PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Inhibitory Postsynaptic Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 955 records · Page 53Linked to original sources

Axonal trajectories of inhibitory vestibulocollic neurons activated by the anterior semicircular canal nerve and their synaptic effects on neck motoneurons in the cat.

Somatic location, axonal trajectories and synaptic effects of inhibitory vestibulocollic neurons which were activated by selective stimulation of the anterior semicircular canal nerve (ACN) were studied in the anesthetized cat. ACN stimulation evoked disynaptic inhibitory postsynaptic potentials (IPSPs) in neck flexor motoneurons. This was seen in all the (64/64) tested motoneurons innervating the ipsilateral (i-) longus capitis (LC) and the i-sternocleidomastoideus (SCM) muscles and in 86% (38/44) of the motoneurons innervating the contralateral (c-) LC muscle. The inhibitory relay neurons, identified by orthodromic and antidromic responses to stimulation of the ACN and the i- and c-LC motoneuron pools, were classified as VCi (vestibulocollic neurons sending an axon to the i-LC motoneuron pool) and VCc (vestibulocollic neurons sending an axon to the c-LC motoneuron pool) neurons. Neither VCi nor VCc neurons were activated antidromically by localized stimulation of the ascending medial longitudinal fasciculus (asc. MLF) or the 3rd nuclei. They were located in the medial, descending and ventral lateral vestibular nuclei. It was also observed that VCi neurons produced unitary IPSPs in i-LC and i-SCM motoneurons in the C1 segment. Inhibitory synapses were estimated to be on the cell somata and/or the proximal dendrites of the motoneurons.

Animals↗

Synaptic inhibition of phrenic motoneurones evoked by stimulation of the superior laryngeal nerve.

Synaptic responses evoked in phrenic motoneurones (PMNs) by stimulation of the superior laryngeal nerve (SLN) were analysed in anaesthetised cats. Stimulation of the SLN was followed by inhibition of ipsilateral phrenic nerve discharge with the latency of 9.5 +/- 2.3 ms (mean +/- S.D.) and hyperpolarizations of ipsilateral PMN membrane potentials (latency, 8.4 +/- 2.1 ms) which were observed after stimuli applied both during inspiration and expiration. During the injection of Cl ions, the hyperpolarizations were either reversed or flattened in all 28 tested PMNs, thus indicating a direct inhibition. The possibility that the inhibitory postsynaptic potentials are produced by segmental respiratory interneurones is discussed.

Action Potentials↗

Carbachol reduces IK,baclofen, but not IK,GABA in guinea pig hippocampal slices.

In the presence of bicuculline and/or picrotoxin (-)-baclofen and gamma-aminobutyric acid (GABA) induced outward currents (IBac and IGABA) at holding potentials of -55 to -75 mV in guinea pig CA3 neurones of hippocampal slices. Zero potentials for these currents were at the K-equilibrium potential indicating that they were carried by K-ions (IK.Bac, IK.GABA). IK.Bac was strongly reduced by carbachol (Cch) in low concentration (0.1 0.3 microM), while IK.GABA was not affected by Cch concentrations even up to 20 microM. The K-dependent late inhibitory postsynaptic potential (IPSP) was reduced significantly by Cch concentrations higher than 1 microM, but with these concentrations the early, Cl-dependent IPSP was reduced as well. The baclofen-derivative phaclofen, considered a selective antagonist of both the postsynaptic action of baclofen and the bicuculline - and picrotoxin - resistant action of GABA, exhibited, in our hands, partial agonistic effects and effects on non-transmitter gated K-currents. Our findings cast some doubt on the assumption that IK.Bac, IK.GABA and the late IPSP are all mediated by the same receptor and generated by the same mechanism.

Animals↗

Calcineurin-mediated LTD of GABAergic inhibition underlies the increased excitability of CA1 neurons associated with LTP.

