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PubMed1989

Excitatory amino acid receptors in the parallel fibre pathway in rat cerebellar slices.

The grease-gap technique was used on young rat cerebellar slices to study the synaptic pharmacology of the parallel fibre pathway. Electrical stimulation of the parallel fibres produced a characteristic response in Purkinje cells: a sharp negative (N) potential, representing the population action potential and underlying parallel fibre EPSP, followed by a slow positive (P) wave, the population inhibitory postsynaptic potential (IPSP). In the presence of 1.2 mM Mg2+, D-2-amino-5-phosphonovalerate (APV, 30 microM) had no effect but both potentials could be inhibited by 6-cyano-2,3-dihydroxy-7-nitro-quinoxaline (CNQX, 10 microM). Removal of Mg2+ had no effect on the N-potential but enhanced the P-wave in an APV-sensitive fashion, particularly when CNQX was present. The results provide further evidence that glutamate is the parallel fibre transmitter and suggest that its acts only on non-NMDA (non-N-methyl-D-aspartate) receptors at synapses with Purkinje cells but on both NMDA and non-NMDA receptors at synapses with inhibitory interneurones. At the latter synapses, the NMDA system is likely to be brought into operation in an activity-dependent manner.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1997

Sacculocollic reflex arcs in cats.

Neuronal connections and pathways underlying sacculocollic reflexes were studied by intracellular recordings from neck extensor and flexor motoneurons in decerebrate cat. Bipolar electrodes were placed within the left saccular nerve, whereas other branches of the vestibular nerve were removed in the inner ear. To prevent spread of stimulus current to other branches of the vestibular nerve, the saccular nerve and the electrodes were covered with warm semisolid paraffin-Vaseline mixture. Saccular nerve stimulation evoked disynaptic (1.8-3.0 ms) excitatory postsynaptic potentials (EPSPs) in ipsilateral neck extensor motoneurons and di- or trisynaptic (1.8-4.0 ms) EPSPs in contralateral neck extensor motoneurons, and di- and trisynaptic (1.7-3.6 ms) inhibitory postsynaptic potentials (IPSPs) in ipsilateral neck flexor motoneurons and trisynaptic (2.7-4.0 ms) IPSPs in contralateral neck flexor motoneurons. Ipsilateral inputs were about twice as strong as contralateral ones to both extensor and flexor motoneurons. To determine the pathways mediating this connectivity, the lateral part of the spinal cord containing the ipsilateral lateral vestibulospinal tract (i-LVST) or the central part of the spinal cord containing the medial vestibulospinal tracts (MVSTs) and possibly reticulospinal fibers (RSTs) were transected at the caudal end of the C1 segment. Subsequent renewed intracellular recordings following sacculus nerve stimulation indicated that the pathway from the saccular nerve to the ipsilateral neck extensor motoneurons projects though the i-LVST, whereas the pathways to the contralateral neck extensors and to the bilateral neck flexor motoneurons descend in the MVSTs/RSTs. Our data show that sacculo-neck reflex connections display a qualitatively bilaterally symmetrical innervation pattern with excitatory connections to both neck extensor motoneuron pools, and inhibitory connections to both neck flexor motoneuron pools. This bilateral organization contrasts with the unilateral innervation scheme of the utriculus system. These results suggest a different symmetry plane along which sacculus postural reflexes are organized, thus supplementing the reference planes of the utriculus system and allowing the gravistatic system to represent all three translational spatial degrees of freedom. We furthermore suggest that the sacculocollic reflex plays an important role in maintaining the relative position of the head and the body against the vertical linear acceleration of gravity.

Afferent Pathways↗

PubMed1994

Synaptic responses of substantia gelatinosa neurones to dorsal column stimulation in rat spinal cord in vitro.

