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PubMed2001

Dynamic modulation of excitation and inhibition during stimulation at gamma and beta frequencies in the CA1 hippocampal region.

Fast oscillations at gamma and beta frequency are relevant to cognition. During this activity, excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) are generated rhythmically and synchronously and are thought to play an essential role in pacing the oscillations. The dynamic changes occurring to excitatory and inhibitory synaptic events during repetitive activation of synapses are therefore relevant to fast oscillations. To cast light on this issue in the CA1 region of the hippocampal slice, we used a train of stimuli, to the pyramidal layer, comprising 1 s at 40 Hz followed by 2--3 s at 10 Hz, to mimic the frequency pattern observed during fast oscillations. Whole cell current-clamp recordings from CA1 pyramidal neurons revealed that individual stimuli at 40 Hz produced EPSPs riding on a slow biphasic hyperpolarizing-depolarizing waveform. EPSP amplitude initially increased; it then decreased concomitantly with the slow depolarization and with a large reduction in membrane resistance. During the subsequent 10-Hz train: the cells repolarized, EPSP amplitude and duration increased to above control, and no IPSPs were detected. In the presence of GABA(A) receptor antagonists, the slow depolarization was blocked, and EPSPs of constant amplitude were generated by 10-Hz stimuli. Altering pyramidal cell membrane potential affected the time course of the slow depolarization, with the peak being reached earlier at more negative potentials. Glial recordings revealed that the trains were associated with extracellular potassium accumulation, but the time course of this event was slower than the neuronal depolarization. Numerical simulations showed that intracellular chloride accumulation (due to massive GABAergic activation) can account for these observations. We conclude that synchronous activation of inhibitory synapses at gamma frequency causes a rapid chloride accumulation in pyramidal neurons, decreasing the efficacy of inhibitory potentials. The resulting transient disinhibition of the local network leads to a short-lasting facilitation of polysynaptic EPSPs. These results set constraints on the role that synchronous, rhythmic IPSPs may play in pacing oscillations at gamma frequency in the CA1 hippocampal region.

2-Amino-5-phosphonovalerate↗

PubMed1989

Slow active potentials in ventral inhibitory motor neurons of the nematode Ascaris.

The ability of ventral inhibitory motor neurons of the nematode Ascaris to generate slow depolarizing potentials was investigated using intracellular recording and current injection. In quiescent cells, regenerative depolarizations with peak amplitudes of approximately 20 mV and durations of several 100 ms were evoked in response to brief depolarizing current pulses. Repetitive slow potentials were produced in response to sustained depolarizing currents in a threshold-dependent manner. Repetitive slow potentials also occurred spontaneously, exhibiting cycle periods of about 700 ms. The ability of inhibitory motor neurons to generate slow potentials was blocked by addition of Co++, Cd++, or other Ca-channel blockers to the saline but not by TTX or substitution of Na+ with Tris. The amplitude and duration of slow potentials were increased in the presence of Ba++, Sr++, and TEA. Spontaneous slow potentials exhibited characteristics expected of intrinsically generated oscillations, including frequency modulation by injection of prolonged offset currents, phase resetting by brief current pulses, and suppression by strong hyperpolarization. Slow potentials appear to be generated in the ventral nerve cord processes and/or cell body of the motor neuron, and they produce rhythmic inhibitory postsynaptic potentials in ventral muscle cells. Slow potentials may therefore contribute to locomotory or other motor behaviors of the animal.

Animals↗

PubMed1984

The role of inhibitory mechanisms in hippocampal long-term potentiation.

The role of inhibitory processes in long-term potentiation (LTP) was investigated in hippocampal slices of the rat. GABAergic inhibition, tested by double shock experiments and by intracellular recording of inhibitory postsynaptic potentials, was not reduced in CA 1 pyramidal neurones after the induction of LTP. In cells recorded with caesium chloride-filled electrodes LTP could not be elicited. A reduction of intrinsic potassium-dependent inhibition may thus be responsible for LTP.