Coincident pre- and postsynaptic activity generates long-term potentiation (LTP), a possible cellular model of learning and memory. LTP has two components: (1) an increase in the excitatory postsynaptic potential (EPSP), and (2) an increase in the ability of the EPSP to generate a spike (E-S coupling of LTP). We have used pharmacological and genetic approaches to address the molecular nature of E-S coupling in CA1 pyramidal neurons. Blockade of the Ca2+-sensitive phosphatase, calcineurin, prevents induction of E-S coupling without interfering with LTP of the EPSP. Calcineurin produces its effect on E-S coupling by inducing a long-lasting depression (LTD) of the GABA(A)-mediated inhibitory postsynaptic potentials (IPSPs). This LTD of the IPSP was prevented by blockade of NMDA receptors. Thus, the tetanus that elicits NMDA-dependent LTP mediates a coordinately regulated double function. It produces LTP of the EPSP and, concomitantly, LTD of the IPSP that leads to enhancement of E-S coupling.

Animals↗

Mechanisms and functional significance of a slow inhibitory potential in neurons of the lateral amygdala.

A slow inhibitory potential (sIP) elicited upon synaptic activation in spiny, pyramidal-like cells with properties indicative of projection neurons was investigated in slices of the rat and guinea-pig lateral amygdala in vitro. The sIP succeeded the triphasic sequence of excitatory and fast/slow inhibitory postsynaptic potentials mediated via glutamate and GABA(A/B) receptors, respectively, was readily evoked upon repetitive stimulation of the external capsule and appeared to terminate epileptiform burst discharges during pharmacologically reduced GABAergic influence. The sIP reversed close to the Cl- equilibrium potential, but was not affected by altered transmembrane Cl- gradients and not abolished by antagonists to ligand-gated Cl- channels. Intracellular injection of QX 314 and resulting blockade of sodium spikes had no effect, whereas the Ca2+ chelator BAPTA blocked the sIP concomitantly with slow hyperpolarizing afterpotentials following intrinsically generated spike firing, thereby indicating the contribution of Ca2+-dependent mechanisms secondary to synaptic activation. During action of BAPTA and QX 314, an N-methyl-D-aspartate (NMDA) receptor-mediated potential was unmasked, which contributed to the sIP. The Ca2+-dependent mechanisms of the sIP involved a membrane K+ conductance, as was indicated by the dependence on the K+ gradient and the shift of the reversal potential towards the K+ equilibrium potential during blocked NMDA receptors. During the presence of GABA receptor antagonists, reduction of the Ca2+-activated K+ conductance through injection of BAPTA or application of dopamine induced a gradual shift of interictal-like single bursts of spikes towards the generation of re-occurring ictal-like activity. It is concluded that pyramidal-like projection cells in the AL can generate a sIP upon synaptic activation, which reflects the combined activation of an NMDA receptor-mediated cation current and a K+ current that is secondary to the rise in intracellular Ca2+ concentration resulting from the preceding depolarizing response. The sIP may play an important role in controlling excitatory activity in the amygdala, particularly in preventing the transformation of interictal-like activity towards recurrent epileptic discharges during periods of decreased GABAergic influence.

Amygdala↗

Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential.

We used intracellular recording in the hippocampal slice in vitro to characterize further the mechanisms behind the unusual excitatory action of opiates and opioid peptides on hippocampal pyramidal cells in vivo. No significant effect on resting membrane potential, input resistance, or action potential size in cortical area 1 (CA1) pyramidal cells was observed with morphine sulfate, beta-endorphin, [Met5]enkephalin, or [D-Ala2, D-Leu5]enkephalin at 1-50 microM. However, in all cells studied, these agents markedly reduced the size of inhibitory postsynaptic potentials generated by stimulation of the stratum radiatum or alveus. Excitatory postsynaptic potentials were also diminished in many of these cells. The effects of the opioids were antagonized by naloxone. These results are consistent with excitation of pyramidal neurons by a disinhibitory mechanism.

Animals↗

Dopamine modulates graded and spike-evoked synaptic inhibition independently at single synapses in pyloric network of lobster.