1. To study the mechanism of dorsal column stimulation-induced depression of nociceptive transmission in the spinal cord, synaptic responses evoked in dorsal horn neurones by dorsal column and dorsal root stimulations were examined in a horizontal spinal cord slice of the adult rat. Intracellular recordings were made from substantia gelatinosa (SG) neurones. 2. All SG neurones examined received monosynaptic inputs and/or polysynpatic inputs from both dorsal column and dorsal root. A delta fibres were probably responsible for the synaptic responses. The responses evoked by dorsal column stimulation were similar to those evoked by primary afferent A delta fibre stimulation. 3. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by dorsal column A delta fibres were depressed by 6-cyano-7-nitroquinoxaline-2,3-dione, suggesting that these fibres released L-glutamate or a related amino acid as a transmitter. 4. In 38 of 101 SG neurones, dorsal column stimulation evoked an initial EPSP followed by fast and/or slow inhibitory postsynaptic potentials (IPSPs). These IPSPs reversed polarity at a membrane potential of -73 +/- 2 mV. The fast IPSPs observed in 16 of the SG neurones (42%) that received inhibitory inputs were depressed by strychnine, while the slow IPSPs observed in 22 SG neurones were depressed by bicuculline. In a few cells, a long-lasting slow IPSP with a much slower time course was detected; this IPSP was insensitive to strychnine and bicuculline, and reversed polarity at a membrane potential near -90 mV. 5. Repetitive stimulation of the dorsal column depressed the amplitude of monosynaptic EPSPs evoked by dorsal root stimulation. 6. The responses of SG neurones to dorsal column stimulation had configurations and durations similar to responses to dorsal root stimulation, and may be mediated largely by the same A delta fibres. However, a C fibre-mediated response could not be detected in SG neurones from dorsal column stimulation, although dorsal root stimulation could evoke C fibre-mediated monosynaptic EPSPs in 18 of 88 SG neurones (20%). 7. These observations suggest that SG neurones receive abundant A delta but not C fibre inputs from the dorsal column and that dorsal column stimulation inhibits primary afferent transmission in the spinal cord both by reducing transmitter release from primary A delta fibres and by hyperpolarizing SG neurones.

2-Amino-5-phosphonovalerate↗

PubMed1989

Excitatory and inhibitory effects of epinephrine on neonatal rat sympathetic preganglionic neurons in vitro.

Current and voltage recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices removed from neonatal rats. When applied by either pressure ejection or superfusion, epinephrine (Epi) caused a slow depolarization or an inward current in 62 SPNs (42%) and a slow hyperpolarization or an outward current in 21 SPNs (14%). The responses persisted in low calcium- or tetrodotoxin-containing media. The Epi-induced depolarization or inward current was associated with increased membrane resistance; it was reduced by membrane hyperpolarization and nullified at a membrane potential of about -100 mV; a clear reversal however was not observed at more negative potential levels. In a number of SPNs the Epi-induced depolarization was accompanied by small inhibitory postsynaptic potentials. The latter were eliminated by a low calcium solution and by the glycine antagonist strychnine, suggesting that they were caused by glycine or a glycine-like substance released from interneurons subsequent to activation by Epi. The Epi-induced hyperpolarization or outward current was associated with decreased membrane resistance, and nullified around -100 mV. The alpha-adrenergic antagonist, dihydroergotamine, and alpha 1-antagonist, prazosin, reversibly blocked the excitatory, whereas the alpha 2-antagonist, yohimbine, abolished the inhibitory response, respectively. It is concluded that Epi acting on alpha 1- and alpha 2-adrenergic receptors depolarizes and hyperpolarizes the rat SPNs by decreasing or increasing membrane conductances to potassium ions.

Adrenergic Fibers↗

PubMed1994

Oscillatory synaptic interactions between ventroposterior and reticular neurons in mouse thalamus in vitro.