Afferent Pathways↗

PubMed1988

Lowering extracellular calcium reverses paired pulse habituation into facilitation in dentate granule cells and removes a late IPSP.

Simultaneous measurements of cellular responses and extracellular field potentials as well as extracellular Ca2+ concentration [( Ca2+]0) were performed in the dentate gyrus granule cell layer during paired pulse stimulation of the lateral perforant path at resting [Ca2+]o and during washout of calcium. At resting [Ca2+]o the second response to a paired stimulus was smaller than the first response. This frequency habituation reversed into frequency potentiation (second response larger than the first one) during lowering of [Ca2+]o at about the same time when a late presumed inhibitory postsynaptic potential (IPSP) was abolished. This suggests that a slow inhibition can account for part of frequency habituation in the dentate gyrus.

Action Potentials↗

PubMed1998

Stimulation-induced responses of the trigeminal caudal neurons in the brainstem preparation isolated from newborn rats.

The brainstem preparation with the trigeminal mandibular nerve attached was isolated from rats postnatal day 0-6 (P0-P6) to test if the potentiation could be induced in neonatal neurons in the trigeminal subnucleus caudalis by stimulation of the primary afferents. The stimulation-induced potentials in 92 neurons recorded extracellularly, and the synaptic potentials in 16 neurons recorded by the whole-cell patch clamp technique were examined. The extracellularly recorded neurons responded to stimulation (0.5 Hz) with either an increase, a decrease, or little change in spike numbers, and were classified as Type 1, Type 2, and Type 3, respectively. Type 1 neurons at P4 and older responded in a low Mg2+ solution with a progressive increase in spike number lasting for several minutes after the cessation of stimulation, i.e., short-term potentiation, STP. This potentiation was antagonized by 20 microM of (+)-MK-801 hydrogen maleate (MK-801) or 25 microM of 2-amino-5-phosphonovaleric acid. In contrast, Type 1 at P3 and younger did not exhibit STP. The age-related distinct response properties were observed between Type 1 neurons at P4-P6 and at P0-P3. The percentage of Type 1 in studied neurons increased from 24% at P0-P3 to 53% at P4-P6. In the intracellular experiment, the mean latency of excitatory postsynaptic potential (EPSP) of recorded neurons indicated that the conduction velocity of the convergent afferents was 0.37 m/s, in the range of C-fiber. Neurons were classified as Type E and Type I. Type E responded with EPSP only, or with both EPSP and inhibitory postsynaptic potentials (IPSP), while Type I responded with IPSP only. In Type E at P4 and older, a single stimulation produced a burst of spike discharges that lasted for several seconds. Stimulation at a hyperpolarized membrane potential showed that aggregated slow EPSPs lay under a burst of spike discharges, and that slow EPSPs, but not a short-latency EPSP, were completely blocked by MK-801. In contrast, Type E at P3 and younger did not evoke a burst of spikes. Morphological examination of recorded neurons showed that the formation of networks was sparse at P1 and rapidly developed up to P4. The results suggest that: (1) short-term potentiation is induced with the development of synaptic network formation in the caudal nucleus at P4 and older; (2) the summation of N-methyl-d-aspartate (NMDA)-mediated slow EPSPs build up a prolonged depolarization; and (3) the brainstem preparation is applicable for neurophysiological studies on the trigeminal pain system.

2-Amino-5-phosphonovalerate↗

PubMed2000

The G protein alpha subunit has a key role in determining the specificity of coupling to, but not the activation of, G protein-gated inwardly rectifying K(+) channels.