Bath application of dopamine (DA) modifies the rhythmic motor pattern generated by the pyloric network in the stomatogastric ganglion of the spiny lobster, Panulirus interruptus. Synaptic transmission between network members is an important target of DA action. All pyloric neurons employ both graded transmitter release and action-potential-mediated synaptic inhibition. DA was previously shown to alter the graded synaptic strength of every pyloric synapse. In this study, we compared DA's effects on action-potential-mediated and graded synaptic inhibition at output synapses of the lateral pyloric (LP) neuron. At each synapse the postsynaptic cell tested was isolated from other descending and pyloric synaptic inputs. DA caused a reduction in the size of the LP spike-evoked inhibitory postsynaptic potentials (IPSPs) in the pyloric dilator (PD) neuron. The change in IPSP size was significantly and linearly correlated with DA-induced reduction in the input resistance of the postsynaptic PD neuron. In contrast, graded inhibition, tested in the same preparations after superfusing the stomatogastric ganglion (STG) with tetrodotoxin (TTX), was consistently enhanced by DA. DA shifted the amplitude of spike-evoked IPSPs in the same direction as the alteration of the postsynaptic cell input resistance at two additional synapses tested: DA weakened the LP spike-mediated inhibition of the ventricular dilator (VD) and reduced the VD input resistance, while strengthening the LP --> pyloric constrictor (PY) synapse and increasing PY input resistance. As previously reported, graded inhibition was enhanced at these two LP output synapses. We conclude that DA can differentially modulate the spike-evoked and graded components of synapses between members of a central pattern generator network. At the synapses we studied, actions on the presynaptic cell predominate in the modulation of graded transmission, whereas effects on postsynaptic cells predominate in the regulation of spike-evoked IPSPs.

Action Potentials↗

Propagation of spindle waves in a thalamic slice model.

1. We study the propagation and dynamics of spindle waves in thalamic slices by developing and analyzing a model of reciprocally coupled populations of excitatory thalamocortical (TC) neurons and inhibitory thalamic reticular (RE) neurons. 2. Each TC neuron has three intrinsic ionic currents: a low-threshold T-type Ca+2 current (ICa-T), a hyperpolarization-activated cation ("sag") current (Ih) and a leak current. Each RE cell also has three currents: ICa-T, a leak current, and a calcium-activated potassium current (IAHP). Isolated TC cells are at rest, can burst when released or depolarized from a hyperpolarized level, and burst rhythmically under moderate constant hyperpolarizing current. Isolated RE cells are at a hyperpolarized resting membrane potential and can burst when depolarized. 3. TC cells excite RE cells with fast alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) synapses, and RE cells inhibit TC cells with fast gamma-aminobutyric acid-A (GABAA) and slow GABAB synapses and inhibit each other with GABAA synapses only. GABAB postsynaptic conductances operate far from saturation, and the slow inhibitory postsynaptic potentials (IPSPs) increase with the width of the presynaptic burst. The model network is a one-dimensional cellular array with localized coupling. The synaptic coupling strength decays with the distance between the pre- and postsynaptic cells, either exponentially or as a step function. 4. The "intact" network can oscillate with partial synchrony and a population frequency of approximately 10 Hz. RE cells emit bursts almost at every oscillation cycle, whereas TC cells do so almost at every other cycle. Block of GABAB receptors hardly changes the network behavior. Block of GABAA receptors leads the network to a slowed oscillatory state, where the population frequency is approximately 4 Hz and both RE and TC cells fire unusually long bursts at every cycle and in full synchrony. These results are consistent with the experimental observations of von Krosigk, Bal, and McCormick. We obtain such consistency only when the above assumptions regarding the synaptic dynamics, particularly nonsaturating GABAB synapses, are fulfilled. 5. The slice model has a stable rest state with no neural activity. By initially depolarizing a few neurons at one end of the slice while all the other cells are at rest, a recruitment process may be initiated, and a wavefront of oscillatory activity propagates across the slice. Ahead of the wavefront, neurons are quiescent; neurons behind it oscillate. We find that the wave progresses forward in a lurching manner. TC cells that have just become inhibited must be hyperpolarized for a long enough time before they can fire rebound bursts and recruit RE cells. This step limits the wavefront velocity and may involve a substantial part of the cycle when no cells at the front are depolarized. 6. The wavefront velocity increases linearly with the characteristic spatial length of the connectivity (the footprint length). It increases only gradually with the synaptic strength, logarithmically in the case of an exponential connection function and only slightly for a step connection function. It also decreases gradually with a potassium leak conductance that hyperpolarizes RE cells. 7. To reproduce the experimentally measured wavefront velocity of approximately 1 mm/s, together with other in vitro observations, both the RE-to-TC and the TC-to-RE projections in the model should be spatially localized. The sum of the RE-to-TC and the TC-to-RE synaptic footprint lengths should be on the order of 100 microns. (ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Synaptic organization of tectal-facial pathways in cat. II. Synaptic potentials following midbrain tegmentum stimulation.