1. The thalamic reticular nucleus (RTN) has reciprocal connections with relay neurons in the dorsal thalamus. We used whole cell recording in a mouse in vitro slice preparation maintained at room temperature to study the synaptic interactions between the RTN and the ventroposterior thalamic nucleus (VP) during evoked low-frequency oscillations. 2. After a single electrical stimulus of the internal capsule, postsynaptic potentials (PSPs) were recorded in all VP and RTN neurons. In 76% of slices, there was an initial response followed by recurrent PSPs lasting for up to 8 s and with a frequency of approximately 2 Hz in both the VP and RTN. 3. In RTN neurons the initial response consisted of a fast excitatory postsynaptic potential (EPSP) that generated a burst of action potentials. Recurrent PSPs consisted of barrages of EPSPs that often reached burst threshold. The structure of subthreshold EPSP barrages in RTN neurons suggested that they were generated by bursting VP neurons. 4. In VP neurons the stimulus usually evoked a small EPSP followed by a large inhibitory postsynaptic potential (IPSP) that was often followed by a rebound burst. This initial response was often followed by a series of recurrent IPSPs presumably generated by RTN bursts, because intrinsic inhibitory neurons are absent in rodent VP. 5. IPSPs in VP neurons and recurrent EPSPs in RTN neurons were completely abolished by application of a gamma-aminobutyric acid-A (GABAA) receptor antagonist. A GABAB receptor antagonist produced no or little change in either the initial or recurrent response. 6. Recurrent IPSPs in VP neurons were abolished by glutamate receptor antagonists before the initial IPSP, which always remained stimulus dependent. 7. The dependency of recurring IPSPs in VP and recurring EPSPs in RTN upon GABA-mediated inhibition and excitatory amino acid-mediated excitation, plus the character of recurring EPSPs in the RTN strongly suggest that the recurring events were generated through reverse-reciprocal synaptic interactions between VP and RTN neurons. These synaptic interactions most likely play an important role in thalamic oscillations in behavior.

Animals↗

PubMedDate not supplied

The action of thallium on the excitability of CA1 pyramidal cells in hippocampal slices.

The effect of thallium ions on central neuronal activity was investigated in hippocampal slice preparations from guinea pigs and rats using extra- and intracellular recording techniques. Thallium induced a reversible and concentration-dependent reduction of the orthodromically evoked compound action potential of CA1 pyramidal cells with only weak effects on either afferent fiber activity, postsynaptic potentials or antidromically evoked responses. The membrane potential and input resistance of the pyramidal cells were not impaired by thallium. In contrast, variations in the maintained spike activity and spontaneously occurring inhibitory postsynaptic potentials were observed. It is concluded, that in contrast to its presynaptic action in the peripheral nervous system, thallium has a predominant postsynaptic target site in the hippocampal slice preparation. It is suggested that the neurotoxic action of thallium is not mediated by an interaction with specific ion channels of the cell membrane, but rather by an unspecific influence on the intracellular metabolism of the CA1 pyramidal cell.

Action Potentials↗

PubMed1996

Modulation of excitatory synaptic transmission by adenosine released from single hippocampal pyramidal neurons.

Adenosine is a potent neuromodulator in the CNS, but the mechanisms that regulate adenosine concentrations in the extracellular space remain unclear. The present study demonstrates that increasing the intracellular concentration of adenosine in a single hippocampal CA1 pyramidal neuron selectively inhibits the excitatory postsynaptic potentials in that cell. Loading neurons with high concentrations of adenosine via the whole-cell patch-clamp technique did not affect the GABAA-mediated inhibitory postsynaptic potentials, the membrane resistance, or the holding current, whereas it significantly increased the adenosine receptor-mediated depression of excitatory postsynaptic currents. The effects of adenosine could not be mimicked by an agonist at the intracellular adenosine P-site, but the effects could be antagonized by a charged adenosine receptor antagonist and by adenosine deaminase, demonstrating that the effect was mediated via adenosine acting at extracellular adenosine receptors. The effect of adenosine loading was not blocked by BaCl2 and therefore was not caused by an adenosine-activated postsynaptic potassium conductance. Adenosine loading increased the paired-pulse facilitation ratio, demonstrating that the effect was mediated by presynaptic adenosine receptors. Finally, simultaneous extracellular field recordings demonstrated that the increase in extracellular adenosine was confined to excitatory synaptic inputs to the loaded cell. These data demonstrate that elevating the intracellular concentration of adenosine in a single CA1 pyramidal neuron induces the release of adenosine into the extracellular space in such a way that it selectively inhibits the excitatory inputs to that cell, and the data support the general conclusion that adenosine is a retrograde messenger used by pyramidal neurons to regulate their excitatory input.

Adenosine↗

PubMed1997

Electrophysiological properties of rat pontine nuclei neurons In vitro II. Postsynaptic potentials.