In neuronal and atrial tissue, G protein-gated inwardly rectifying K(+) channels (Kir3.x family) are responsible for mediating inhibitory postsynaptic potentials and slowing the heart rate. They are activated by Gbetagamma dimers released in response to the stimulation of receptors coupled to inhibitory G proteins of the G(i/o) family but not receptors coupled to the stimulatory G protein G(s). We have used biochemical, electrophysiological, and molecular biology techniques to examine this specificity of channel activation. In this study we have succeeded in reconstituting such specificity in an heterologous expression system stably expressing a cloned counterpart of the neuronal channel (Kir3.1 and Kir3.2A heteromultimers). The use of pertussis toxin-resistant G protein alpha subunits and chimeras between G(i1) and G(s) indicate a central role for the G protein alpha subunits in determining receptor specificity of coupling to, but not activation of, G protein-gated inwardly rectifying K(+) channels.

Adenosine↗

PubMed1997

Deafferentation weakens excitatory synapses in the developing central auditory system.

Decreased excitatory synaptic activity during development often leads to pre- and postsynaptic atrophy, as assessed anatomically. The present study considers the effect of decreased excitatory transmission on the maturation of synaptic strength. Towards this end, cochlear nucleus neurons, which project to the ipsilateral lateral superior olive (LSO), were denervated in gerbils at postnatal day 7, before the onset of hearing. This manipulation was intended to disrupt spontaneous glutamatergic transmission in the LSO while sparing the glycinergic afferents from the medial nucleus of the trapezoid body (MNTB). Afferent-evoked synaptic activity was assessed 1-6 days after ablation in a brain slice preparation using whole-cell current- and voltage-clamp recordings. In control animals, ipsilaterally evoked excitatory postsynaptic potentials (EPSPs) were present in 91% of neurons tested, but were observed in only 60% of neurons following cochlea removal. The maximum EPSP amplitude was significantly smaller in manipulated neurons compared with controls, and this was accompanied by a higher incidence of ipsilaterally evoked inhibitory postsynaptic potentials (IPSPs). To study the efficacy of excitatory synapses in greater detail, voltage-clamp recordings were made in the presence of strychnine and AP-5 [D(O)-2-amino-5-phosphonopentanoic acid]. The minimum excitatory postsynaptic current (EPSC) amplitude, presumed to reflect the efficacy of a single glutamatergic afferent, was approximately 40% smaller in manipulated neurons. In contrast, MNTB-evoked IPSPs were similar in neurons from control and ablated animals. However, manipulated neurons often exhibited a rebound depolarization after a hyperpolarizing current pulse or an afferent-evoked IPSP. In 70% of manipulated neurons, synaptically evoked rebound depolarizations were reduced, but not eliminated, by glutamate receptor antagonists. The glycine receptor antagonist strychnine did eliminate the IPSP-associated depolarization in these neurons. Collectively, these results suggest that functional denervation of excitatory afferents decreases their synaptic efficacy as result of both cell loss as well as decreased strength of individual surviving synapses.

Acoustic Stimulation↗

PubMed2002

Adrenomedullin influences magnocellular and parvocellular neurons of paraventricular nucleus via separate mechanisms.

We previously reported that adrenomedullin (AM) decreases blood pressure following microinjection into the paraventricular nucleus of the hypothalamus (PVN) of the rat. With the use of whole cell recordings in rat hypothalamic slice preparations, we characterized the effects of AM on electrophysiologically identified PVN neurons and described the membrane events underlying such actions. AM hyperpolarized magnocellular (type I) neurons in a dose-dependent manner, a response associated with an increase in the frequency and amplitude of inhibitory postsynaptic potentials. Blockade of action potentials with tetrodotoxin (TTX) abolished AM effects on membrane potential and synaptic activity in magnocellular neurons, suggesting direct actions on inhibitory interneurons. Furthermore, blockade of inhibitory synaptic transmission with the GABA(A) receptor antagonist bicuculline methiodide also abolished AM effects on membrane potential in magnocellular neurons. In contrast, parvocellular (type II) neurons depolarized following AM receptor activation. AM effects on parvocellular neurons were dose dependent and were maintained in the presence of TTX, indicating direct effects on this population of neurons. Voltage-clamp recordings from parvocellular neurons showed AM enhances a nonselective cationic conductance, suggesting a potential mechanism through which AM influences membrane potential. These observations show clear population-specific actions of AM on separate identified groups of PVN neurons. Such effects on magnocellular neurons likely contribute to the hypotensive actions of this peptide in PVN. Although the effects on parvocellular neurons may also contribute to such cardiovascular effects of AM, it is more likely that actions on this population of PVN neurons underlie the previously demonstrated activational effects of AM on the hypothalamic-pituitary-adrenal axis.