1. The organization of the synaptic pathways underlying midbrain tegmentum influence over the facial musculature was studied with the use of an acute electrophysiological approach in the cat. Under pentobarbital sodium anesthesia, synaptic potentials were recorded intracellularly in antidromically identified facial motoneurons following electrical stimulation of the paralemniscal zone. The cells of origin and the pathways responsible for the potentials evoked from the paralemniscal zone were defined with the use of retrograde transport of horseradish peroxidase (HRP). The putative role of the paralemniscal zone with regard to the production of disynaptic, tectally evoked potentials in facial motoneurons was investigated both by inactivating this nucleus with injections of lidocaine and by making acute brain stem lesions to sever the paralemniscal-facial and other afferent pathways. 2. Following paralemniscal stimulation, monosynaptic, excitatory postsynaptic potentials (EPSPs) with latencies ranging from 0.6 to 0.9 ms, steep rising phases, and amplitudes in excess of 4.0 mV were recorded in motoneurons of the temporal and auriculoposterior subdivisions, which supply the pinna muscles. Smaller amplitude EPSPs (less than 1.0 mV) with monosynaptic latencies were observed in the zygomatic subdivision. Polysynaptic EPSPs with latencies ranging from 1.0 to 1.8 ms were also observed in all three of these subdivisions. However, only long-latency EPSPs, arriving at 2.0 ms or later, were present in ventral subdivision motoneurons. 3. Inhibitory postsynaptic potentials (IPSPs) were also frequently recorded in facial motoneurons after paralemniscal stimulation. Monosynaptic IPSPs with latencies ranging from 0.8 to 1.2 ms and amplitudes in excess of 4.0 mV were recorded in facial motoneurons of the temporozygomatic and auriculoposterior subdivisions, as were polysynaptic IPSPs with latencies ranging from 1.2 to 1.8 ms. IPSPs were sometimes observed in combination with a smaller, shorter latency EPSPs. Only long-latency IPSPs of greater than 2.0 ms were recorded in ventral subdivision motoneurons. In all cases, both the EPSPs and the IPSPs were graded in character and could be augmented by multiple stimuli. 4. The contralateral paralemniscal zone and the supraoculomotor area, bilaterally, represented the two most prominent afferent sources labeled after HRP injection of the facial nucleus. The superior colliculus and numerous reticular formation regions were also identified as facial nucleus afferents by the presence of retrogradely labeled cells. The retrogradely labeled cells in the paralemniscal zone exhibited heterogeneous soma size. HRP-labeled axons of the paralemniscal-facial pathway were observed to cross the midline by traveling ventral to the brachium conjunctivum in the caudal mesencephalon.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Discharge properties of medullary reticulospinal neurons during postural changes induced by intrapontine injections of carbachol, atropine and serotonin, and their functional linkages to hindlimb motoneurons in cats.

The present study was aimed at elucidating the pontomedullary and spinal cord mechanisms of postural atonia induced by microinjection of carbachol and restored by microinjections of serotonin or atropine sulfate into the nucleus reticularis pontis oralis (NRPo). Medullary reticulospinal neurons (n = 132) antidromically activated by stimulating the L1 spinal cord segment were recorded extracellularly. Seventy-eight of them were orthodromically activated with mono- or disynaptic latencies by stimulating the NRPo area at the site where carbachol injections effectively induced postural atonia. Most of these reticulospinal neurons (71 of 78) were located in the nucleus reticularis gigantocellularis (NRGc). Following carbachol injection into the NRPo, discharge rates of the NRGc reticulospinal neurons (29 of 34) increased, while the activity of soleus muscles decreased bilaterally. Serotonin or atropine injections into the same NRPo area resulted in a decrease in the discharge rates of the reticulospinal neurons with a concomitant increase in the levels of hindlimb muscle tone. Membrane potentials of hindlimb extensor and flexor alpha motoneurons (MNs) were hyperpolarized and depolarized by carbachol and serotonin or atropine injections, respectively. In all pairs of reticulospinal neurons and MNs (n = 11), there was a high correlation between the increase in the discharge rates and the degree of membrane hyperpolarization of the MNs. Spike-triggered averaging during carbachol-induced atonia revealed that inhibitory postsynaptic potentials (IPSPs) were evoked in 15 MNs by the discharges of nine reticulospinal neurons. Four of them evoked IPSPs in more than one MN. The mean segmental delay and the mean time to the peak of IPSPs were 1.6 ms and 2.0 ms, respectively. Axonal trajectories of reticulospinal neurons (n = 6), which evoked IPSPs in MNs, were investigated in the lumbosacral segments (L1-S1) by antidromic threshold mapping. The stem axons descended through the ventral (n = 2) and ventrolateral (n = 4) funiculi in the lumbar segments. All axons projected their collaterals to the intermediate region (laminae V, VI) and ventromedial part (laminae VII, VIII) of the gray matter. All these results suggest that the reticulospinal pathway originating from the NRGc is involved in postural atonia induced by pontine microinjection of carbachol, and that the pathway is inactivated during the postural restoration induced by subsequent injections of serotonin or atropine. It is further suggested that the pontine inhibitory effect is mediated via segmental inhibitory interneurons projecting to MNs.