We investigated the postsynaptic responses of neurons of the rat pontine nuclei (PN) by performing intracellular recordings in parasagittal slices of the pontine brain stem. Postsynaptic potentials (PSPs) were evoked by brief (0.1 ms) negative current pulses (10-250 microA) applied to either the cerebral peduncle or the pontine tegmentum. First, excitatory postsynaptic potentials (EPSPs) could be evoked readily from peduncular stimulation sites. These EPSPs exhibited short latencies, a nonlinear increment in response to increased stimulation currents, and an unconventional dependency on the somatic membrane potential. Pharmacological blockade of the synaptic transmission using 6,7-dinitroquinoxaline-2, 3-dione and ,-2-amino-5-phosphonovaleric acid, selective antagonists of the alpha-amino-3-hydroxy-5-methyl-4-isoxazilepropionate- (AMPA) and the N-methyl--aspartate (NMDA)-type glutamate receptors, showed that these EPSPs were mediated exclusively by excitatory amino acids via both AMPA and NMDA receptors. Moreover, the pharmacological experiments indicated the existence of voltage-sensitive but NMDA receptor-independent amplification of EPSPs. Second, stimulations at peduncular and tegmental sites also elicited inhibitory postsynaptic potentials (IPSPs) in a substantial proportion of pontine neurons. The short latencies of all IPSPs argued against the participation of inhibitory interneurons. Their sensitivity to bicuculline and reversal potentials around -70 mV suggested that they were mediated by gamma-aminobutyric acid-A (GABAA) receptors. In addition to single PSPs, sequences consisting of two to four distinct EPSPs could be recorded after stimulation of the cerebral peduncle. Most remarkably, the onset latencies of the following EPSPs were multiples of the first one indicating the involvement of intercalated synapses. Finally, we used the classic paired-pulse paradigm to study whether the temporal structure of inputs influences the synaptic transmission onto pontine neurons. Pairs of electrical stimuli applied to the cerebral peduncle resulted in a marked enhancement of the amplitude of the second EPSP for interstimulus intervals of 10-100 ms. Delays >200 ms left the EPSP amplitude unaltered. These data provide evidence for a complex synaptic integration and an intrinsic connectivity within the PN too elaborate to support the previous notion that the PN are simply a relay station.

Animals↗

PubMed1979

Avermectin B1a irreversibly blocks postsynaptic potentials at the lobster neuromuscular junction by reducing muscle membrane resistance.

Avermectin B1a, a macrocyclic lactone with broad spectrum anthelmintic activity, affects neuromuscular transmission in the lobster stretcher muscle. Perfusion of the muscle with 1-10 microgram of the drug per ml eliminates inhibitory postsynaptic potentials within a few minutes. Intracellularly recorded excitatory postsynaptic potentials are gradually reduced in amplitude over 20-30 min, and their falling phases become faster; there is no effect, however, on extracellularly recorded excitatory potentials. Avermectin B1a reduced the input resistance of the muscle fibers with a time course similar to that of the reduction of excitatory potentials. Washing for up to 2 hr with drug-free solution fails to reverse the drug's effects. However, perfusion with 20 microgram of picrotoxin per ml results in recovery of the excitatory potentials and input resistance. Avermectin B1a also blocks the firing of the crayfish stretch receptor neuron, and this block is also reversed by picrotoxin. We hypothesize that the reduction in excitatory postsynaptic potentials after avermectin B1a treatment is caused solely by reduction in membrane resistance; additional experiments suggest that the reduction in membrane resistance is due to the opening of membrane Cl- channels, perhaps including those regulated by gamma-aminobutyric acid at the inhibitory synapse.

Animals↗

PubMed1990

Synaptic and intrinsic control of membrane excitability of neostriatal neurons. I. An in vivo analysis.