Adrenomedullin↗

PubMed2000

Nitric oxide and carbon monoxide modulate oscillations of olfactory interneurons in a terrestrial mollusk.

Spontaneous or odor-induced oscillations in local field potential are a general feature of olfactory processing centers in a large number of vertebrate and invertebrate species. The ubiquity of such oscillations in the olfactory bulb of vertebrates and analogous structures in arthropods and mollusks suggests that oscillations are fundamental to the computations performed during processing of odor stimuli. Diffusible intercellular messengers such as nitric oxide (NO) and carbon monoxide (CO) also are associated with central olfactory structures in a wide array of species. We use the procerebral (PC) lobe of the terrestrial mollusk Limax maximus to demonstrate a role for NO and CO in the oscillatory dynamics of the PC lobe: synthesizing enzymes for NO and CO are associated with the PC lobes of Limax, application of NO to the Limax PC lobe increases the local field potential oscillation frequency, whereas block of NO synthesis slows or stops the oscillation, the bursting cells of the PC lobe that drive the field potential oscillation are driven to higher burst frequency by application of NO, the nonbursting cells of the PC lobe receive trains of inhibitory postsynaptic potentials, presumably from bursting cells, due to application of NO, and application of CO to the PC lobe by photolysis of caged CO results in an increase in oscillation frequency proportional to CO dosage.

Animals↗

PubMed1996

Excitatory actions of norepinephrine on multiple classes of hippocampal CA1 interneurons.

Norepinephrine (NE) causes an increase in the frequency of inhibitory postsynaptic potentials in CA1 pyramidal neurons in vitro. The possibility that this increase in tonic inhibition is caused by an excitatory effect on inhibitory interneurons was investigated through whole-cell recordings from pyramidal cells and both whole-cell and cell-attached patch recordings from visualized interneurons in acute slices of rat hippocampus. Adrenergic agonists caused a large increase in the frequency and amplitude of spontaneous IPSCs recorded from pyramidal cells in the presence of ionotropic glutamate receptor blockers, but they had no effect on either the frequency or the amplitude of action potential-independent miniature IPSCs recorded in tetrodotoxin. This effect was mediated primarily by an alpha adrenoceptor, although a slight beta adrenoceptor-dependent increase in IPSCs was also observed. NE caused interneurons located in all strata to depolarize and begin firing action potentials. Many of these cells had axons that ramified throughout the stratum pyramidale, suggesting that they are responsible for the IPSCs observed in pyramidal neurons. This depolarization was also mediated by an alpha adrenoceptor and was blocked by a selective alpha 1- but not a selective alpha 2-adrenoceptor antagonist. However, a slight beta adrenoceptor-dependent depolarization was detected in those interneurons that displayed time-dependent inward rectification. In the presence of a beta antagonist, NE induced an inward current that reversed near the predicted K+ equilibrium potential and was not affected by changes in intracellular Cl- concentration. In the presence of an alpha 1 antagonist, NE induced an inwardly rectifying current at potentials negative to approximately -70 mV that did not reverse (between -130 and -60 mV), characteristics similar to the hyperpolarization-activated current (lh). However, the depolarizing action of NE is attributable primarily to the alpha 1 adrenoceptor-mediated decrease in K+ conductance and not the beta adrenoceptor-dependent increase in lh. These results provide evidence that NE increases action potential-dependent IPSCs in pyramidal neurons by depolarizing surrounding inhibitory interneurons. This potent excitatory action of NE on multiple classes of hippocampal interneurons may contribute to the NE-induced decrease in the spontaneous activity of pyramidal neurons and the antiepileptic effects of NE observed in vivo.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1994

Clonazepam suppresses GABAB-mediated inhibition in thalamic relay neurons through effects in nucleus reticularis.