Action Potentials↗

Synaptic mechanisms acting on lumbar motoneurons during postural augmentation induced by serotonin injection into the rostral pontine reticular formation in decerebrate cats.

Intrapontine microinjections of serotonin in acutely decerebrated cats resulted in the bilateral augmentation of the postural muscle tone of the hindlimbs. Optimal injection sites were located in the dorsomedial part of the rostral pontine reticular formation corresponding to the nucleus reticularis pontis oralis (NRPo). In this study, attempts were made to elucidate the cellular basis for the serotoninergically induced augmentation of postural muscle tone by recording the electromyographic (EMG) activity of hindlimb extensor muscles, the monosynaptic reflex responses evoked by electrical stimulation of group Ia muscle afferent fibres and the membrane potentials of hindlimb alpha-motoneurons (MNs). Serotonin injections resulted not only in the augmentation of the EMG activity of gastrocnemius soleus muscles, but also in the restoration of EMG suppression, which was induced by previous injection of carbachol into the NRPo. Extensor and flexor monosynaptic reflex responses were facilitated by serotonin injections into the NRPo. Such reflex facilitation was not induced by serotonin injections into the mesencephalic or the medullary reticular formation. Intrapontine serotonin injections resulted in membrane depolarization of extensor and flexor MNs with decreases in input resistance and rheobase. Spontaneous depolarizing synaptic potentials (EPSPs) increased in both frequency and amplitude. Peak voltage of Ia monosynaptic EPSPs also increased. Serotonin injections which followed carbachol injections resulted in membrane depolarization of MNs along with an increase in the frequency of spontaneous EPSPs and a decrease in carbachol-induced inhibitory postsynaptic potentials. Following pontine carbachol injections, antidromic and orthodromic responses in MNs were suppressed. Discharges of MNs evoked by intracellular current injections were also suppressed, but were restored following serotonin injections. These results indicate that postsynaptic excitation, presynaptic facilitation and disinhibition (withdrawal of postsynaptic inhibition) simultaneously act on the hindlimb MNs during serotonin-induced postural augmentation and restoration.

Animals↗

Identification of two populations of corticothalamic neurons in cat primary somatosensory cortex.

Extracellular and intracellular recordings of corticothalamic (CT) cells were performed in the primary somatosensory cortex of the cat. CT neurons were antidromically activated by electrically stimulating the ventroposterior lateral (VPL) nucleus of the thalamus and were classified into two types according to their physiological properties. Type 1 had no spontaneous activity and no identifiable somatic receptive field. Type 2 fired action potentials spontaneously and responded to mechanical stimulation of the skin or underlying tissues. Axonal conduction velocities were slower for type 1 cells and their cell bodies were located slightly deeper in the cortex than those of type 2 cells. Both types of CT neurons exhibited inhibitory postsynaptic potentials in response to VPL stimulation but an early synaptic excitation and rebound discharge was observed almost exclusively in type 2 cells. These results suggest that only type 2 CT cells can modify the activity of thalamic neurons through a corticothalamic feedback loop.

Action Potentials↗

Inhibitory input to pause neurons from pontine burst neuron area in the cat.

