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PubMed1993

Membrane potential oscillations and corticothalamic connectivity in rat associational thalamic neurons in vitro.

Thalamic relay neurons were recorded from the dorsolateral and lateroposterior nuclei of the rat thalamus in a superfused explant preparation. The mean membrane potential of these cells was -67 +/- 7 mV, input resistance 114 +/- 31 M omega and spike amplitude 75 +/- 6 mV. Low-threshold slow membrane potential oscillations (1-4 Hz) were present in about 46% of the neurons. They occurred either spontaneously or following a membrane potential perturbation. In a subpopulation of cells, we also observed a high-threshold membrane oscillation when cells were depolarized above -45 mV. This oscillation consisted of bursts of low-amplitude spikes interrupted by rhythmic after-hyperpolarizations. Stimulation of the corticothalamic pathway elicited prolonged inhibitory postsynaptic potentials in associational thalamic neurons. In the presence of picrotoxin, corticothalamic input evoked prominent excitatory postsynaptic responses that showed marked short-term synaptic plasticity. Our results suggest that associational thalamic neurons maintained in vitro have a strong tendency to exhibit membrane oscillations. In addition, they receive a direct excitatory cortical input that remained functional in explant preparation.

Animals↗

PubMed1993

Elevation of cAMP facilitates noradrenergic transmission in submucous neurons of guinea pig ileum.

Slow synaptic excitation and inhibition were studied with intracellular microelectrodes in submucous ganglion cells of the guinea pig ileum. Elevation of adenosine 3',5'-cyclic monophosphate (cAMP) after application of forskolin or the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (IBMX) resulted in slowly activating depolarization of the membrane potential. The depolarization was associated with increased input resistance, enhanced excitability, and suppression of hyperpolarizing afterpotentials. This occurred in AH/type 2 but not S/type 1 neurons. The action of forskolin or IBMX mimicked slow synaptic excitation in the same neurons. Focal electrical stimulation also evoked slow inhibitory postsynaptic potentials (IPSPs). The amplitude and duration of the IPSPs were increased by forskolin or a membrane-permeant analogue of cAMP. Treatment with phentolamine, yohimbine or idazoxan suppressed the IPSPs before and after potentiation by forskolin, suggesting that the IPSPs were mediated by release of norepinephrine acting at alpha 2-adrenoceptors. Application of adenosine or selective adenosinergic A1 agonists suppressed or abolished the IPSPs. The results suggest that elevation of cAMP facilitates the release of norepinephrine at alpha 2-synapses on submucous neurons of guinea pig small bowel.

1-Methyl-3-isobutylxanthine↗

PubMed1989

Membrane Characteristics and Synaptic Responsiveness of Superficial Dorsal Horn Neurons in a Slice Preparation of Adult Rat Spinal Cord.

Intracellular recordings have been made from neurons of the superficial dorsal horn in slices of the lumbar and thoracic spinal cord of young adult rats. Three broad categories of neurons could be distinguished on the basis of their firing patterns to intracellular current pulses and their afterhyperpolarizations (AHP); there was no detectable difference in the regional distribution of the three types. Category 1 cells were characterized by maintained firing to intracellular depolarizing current pulses, brief action potential durations and polyphasic AHPs. Category 2 cells showed spike adaptation, without spike attenuation, during intracellular current pulses, and had monophasic AHPs. Category 3 cells fired only 1 or 2 spikes to maintained depolarizing pulses and had smaller monophasic AHPs than category 2 neurons. Spontaneous excitatory and inhibitory postsynaptic potential (epsp and ipsp) activity was seen with psp durations varying widely. Low intensity electrical stimulation of afferent fibres, or of superficial white matter, resulted in polyphasic epsps and/or ipsps. The spike discharge in response to such afferent inputs correlated with the membrane properties of the cells, such that the synaptic responses of category 1 neurons were usually bursts of spikes, whereas category 2 and 3 neurons either failed to fire or fired only a single spike. These results in adult rat spinal cord suggest that the discharge pattern within synaptic sensory responses of superficial dorsal horn neurons is determined by postsynaptic membrane properties as well as by the pattern of the afferent input.