1. Experiments were carried out using patch-clamp techniques in rat thalamic slices, maintained in vitro, to examine the effects of the benzodiazepine compound, clonazepam (CZP), on intrathalamic inhibition. Bath-applied CZP reduced the gamma-aminobutyric acid-B (GABAB) component of inhibitory postsynaptic potentials and currents (IPSPs and IPSCs, respectively) evoked in rat thalamic somatosensory relay neurons by stimulation of nucleus reticularis thalami (nRt), without consistently affecting the GABAA IPSP. Secondary IPSPs, which occur as a result of intrathalamic oscillations, were dramatically reduced. 2. Voltage-clamp experiments combined with local or bath perfusion of the GABAA antagonist bicuculline methiodide (BMI), demonstrated that nRt is a site of GABAA-mediated postsynaptic inhibition that affects inhibitory output onto relay neurons. BMI enhanced both GABAA and GABAB postsynaptic inhibition in relay neurons when applied to nRt. Focal applications in the ventrobasal relay nucleus near the recording electrode blocked the GABAA-mediated IPSP but had no effects on GABAB inhibitory potentials. 3. Results suggest that CZP acts to facilitate recurrent inhibition in nRt and decrease its inhibitory output onto relay neurons. Intra-nRt GABAA-mediated inhibition thus has an important role in controlling thalamic excitability and in the anti-absence actions of CZP.

Animals↗

PubMed1980

Excitation and inhibition of marginal layer and interstitial interneurons in cat nucleus caudalis by mechanical stimuli.

In cats anesthetized with urethane, the caudal medulla was stabilized in preparation for intracellular recording from interstitial neurons in the descending tract of the trigeminal nerve and from neurons in lamina I of nucleus caudalis. Glass micropipets (10-50 M ohms) were advanced from the surface to a maximum depth of 350 micrometer. When DC potential shifts occurred, it was found that mechanical stimuli to the face generated bursts of positive-going spikes, followed in some cases by inhibitory postsynaptic potentials (IPSPs). Subdermal electrical stimulation of the face in each receptive field almost always enabled the same neuron to be driven electrically. Recordings were classified as from primary afferent fibers or from interneurons. Primary fibers had a purely positive spike, with a latency varying by no more than 0.05 msec, and could follow stimulation at 500 Hz. The mean latency for the fibers was 1.87 +/- 0.06 msec (n=75), and their absolute refractory period was 0.42 +/- 0.02 msec (n=36). Recordings were classed as from interneurons if there was an IPSP or the latency was at least 4 msec, with a variation of latency of at lest 0.5 msec. Responses thought to be monosynaptically driven had a mean latency of 2.09 +/0 0.07 msec (n=32) and could follow pairs of stimuli at a mean minimum interval of 0.70 +/- 0.06 msec (n=20). Responses thought to be polysynaptically driven had a mean latency of 7.9 +/- 1.08 msec (n=49) and a mean interstimulus interval of 2.96 +/- 0.84 (n=20). Most responses were generated by brushing the face (n=87), some by pressure on the face (n=25), and a few by pinching the skin of the face (n=6). Interneuron responses were most commonly recorded in the first 200 micrometer of the descending tract, and this position was confirmed by the injection of pontamine sky blue and the examination of frozen sections. The recordings were thought to be from dendrites of marginal and interstitial cells or the somas of interstitial cells. The IPSPs which followed spike potentials could only follow stimuli at 10 Hz or less. The failure appeared to be at a primary afferent synapse upon an inhibitory interneuron. Collision tests between mechanically evoked and electrically evoked responses showed long-lasting inhibition of the response to electrical stimulation after collision. Presynaptic inhibition exerted on the primary afferent excitation was suggested as the explanation.