1. The relationship between membrane properties of neostriatal neurons and spontaneous and evoked synaptic potentials was studied with the use of intracellular recordings from anesthetized rats. Most of these neurons showed regular or irregular spontaneous depolarizing potentials that only in a few cases triggered action potentials at resting level. 2. The stimulation of the ipsilateral substantia nigra or of the sensorimotor cortex produced a relatively fast depolarizing post-synaptic potential (EPSP). In some cells this potential was followed by an inhibitory period that appeared as an hyperpolarization when the cell was depolarized from the resting level (inhibitory postsynaptic potential, IPSP). A late and long-lasting depolarization (LD) followed the EPSP or the EPSP-IPSP sequence. 3. Repetitive discharge with little adaptation was observed during direct depolarization. Most of the neurons tested for current-voltage (I-V) relationship showed nonlinearity of the input resistance in the hyperpolarizing direction. Spontaneous and evoked EPSPs were decreased in their amplitude and duration when the membrane potential was held at levels more hyperpolarized than -85 mV because of the strong rectification at these levels of hyperpolarization. 4. Local microiontophoretic application of bicuculline (BIC) or systemic administration of BIC and pentylenetetrazole (PTZ) produced a reduction of the IPSPs. The reduction of the inhibitory transmission caused a strong increase of the LD. The current-evoked firing pattern was not greatly altered. 5. The intracellular application of cesium increased the amplitude and the duration of the spontaneous depolarizations that triggered bursts of action potentials under this condition. Spikes were broadened and the rectification in the hyperpolarization direction was reduced. 6. Iontophoretically applied cadmium strongly depressed the amplitude of the spontaneous and evoked postsynaptic potentials. During cadmium application, nigral stimulation produced constant latency, all-or-none spikes in the absence of any synaptic potential. 7. Repetitive stimulation of the ipsilateral substantia nigra by electrical shocks (5 Hz, 25 s) produced a progressive and reversible decrease of the spontaneous depolarizing potentials (SDPs) and a decrease of the firing rate. In the same cells, when the train of stimulation was delivered in the ipsilateral cortex, a membrane depolarization coupled with an increase of the firing rate was observed. 8. We conclude that although synaptic circuits mediate a phasic inhibition in neostriatum, the low level of spontaneous firing of most neostriatal neurons is mainly because of the effects that membrane properties exert on the spontaneous and the evoked synaptic depolarizations in the striatum.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1985

Synaptic responses of neurons of the nucleus tractus solitarius in vitro.

Postsynaptic responses of neurons in the nucleus tractus solitarius (NTS) have been studied in an in vitro slice preparation using extra- and intracellular recording. Single or paired pulse stimulations were delivered to afferent fibers within the tractus solitarius (TS) to activate orthodromic responses in these neurons. Most NTS neurons displayed an initial synaptic excitation followed by inhibition of spontaneous or evoked firing lasting up to 150-200 ms after stimulation. Excitatory postsynaptic potentials (EPSPs), recorded intracellularly, were increased in amplitude by membrane hyperpolarization. Large afterhyperpolarizations followed action potentials triggered by the EPSPs or evoked by intracellular current injections. Intracellular evidence for synaptic inhibition within the NTS included: (1) the presence, after Cl-injection, of flurries of spontaneous PSPs likely to be inverted inhibitory postsynaptic potentials; (2) reduction of the size of a test EPSP by a previous subthreshold TS conditioning volley; and (3) hyperpolarizing PSPs recorded in some neurons. Other NTS neurons exhibited prolonged excitatory responses to TS stimulation and could be local inhibitory interneurons. These results may help specify synaptic mechanisms in the NTS that could play an integrative role in the relay of visceral sensory inputs to higher order effectors.

Animals↗

PubMed2000

Serotonin-induced spike narrowing in a locomotor pattern generator permits increases in cycle frequency during accelerations.

During serotonin-induced swim acceleration in the pteropod mollusk Clione limacina, interneurons of the central pattern generator (CPG) exhibit significant action potential narrowing. Spike narrowing is apparently necessary for increases in cycle frequency during swim acceleration because, in the absence of narrowing, the combined duration of the spike and the inhibitory postsynaptic potential (IPSP) of a single cycle is greater than the available cycle duration. Spike narrowing could negatively influence synaptic efficacy in all interneuron connections, including reciprocal inhibitory connections between the two groups of antagonistic CPG interneurons as well as the interneuron-to-motoneuron connections. Thus compensatory mechanisms must exist to produce the overall excitatory behavioral change of swim acceleration. Such mechanisms include 1) a baseline depolarization of interneurons, which brings them closer to spike threshold, 2) enhancement of their postinhibitory rebound, and 3) direct modulation of swim motoneurons and muscles, all through inputs from serotonergic modulatory neurons.