Journal Article↗

PubMed1998

Mechanisms underlying the enhancement of excitatory synaptic transmission in basolateral amygdala neurons of the kindling rat.

To elucidate the mechanism underlying epileptiform discharges in kindled rats, synaptic responses in kindled basolateral amygdala neurons in vitro were compared with those from control rats by using intracellular and whole cell patch-clamp recordings. In kindled neurons, electrical stimulation of the stria terminalis induced epileptiform discharges. The resting potential, apparent input resistance, current-voltage relationship of the membrane, and the threshold, amplitude, and duration of action potentials in kindled neurons were not different from those in control neurons. The electrical stimulation of stria terminalis elicited excitatory postsynaptic potentials (EPSPs) and DL-2-amino-5-phosphonopentanoic acid (AP5)-sensitive and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive excitatory postsynaptic currents (EPSCs). The amplitude of evoked EPSPs and of evoked AP5-sensitive and CNQX-sensitive EPSCs were enhanced markedly, whereas fast and slow inhibitory postsynaptic potentials (IPSPs) induced by electrical stimulation of lateral amygdaloid nucleus were not significantly different. The rise time and the decay time constant of the evoked CNQX-sensitive EPSCs were shortened, whereas the rise time of the evoked AP5-sensitive EPSCs was shortened, but the decay time constants were not significantly different. In both tetrodotoxin (TTX)-containing medium and low Ca2+ and TTX-containing medium, the frequency and amplitude of spontaneous EPSCs were increased in kindled neurons. These increases are presumably due to nearly synchronous multiquantal events resulted from the increased probability of Glu release at the nerve terminals. The rise time of evoked CNQX- and AP5-sensitive EPSCs and the decay time constant of evoked CNQX-sensitive EPSCs were shortened, suggesting that excitatory synapses at the proximal dendrite and/or the soma in kindled neurons may contribute more effectively to generate evoked EPSCs than those at distal dendrites. In conclusion, the increases in the amplitudes of spontaneous and evoked EPSCs and in the frequency of spontaneous EPSCs may contribute to the epileptiform discharges in kindled neurons.

2-Amino-5-phosphonovalerate↗

PubMed2000

Floccular modulation of vestibuloocular pathways and cerebellum-related plasticity: An in vitro whole brain study.

The isolated whole brain (IWB) preparation of the guinea pig was used to investigate the floccular modulation of vestibular-evoked responses in abducens and oculomotor nerves and abducens nucleus; for identification of flocculus target neurons (FTNs) in the vestibular nuclei and intracellular study of some of their physiological properties; to search for possible flocculus-dependent plasticity at the FTN level by pairing of vestibular nerve and floccular stimulations; and to study the possibility of induction of long-term depression (LTD) in Purkinje cells by paired stimulation of the inferior olive and vestibular nerve. Stimulation of the flocculus had only effects on responses evoked from the ipsilateral (with respect to the stimulated flocculus) vestibular nerve. Floccular stimulation significantly inhibited the vestibular-evoked discharges in oculomotor nerves on both sides and the inhibitory field potential in the ipsilateral abducens nucleus while the excitatory responses in the contralateral abducens nerve and nucleus were free from such inhibition. Eleven second-order vestibular neurons were found to receive a short-latency monosynaptic inhibitory input from the flocculus and were thus characterized as FTNs. Monosynaptic inhibitory postsynaptic potentials from the flocculus were bicuculline sensitive, suggesting a GABA(A)-ergic transmission from Purkinje cells to FTNs. Two of recorded FTNs could be identified as vestibulospinal neurons by their antidromic activation from the cervical segments of the spinal cord. Several pairing paradigms were investigated in which stimulation of the flocculus could precede, coincide with, or follow the vestibular nerve stimulation. None of them led to long-term modification of responses in the abducens nucleus or oculomotor nerve evoked by activation of vestibular afferents. On the other hand, pairing of the inferior olive and vestibular nerve stimulation resulted in approximately a 30% reduction of excitatory postsynaptic potentials evoked in Purkinje cells by the vestibular nerve stimulation. This reduction was pairing-specific and lasted throughout the entire recording time of the neurons. Thus in the IWB preparation, we were able to induce a LTD in Purkinje cells, but we failed to detect traces of flocculus-dependent plasticity at the level of FTNs in vestibular nuclei. Although these data cannot rule out the possibility of synaptic modifications in FTNs and/or at other brain stem sites under different experimental conditions, they are in favor of the hypothesis that the LTD in the flocculus could be the essential mechanism of cellular plasticity in the vestibuloocular pathways.