Animals↗

PubMed1990

Low magnesium epileptogenesis in the rat hippocampal slice: electrophysiological and pharmacological features.

Extra- and intracellular recording techniques were used to study the epileptiform activity generated by rat hippocampal slices perfused with Mg2(+)-free artificial cerebrospinal fluid (ACSF). This procedure induced in both CA1 and CA3 subfields the appearance of synchronous, spontaneously occurring epileptiform discharges which consisted of extracellularly recorded 100-800 ms long, positive shifts with superimposed negative going population spikes. Simultaneous, extracellular recordings from CA1 and CA3 subfields revealed that the epileptiform discharges in CA3 preceded those occurring in CA1 by 5-25 ms. Surgical separation of the two areas led to the disappearance of spontaneous events in the CA1 but not in the CA3 subfield. In this type of experiment CA1 pyramidal cells still generated epileptiform discharges following orthodromic stimuli. The intracellular counterpart of both spontaneous and stimulus-induced epileptiform discharges in CA1 and CA3 pyramidal cells was a large amplitude depolarization with high frequency discharge of action potentials which closely resembled the paroxysmal depolarizing shift recorded in the experimental epileptogenic focus. A hyperpolarizing potential triggered by alvear stimuli was recorded in CA1 cells perfused with Mg2(+)-free ACSF. This hyperpolarization was blocked by bicuculline methiodide (BMI) indicating that it represented a GABAergic inhibitory postsynaptic potential (IPSP). BMI also caused a prolongation of both spontaneous and stimulus-induced Mg(+)-free epileptiform discharges. Perfusion of the slices with the N-methyl-D-aspartate (NMDA) receptor antagonist DL-2-amino-5-phosphono-valerate (APV) reduced and eventually abolished the Mg(+)-free epileptiform discharges. These effects were more pronounced in the CA1 than in the CA3 subfield. APV also reduced the amplitude and the duration of the alveus-induced IPSP. These data demonstrate that Mg(+)-free epileptiform activity is present in the hippocampal slice at a time when inhibitory GABAergic potentials are operant as well as that in the CA1 subfield this type of epileptiform activity is dependent upon NMDA-activated conductances. Our experiments also indicate that NMDA receptors might be involved in the neuronal circuit responsible for the hyperpolarizing IPSP generated by CA1 pyramidal neurons.

2-Amino-5-phosphonovalerate↗

PubMed1998

Ontogeny of altered synaptic function in a rat model of chronic temporal lobe epilepsy.

In the limbic status model of chronic temporal lobe epilepsy, hippocampal stimulation induces acute status epilepticus in rats; recurrent, spontaneous seizures develop following an asymptomatic silent period lasting several weeks. Previous work has shown increased excitability and decreased inhibition in CA1 pyramidal neurons in chronically epileptic animals. To determine the relationship of altered cellular responses to seizure onset, in vitro intracellular recording was used to follow the evolution of changes in synaptic physiology occurring during the seizure-free silent period. Pyramidal cells displayed increasing epileptiform activity throughout the period investigated, 3-14 days following status; the mean number of evoked action potentials from 1.1+/-0.05 in control cells to 2.4+/-0.4 early (3 days after status) and 4. 3+/-0.7 late (14 days) in the silent period. Monosynaptic inhibitory postsynaptic potentials mediated by gamma-aminobutyric acid-A receptors in silent period cells differed markedly from controls. Area, rise time, and duration of these potentials decreased by 40-60% within 3 days following status and to values commensurate with chronically epileptic animals in 7 to 10 days. gamma-Aminobutyric acid-B receptor-mediated IPSPs diminished more gradually in the silent period, reaching a minimum at day 14. In contrast, presynaptic gamma-aminobutyric acid-B receptor function showed maximum impairment 3 days after status. The benzodiazepine type 1 receptor agonist zolpidem reduced hyperexcitability in both silent period and chronically epileptic cells, but was more effective at unmasking the underlying IPSP in silent period neurons. The results indicate that changes in different components of pyramidal cell inhibitory synaptic physiology associated with chronic epilepsy in this model evolve individually at different rates, but are all complete before seizure onset. Although the results do not imply causality, they do suggest that the development of physiological changes in CA1 pyramidal cells may contribute to the lag period preceding the onset of chronic seizures.