Acceleration↗

PubMed1982

The pharmacology of Limulus central neurons.

1. Intracellular recordings have been made from neurons in the central nervous system of the horse-shoe crab, Limulus polyphemus. Neurons possess resting potentials between -40 and -60 mV, with action potentials ranging from 2-3 mV up to 60 mV in amplitude. Neurons also have excitatory and inhibitory postsynaptic potentials. 2. All the neurons studied are inhibited by GABA and excited by cholinomimetics. The GABA response is chloride mediated and reversibly antagonised by picrotoxinin but not by bicuculline or bicuculline methochloride or methoiodide. The cholinergic response is nicotinic and blocked by pentolinium, hexamethonium, chlorisondamine and dihydro-beta-erythroidine. 3. L-Glutamate can excite some cells, inhibit others and have a biphasic action, inhibition followed by excitation, on other cells. The inhibitory effect is chloride mediated and blocked by picrotoxinin. Ibotenate mimics the action of glutamate both in terms of inhibition and excitation but kainate and quisqualate only mimic the excitatory action of L-glutamate. 4. Dopamine, octopamine, 5-hydroxytryptamine and histamine excite some neurons while inhibiting others or have a biphasic action. Dopamine and octopamine normally have different effects on the same cell, suggesting they act via different receptors. Octopamine shows stereospecificity for the (-) isomer which is more than 100 times more active than the (+) isomer and octopamine is reversibly antagonised by phentolamine and cyproheptadine. 5. Proctolin has an excitatory action on these neurons and this effect is long lasting and can be potentiated by dibutyl cyclic AMP. 6. The pharmacology of Limulus central neurons is compared to the pharmacology of insect and crustacean central neurons. It is concluded that GABA and acetylcholine are central transmitters throughout the arthropods. It is also probable that L-glutamate and octopamine have a physiological role in the arthropod central nervous system. Proctolin appears to modify neuronal and muscle activity in the arthropods and has a modulatory or transmitter function.

Acetylcholine↗

PubMed1992

Introduction to slow synaptic potentials and their neuromodulation by dopamine.

The existence of two muscarinically mediated slow postsynaptic potentials (PSPs) and a noncholinergic (peptidergic) late-slow PSP was established in the 1960s. These have synaptic delays and PSP durations 100-10,000 times those for the nicotinic (fast) excitatory post-synaptic potential (EPSP). Evidence is reviewed for an against the proposal that, in rabbit superior cervical ganglia, the slow (s-) inhibitory postsynaptic potential requires a second transmitter, dopamine, released by muscarinic action on interneurones (the small, intensely fluorescent cells). The s-EPSP in frog ganglia appears only in already depolarized cells by a muscarinic closure of the M (voltage-sensitive K+) channels. But the large s-EPSP in mammalian neurones, not depolarized, is generated largely via other mechanisms, especially one involving cyclic GMP. Dopamine also produces a long-term enhancement (LTE) of the muscarinic slow PSPs in rabbit superior cervical ganglia, whether dopamine is applied exogenously or released intraganglionically by preganglionic nerve impulses at 10 s-1. LTE is producible heterosynaptically, and it persists well over 3 h; a noncholinergic (peptide?) transmitter may contribute to the initial 30 min of LTE. LTE is mediated by a D1 receptor coupled to cyclic AMP; it is blocked by cyclic GMP or low Ca2+ or calmidazolium (a calmodulin inhibitor). The modulatory process of LTE has certain similarities to, but also fundamental differences from, the long-term potentiation known in the hippocampus.

Animals↗

PubMed1994

Feedback inhibition in the cat's lateral geniculate nucleus.

Feedback inhibition is generally believed to be a ubiquitous feature of brain circuitry, but few specific instances have been documented. An example in cats is the supposed feedback circuit involving relay cells of the lateral geniculate nucleus and cells of the perigeniculate nucleus (a part of the thalamic reticular nucleus): geniculate relay cells innervate the perigeniculate nucleus, which, in turn, provides an inhibitory, GABAergic projection back to the lateral geniculate nucleus. However, feedback inhibition at the single-cell level requires that a given perigeniculate cell project back onto the same geniculate relay cell that innervates it. We probed for this in an in vitro slice preparation of the cat's lateral geniculate nucleus. We evoked a single action potential in a geniculate cell via a brief, depolarizing pulse delivered through an intracellular recording electrode and looked for any evoked hyperpolarizations. For 6 of the 36 geniculate cells tested, we observed a long-lasting hyperpolarization after the action potential, and much of this was eliminated by application of bicuculline, suggesting synaptically activated inhibitory postsynaptic potentials. We interpreted this to be clear evidence that a given neuron may inhibit itself via circuitry mediating feedback inhibition in the cat's lateral geniculate nucleus.