Abducens Nerve↗

PubMed1985

Lateral spread of neuronal activity within the motor cortex investigated with intracellular responses to distant epicortical stimulation.

Lateral spread of activity within the motor cortex was examined by means of analyses of the direct cortical responses (DCRs) and intracellular responses to distant epicortical stimulation (EPICS) using cat encéphale isolé preparations. DCRs to the EPICS at a distance of 1.5-6.5 mm consisted of initial small positive (Pd) and subsequent negative waves (Nd). The reversal of polarity in depths occurred at 400-550 microns for Pd and at 150-250 microns for Nd as well as for the initial negative wave elicited by near EPICS. Intracellular responses to distant EPICS consisted of excitatory (EPSP) and inhibitory postsynaptic potentials (IPSP), disfacilitation (DF), and disinhibition (DI). Depth distributions of cells with EPSPs at two peaks in laminae II and V-VI, with IPSPs mainly in lamina III, and with DF or DI in laminae V-VI were the same with those by near EPICS. The inhibitory effects of distant EPICS on middle layer cells were much greater than those by near EPICS. No linear relations of the latency of EPSPs or IPSPs to the depth were seen for distant EPICS. Instead, the latency increased in proportion to the lateral distance in EPSPs at a slower rate than in IPSPs compared in superficial and middle layer cells. Several routes for lateral spread of activity were postulated. Most conspicuous are the excitatory route via horizontal axons in lamina I and the inhibitory route via laterally running axons in laminae II-III, which produce overall excitation of superficial layer cells and depression of middle and deep layer cells. Their possible role in phasic cortical arousal was discussed.

Animals↗

PubMed1988

Fluorescence recordings of electrical activity in goldfish optic tectum in vitro.

Optical methods for recording electrical activity in the goldfish optic tectum were evaluated. Tectal slices, with a short section of the optic nerve attached, were stained with a fluorescent styryl dye. Potential-dependent fluorescence changes following optic nerve stimulation were monitored with a photodiode. We found that large optical signals could be obtained. Experimental manipulations of the slice bathing solution permitted us to identify several events that contributed to the optical response, including activity in afferent fibers, excitatory and inhibitory postsynaptic potentials, and presumptive glial depolarizations. These results suggest that voltage-sensitive dyes can provide a useful alternative method for monitoring synaptic responses in the goldfish tectum, and may prove valuable in studying changes in the functional synaptic organization of the tectum following manipulations of the retinotectal pathway.

Animals↗

PubMed1999

Modulation of inhibitory synaptic potentials in the piriform cortex.

Modulation of inhibitory synaptic potentials in the piriform cortex. Intracellular recordings from pyramidal neurons in brain slice preparations of the piriform cortex were used to test results from a computational model about the effects of cholinergic agonists on inhibitory synaptic potentials induced by stimulation of afferent fibers in layer Ia and association/intrinsic fibers in layer Ib. A simple model of piriform cortex as an associative memory was used to analyze how suppression of inhibitory synaptic transmission influenced performance of the network. Levels of suppression of excitatory synaptic transmission were set at levels determined in previous experimental work. Levels of suppression of inhibitory synaptic transmission were then systematically varied within the model. This modeling work demonstrated that suppression of inhibitory synaptic transmission in layer Ib should be stronger than suppression of inhibitory synaptic transmission in layer Ia to keep activity levels high enough for effective storage. Experimental data showed that perfusion of the cholinergic agonist carbachol caused a significant suppression of inhibitory postsynaptic potentials (IPSPs) in the pyramidal neurons that were induced by stimulation of layer Ib, with a weaker effect on IPSPs induced by stimulation of layer Ia. As previously described, carbachol also selectively suppressed excitatory postsynaptic potentials (EPSPs) elicited by intrinsic but not afferent fiber stimulation. The decrease in amplitude of IPSPs induced by layer Ib stimulation did not appear to be directly related to the decrease in EPSP amplitude induced by layer Ib stimulation. The stimulation necessary to induce neuronal firing with layer Ia stimulation was reduced in the presence of carbachol, whereas that necessary to induce neuronal firing with layer Ib stimulation was increased, despite the depolarization of resting membrane potential. Thus physiological data on cholinergic modulation of inhibitory synaptic potentials in the piriform cortex is compatible with the functional requirements determined from computational models of piriform cortex associative memory function.