Extra- and intracellular recordings were made from pontine pause neurons (PNs) in the cat. Spontaneous spikes of PNs were suppressed after single shock stimulation of excitatory burst neuron (EBN) area immediately rostral to the abducens nucleus. The most effective stimulation site for the suppression was the region where long-lead burst neurons (LLBNs) were predominantly located. Intracellular recordings from PNs showed that stimulation of the LLBN area induced short-latency inhibitory postsynaptic potentials (IPSPs) in PNs and that steep hyperpolarization of PNs associated with quick phases of nystagmus occurred prior to an abrupt change in abducens nerve activity. Results suggest that a pause of PN spikes associated with quick phases is, at least in part, produced by inhibitory action mediated through LLBNs.

Abducens Nerve↗

Trace amines depress GABA B response in dopaminergic neurons by inhibiting G-betagamma-gated inwardly rectifying potassium channels.

Trace amines (TAs) are present in the central nervous system in which they up-regulate catecholamine release and are implicated in the pathogenesis of addiction, attention-deficit/hyper-activity disorder, Parkinson's disease, and schizophrenia. By using intracellular and patch-clamp recordings from dopaminergic cells in the rat midbrain slices, we report a depressant postsynaptic action of two TAs, beta-phenylethylamine (beta-PEA) and tyramine (TYR) on the GABA(B)-mediated slow inhibitory postsynaptic potential and baclofen-activated outward currents. beta-PEA and TYR activated G-proteins, interfering with the coupling between GABA(B) receptors and G-betagamma-gated inwardly rectifying potassium channels. This is the first demonstration that beta-PEA and TYR depress inhibitory synaptic potentials in neurons of the central nervous system, supporting their emerging role as neuromodulators.

Animals↗

Picrotoxin-induced epileptiform activity in hippocampus: role of endogenous versus synaptic factors.

Picrotoxin-(PTX) induced epileptiform activity was studied in guinea pig hippocampal slices maintained in vitro, using intra- and extracellular recording techniques. The observed pattern of spontaneous and evoked epileptiform activity was quite complex. Spontaneous epileptiform events originated in the CA3 region and subsequently spread or propagated to CA1. Activation of CA1 could then reactivate CA3. This reverberation of activity was seen also following stimulation of the mossy fiber afferents from the dentate gyrus to CA3. Stimulation of fibers in the stratum radiatum of the CA1 region could trigger, at short latency, epileptiform activity that either was localized in CA1 or also occurred in CA3, with a late secondary discharge in CA1. This is attributed to a backfiring of the Schaffer collaterals and illustrates the ability of a variety of CA3 inputs to trigger epileptiform activity. Bath-applied PTX, at concentrations of 50-200 microM, had no apparent effect on the resting membrane potential or input resistance of the CA3 cells tested. Depolarizing current pulses elicited characteristic endogenous-burst responses that were not altered by PTX. Synaptic activity evoked by mossy fiber stimulation was altered markedly by PTX. The pattern of observed changes indicated that PTX reduced inhibitory postsynaptic potential (IPSP) amplitudes, resulting in the appearance of repetitive (presumably recurrent) excitatory inputs. Paroxysmal depolarizing shifts ( PDSs ) were generated by the coalescence of these excitatory inputs. Two types of spontaneous bursting were observed after PTX application. The first type was nonepileptiform , all or none in nature, and its frequency was voltage dependent. The second type of spontaneous burst was the PDS. It was epileptiform in character because it was associated with the synchronous discharge of many neurons. It was graded in nature, and its frequency was voltage independent. The graded nature of the PDS was demonstrated by varying the duration and intensity of the orthodromic stimulation. Trains of stimulation could produce PDSs that lasted 500-800 ms. A refractory period was observed following a PDS. By varying the strength of the orthodromic stimulation, it was possible to demonstrate that for the intervals tested this was a relative, not absolute, refractory period. Intracellular recordings in CA3 neurons indicated that each spontaneous PDS was followed by an afterhyperpolarization (AHP).

Animals↗

Dendritic excitability and a voltage-gated calcium current in locust nonspiking local interneurons.

