prolonged hyperpolarization in all three investigated (cortical, thalamic reticular, and thalamocortical) cellular types. 6. We propose that the waxing pattern of spindle oscillation is due to a progressive entrainment of units into the oscillation until a maximum number is reached, depending on the background activity in the network. The phase relations between cortical, thalamic reticular and thalamocortical neurons are ascribed to distributed excitatory signals from thalamocortical neurons to both cortical and reticular neurons at each cycle of the oscillation. In turn, cortical neurons provide a powerful drive to potentiate the genesis of thalamic spindles.

Animals↗

PubMed1993

Sensitization of the gill and siphon withdrawal reflex of Aplysia: multiple sites of change in the neuronal network.

1. Recent studies have emphasized the major contribution of interneuronal transmission to the mediation and learning-associated modulation of the gill and siphon withdrawal (GSW) reflex of Aplysia. We wish to provide more direct support for the hypothesis that inhibitory junctions are crucial sites of plasticity. 2. In parallel experiments we investigated modulation at five major sites of synaptic transmission in the GSW network: 1) from sensory neurons to motor neurons, 2) from sensory neurons to excitatory interneurons (INTs+) 3) from INTs+ to motor neurons (MNs), 4) from inhibitory interneurons (INTs-) to INTs+, and 5) from INTs+ to INTs-. 3. While recording simultaneously from a single sensory neuron of the LE cluster, an INT+, and a MN, we found that both LE-MN and LE-INTs+ synapses were facilitated by the activation of modulator neurons by stimulation of the left pleuroabdominal connective (185 and 93%, respectively) as well as by serotonin (5-HT) (191 and 84%). Junctions of the second type were therefore less facilitated. The difference in the magnitude of facilitation at these two sites is an indication of a branch-specific, differential efficacy in the modulation of different central synapses made by a single neuron. 4. Although INT(+)-MN junctions have the capacity to display marked posttetanic potentiation, they are not significantly potentiated after connective stimulation. Sensitization of the GSW reflex is therefore not necessarily accompanied by a modification of transmission at these synapses. 5. Inhibitory transmission to INTs+ is significantly reduced by connective stimulation (36%) and by 5-HT (71%). This supports the hypothesis that a reduction of feedback inhibition into INTs+ is a major mechanism of reflex sensitization and may account for the increased evoked firing of INTs+ that is observed after connective stimulation. 6. The excitatory input to INTs- is selectively decreased by 5-HT (50%) and by the molluscan neuropeptide small cardioactive peptide B (38%). This latter effect, which could produce disinhibition of INTs+, may explain the previous observation that this peptide is able to potentiate the evoked input to MNs of the reflex at a concentration (1 microM) that fails to modify monosynaptic sensory-motor transmission. 7. These results indicate that transmission through a small neuronal network that mediates a withdrawal reflex in Aplysia may be modulated at multiple sites and by different mechanisms. These mechanisms include: 1) branch-specific facilitation of sensory neuron outputs and 2) inhibition of INT(-)-INT+ inhibitory postsynaptic potentials by endogenous modulatory neurons and by 5-HT.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