Animals↗

PubMed1998

Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo.

Transient neurophysiological changes in CA3 neurons and dentate granule cells after severe forebrain ischemia in vivo. J. Neurophysiol. 80: 2860-2869, 1998. The spontaneous activities, evoked synaptic responses, and membrane properties of CA3 pyramidal neurons and dentate granule cells in rat hippocampus were compared before ischemia and </=7 days after reperfusion with intracellular recording and staining techniques in vivo. A four-vessel occlusion method was used to induce approximately 14 min of ischemic depolarization. No significant change in spontaneous firing rate was observed in both cell types after reperfusion. The amplitude and slope of excitatory postsynaptic potentials (EPSPs) in CA3 neurons decreased to 50% of control values during the first 12 h reperfusion and returned to preischemic levels 24 h after reperfusion. The amplitude and slope of EPSPs in granule cells slightly decreased 24-36 h after reperfusion. The amplitude of inhibitory postsynaptic potentials in CA3 neurons transiently increased 24 h after reperfusion, whereas that in granule cells showed a transient decrease 24-36 h after reperfusion. The duration of spike width of CA3 and granule cells became longer than that of control values during the first 12 h reperfusion. The spike threshold of both cell types significantly increased 24-36 h after reperfusion, whereas the frequency of repetitive firing evoked by depolarizing current pulse was decreased during this period. No significant change in rheobase and input resistance was observed in CA3 neurons. A transient increase in rheobase and a transient decrease in input resistance were detected in granule cells 24-36 h after reperfusion. The amplitude of fast afterhyperpolarization in both cell types increased for 2 days after ischemia and returned to normal values 7 days after reperfusion. The results from this study indicate that the neuronal excitability and synaptic transmission in CA3 and granule cells are transiently suppressed after severe forebrain ischemia. The depression of synaptic transmission and neuronal excitability may provide protection for neurons after ischemic insult.

Animals↗

PubMed1993

Cellular effects of isoflurane on bulbar respiratory neurons in decerebrate cats.

Effects of isoflurane on the membrane potential trajectory and synaptic activity in bulbar respiratory neurons were investigated in decerebrate, vagotomized and artificially ventilated cats. A 2-min inhalation of 1.6% end-tidal concentration of isoflurane produced depolarization of the membrane in 10 out of 18 inspiratory, 8 out of 15 post-inspiratory and 5 out of 12 expiratory neurons and hyperpolarization in the rest of the population recorded in the ventral respiratory group. In both depolarized and hyperpolarized cells, periodically occurring excitatory and inhibitory synaptic waves were decreased, and input resistance was increased. Concomitantly, isoflurane reduced the excitatory and inhibitory postsynaptic potentials evoked by electrical stimulation of the vagus nerve, superior laryngeal nerve and cervical spinal cord. The effects of isoflurane on membrane potential and input resistance became negligible when excitatory and inhibitory synaptic potentials were suppressed by iontophoretically applied tetrodotoxin. The present results suggest that the respiratory neuronal responses induced by isoflurane are attributed mainly to the decrease of excitatory and inhibitory synaptic interactions in the bulbar respiratory network of neurons.

Action Potentials↗

PubMed1994

Surround inhibition among projection neurons is weak or nonexistent in the rat neostriatum.