1. The active properties of axonless nonspiking interneurons in the thoracic nervous system of the locust Schistocerca americana were studied in vivo with the switched current-clamp technique from dendritic impalements, and in vitro with the whole-cell variation of the patch-clamp technique. 2. In 20% of in vivo recordings, depolarization of a dendrite to potentials more positive than about -40 mV evoked resonant behaviour and/or regenerative potentials. The latter were slow (half width: 20-30 ms), small (base-to-peak amplitude: 25-35 mV), and were often followed by a pronounced after hyperpolarization (AHP). 3. The slow regenerative potentials sometimes had multiple peaks separated by incomplete repolarizations. The voltage envelope of such potentials was always broader than that of spikes with single peaks. In other recordings, a same depolarizing pulse could evoke several regenerative potentials with different waveforms. These results suggested the presence of multiple dendritic initiation sites separated by regions of inexcitable membrane, allowing decremental conduction and the passive fusion of spike envelopes. 4. Graded active responses could also be evoked on rebound from short hyperpolarizations such as inhibitory postsynaptic potentials (IPSPs) provided that the membrane was already depolarized to about -40 mV. IPSPs evoked by several presynaptic interneurons differed in their ability to evoke rebound potentials suggesting that some synaptic sites were electrically closer than others to regions of active membrane. 5. Patch-clamp recordings from somata of nonspiking neurons isolated from 75% embryos and grown in culture medium for 1-2 days revealed the presence of an inactivating inward current resistant to 0.5-1 microM tetrodotoxin (TTX). The inward current was carried equally well by Ba2+, and sensitive to blockade by Cd2+ (0.5 mM), Ni2+ (0.75 mM), or Co2+ (2.5 mM). 6. The current activated around -40 mV, with voltage-dependent activation (time-to-peak approximately 20 ms at -35 mV and 1-2 ms at 0 mV). Tail currents evoked upon repolarization were well fitted by a single exponential (tau = 1-2 ms). Deactivation time constants shorter than 300 microseconds, however, could not be measured. 7. The current inactivated rapidly in a voltage-dependent manner, following two-exponential kinetics. A very small persistent component could be explained by the overlap between activation and inactivation curves, greatest at approximately -20 mV. The voltage of half-inactivation was about -25 mV. At a resting potential of -58 mV, 90% of the current was available for activation. Recovery from steady-state inactivation followed the sum of two or more exponential processes.(ABSTRACT TRUNCATED AT 400 WORDS)

Age Factors↗

Spontaneous hyperpolarizations in pyramidal cells of chronically stimulated rabbit hippocampus.

Through daily electrical stimulation of one of the hippocampi in the rabbit, EEG spikes were "kindled" in both hippocampi. Such hippocampi (termed kindled hippocampi) were then studied with the microelectrode in acute experiments. The electrical activities of the kindled hippocampus were characterized by spontaneous occurrence of hyperpolarizing potentials of various magnitudes (3-27 mV) and various durations (50-600 msec) in the pyramidal cell. These hyperpolarizations were never preceded by a prolonged spike burst. Furthermore, they could occur without any preceding depolarizations. They consisted of two components, i.e., Cl-dependent (somatic inhibitory postsynaptic potential) and C1-non-dependent (dendritic hyperpolarization) components. They were the main abnormal events occurring within the pyramidal cell of the kindled hippocampus. It was therefore considered that they were the intracellular correlates of the EEG spikes.

Action Potentials↗

Cocaine induced synchronous oscillations in central noradrenergic neurons in vitro.

Through inhibition of reuptake, cocaine increases monoaminergic tone in the central nervous system. The activities of the neurons within the locus coeruleus play a pivotal role in central noradrenergic transmission and regulate overall levels of arousal and attention. We have found that cocaine in low concentrations (0.3-1.0 microM) induced slow oscillations (0.8 Hz) in membrane potential (2-6 mV). These oscillations were synchronized in neurons throughout the nucleus and were blocked by alpha 2-adrenergic receptor antagonists. The synchrony of these events was thought to arise from within the nucleus, through a combination of spontaneous activity (intrinsic properties) and noradrenergic mediated inhibitory postsynaptic potentials augmented by cocaine. The synchronous firing of noradrenergic neurons may facilitate transmitter release in the widespread projection areas and thus be important for the action of cocaine to increase levels of arousal.

Adrenergic alpha-Antagonists↗