Animals↗

PubMed1988

Septohippocampal disinhibition.

Intracellular recordings from CA1 and CA2/3 neurons in rats under urethane anesthesia revealed the following effects of medial septal stimulation (10 pulse trains at approximately 100 Hz): (1) in most cases only minimal signs of any synaptic potential; (2) a marked and prolonged (200-500 ms) depression of on-going inhibitory postsynaptic potentials (IPSPs), particularly evident when IPSPs were reversed by Cl- injection; (3) a corresponding increase in input resistance: (4) depolarization when recording with non-Cl(-)-containing electrodes; (5) a predominant hyperpolarization when recording with Cl(-)-containing electrodes; and (6) a marked reduction of the variability of resistance and voltage data. These observations indicate that septal stimulation can strongly depress tonic inhibition in the hippocampus. Septal trains also tended to weaken IPSPs evoked in pyramidal cells by fimbrial stimulation, reducing conductance increase during IPSPs by an average of 42% (S.D. +/- 24.3). Septal inputs to the hippocampal CA1 and CA2/3 regions appear to have a major disinhibitory function.

Action Potentials↗

PubMed2006

Synchronization of olfactory bulb mitral cells by precisely timed inhibitory inputs.

Synchronized oscillatory activity at the gamma frequency (30-70 Hz) is thought to be important for information processing in many sensory systems. Here, I used patch-clamp recordings in neuron pairs in rat olfactory bulb slices to assess the mechanisms underlying such "gamma" activity in the olfactory system. Patterned electrical stimulation of afferents that mimicked a natural odor stimulus elicited rapidly synchronized spikes (lag < or = 5 ms) in mitral cells, along with oscillatory activity at the gamma (approximately 50 Hz) frequency. Analysis of coupling potentials, combined with dendritic sectioning, indicated that mitral cell synchrony was mainly driven by inhibitory postsynaptic potentials (IPSPs) imposed by GABAergic granule cells. Recordings in granule cell pairs indicated that granule cells were themselves synchronized by their excitatory inputs from mitral cells, providing a means to coordinate GABA release. These results demonstrate that rapid synchrony can emerge in a network through the precise back-and-forth interplay between neuronal populations.

Animals↗

PubMed2005

Effects of emodin on synaptic transmission in rat hippocampal CA1 pyramidal neurons in vitro.

Rhubarb extracts provide neuroprotection after brain injury, but the mechanism of this protective effect is not known. The present study tests the hypothesis that rhubarb extracts interfere with the release of glutamate by brain neurons and, therefore, reduce glutamate excitotoxicity. To this end, the effects of emodin, an anthraquinone derivative extracted from Rheum tanguticum Maxim. Ex. Balf, on the synaptic transmission of CA1 pyramidal neurons in rat hippocampus were studied in vitro. The excitatory postsynaptic potential (EPSP) was depressed by bath-application of emodin (0.3-30 microM). Paired-pulse facilitation (PPF) of the EPSP was significantly increased by emodin. The monosynaptic inhibitory postsynaptic potential (IPSP) recorded in the presence of glutamate receptor antagonists (DNQX and AP5) was not altered by emodin. Emodin decreased the frequency, but not the amplitude, of the miniature EPSP (mEPSP). The inhibition of the EPSP induced by emodin was blocked by either 8-CPT, an adenosine A1 receptor antagonist, or by adenosine deaminase. These results suggest that emodin inhibits the EPSP by decreasing the release of glutamate from Schaffer collateral/commissural terminals via the activation of adenosine A1 receptors in rat hippocampal CA1 area and that the neuroprotective effects of rhubarb extracts may result from decreased glutamate excitotoxicity.

Adenosine↗