1. Antidromic activation of striatal spiny projection neurons by substantia nigra stimulation in vivo did not evoke inhibitory postsynaptic potentials (IPSPs) in the antidromically activated neurons, or in neighboring spiny neurons. 2. More generalized activation of projection cells by stimulation of the efferent pathway in slices did not evoke IPSPs in spiny neurons. Inhibitory mechanisms were operative in these slices, as indicated by the presence of an IPSP component in the orthodromic response to local stimulation. 3. Dual intracellular recordings, obtained from cells located within 50-200 microns of each other in striatal slices also failed to demonstrate any inhibition among striatal spiny cells. Spikes triggered in one spiny neuron by current injection failed to produce any postsynaptic potential in nearby spiny cells at resting or depolarized membrane potentials. Excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the cortex were not affected by spiking of neighboring cells. 4. It is impossible to rule out the presence of inhibition among striatal spiny neurons in all circumstances. However, the absence of demonstrable IPSPs in these experiments argue against the common view that mutual inhibition among spiny neurons is a central organizing principle of striatal function.

Animals↗

PubMed1999

Dopamine activates two different receptors to produce variability in sign at an identified synapse.

Chemical synaptic transmission was investigated at a central synapse between identified neurons in the freshwater snail, Lymnaea stagnalis. The presynaptic neuron was the dopaminergic cell, Right Pedal Dorsal one (RPeD1). The postsynaptic neuron was Visceral Dorsal four (VD4). These neurons are components of the respiratory central pattern generator. The synapse from RPeD1 to VD4 showed variability of sign, i.e., it was either inhibitory (monophasic and hyperpolarizing), biphasic (depolarizing followed by hyperpolarizing phases), or undetectable. Both the inhibitory and biphasic synapse were eliminated by low Ca2+/high Mg2+ saline and maintained in high Ca2+/high Mg2+ saline, indicating that these two types of connections were chemical and monosynaptic. The latency of the inhibitory postsynaptic potential (IPSP) in high Ca2+/high Mg2+ saline was approximately 43 ms, whereas the biphasic postsynaptic potential (BPSP) had approximately 12-ms latency in either normal or high Ca2+/high Mg2+ saline. For a given preparation, when dopamine was pressured applied to the soma of VD4, it always elicited the same response as the synaptic input from RPeD1. Thus, for a VD4 neuron receiving an IPSP from RPeD1, pressure application of dopamine to the soma of VD4 produced an inhibitory response similar to the IPSP. The reversal potentials of the IPSP and the inhibitory dopamine response were both approximately -90 mV. For a VD4 neuron with a biphasic input from RPeD1, pressure-applied dopamine produced a biphasic response similar to the BPSP. The reversal potentials of the depolarizing phase of the BPSP and the biphasic dopamine response were both approximately -44 mV, whereas the reversal potentials for the hyperpolarizing phases were both approximately -90 mV. The hyperpolarizing but not the depolarizing phase of the BPSP and the biphasic dopamine response was blocked by the D-2 dopaminergic antagonist (+/-) sulpiride. Previously, our laboratory demonstrated that both IPSP and the inhibitory dopamine response are blocked by (+/-) sulpiride. Conversely, the depolarizing phase of both the BPSP and the biphasic dopamine response was blocked by the Cl- channel antagonist picrotoxin. Finally, both phases of the BPSP and the biphasic dopamine response were desensitized by continuous bath application of dopamine. These results indicate that the biphasic RPeD1 --> VD4 synapse is dopaminergic. Collectively, these data suggest that the variability in sign (inhibitory vs. biphasic) at the RPeD1 --> VD4 synapse is due to activation of two different dopamine receptors on the postsynaptic neuron VD4. This demonstrates that two populations of receptors can produce two different forms of transmission, i.e., the inhibitory and biphasic forms of the single RPeD1 --> VD4 synapse.

Animals↗