Animals↗

PubMed1994

A comparison of synapses onto the somata of intrinsically bursting and regular spiking neurons in layer V of rat SmI cortex.

Regular spiking (RS) and intrinsically bursting (IB) neurons show distinct differences in their inhibitory responses. Under various conditions, the synaptic responses of RS cells display marked inhibitory postsynaptic potentials (IPSPs), whereas the responses of most IB cells do not (Silva et al: Soc Neurosci Abstr 14:883, 1988; Chagnac-Amitai and Connors: J Neurophysiol 61:747, 62:1149, 1989; Connors and Gutnick: TINS 13:99, 1990). This investigation is designed to determine if differences in the inhibitory responses of RS versus IB cells are reflected in differences in the concentration of inhibitory synapses onto their somata. RS and IB neurons in rat somatosensory cortex were identified by using intracellular recording and labeling, examined with the light microscope, and then serial thin-sectioned prior to examination with the electron microscope. Axonal terminals presynaptic to their somata and proximal dendrites were identified and classified according to criteria described by Peters and coworkers (Peters et al: J Neurocytol 19:584, 1990; Peters and Harriman: J Neurocytol 19:154, 1990; 21:679, 1992). The locations of these boutons were displayed on the surfaces of 3-D reconstructions of the somata and proximal dendrites. The reconstructions were produced directly from the serial thin sections by using a novel, electron microscopic, image-processing computer resource. Our analysis showed no significant difference in the types and concentration of boutons presynaptic to the cell bodies and proximal dendrites of intrinsically bursting versus regular spiking neurons. We conclude that the differences observed in the inhibitory responses of intrinsically bursting versus regular spiking neurons cannot be explained by differences in the concentrations of synapses onto their somata.

Action Potentials↗

PubMed1985

Characterization of long-lasting histaminergic inhibition in a beating pacemaker neuron of Onchidium.

A single BPSP (excitatory-inhibitory postsynaptic potential) was monosynaptically produced in an identified Onchidium neuron, Be-1, with a beating rhythm upon stimulation of the cardiac nerve. The BPSPs summated to produce an inhibition of long duration (ILD) upon blockage of the beating rhythm after repeated stimulation, so that the BPSPs seemed to be functionally inhibitory. Ten stimuli (1-2 Hz) applied to the cardiac nerve usually evoked an ILD (0.5-1 min) of about 10 mV. The early and middle phases of this ILD reversed near -80 to -85 mV, but the late phase did not reverse at more negative potentials. None of the phases was significantly affected by low Cl or Na solutions or by high Ca solutions. However, by changing the external K, the shift of the reversal potentials for the early and middle phases reached about 65% of that predicted for the K electrode, although the late phase was insensitive to the external K. Intracellular tetraethylammonium (TEA) attenuated the amplitude of the ILD but did not shorten the duration. These suggest that the ILD has another conductance-independent mechanism simultaneously with the increase in K conductance. Several lines of evidence suggested that a ouabain-sensitive Na pump does not contribute to the ILD. Inhibitors of energy supply, 2,4-dinitrophenol sodium salt (DNP) and cyanide, selectively and reversibly reduced the ILD. Simultaneous applications of intracellular TEA and DNP completely abolished the ILD. As for the ionic basis, the histamine-induced inhibitory response in Be-1 was closely related to the ILD. Cimetidine specifically blocked the ILD and histamine-induced inhibitory response, which were mimicked by 2-methylhistamine, but not by dimaprit. It is concluded that the ILD, mediated by some histamine receptor other than the H1 or H2 type, results from an increase in K conductance and a hyperpolarizing ion pump insensitive to ouabain.

Animals↗

PubMed1999

Intracellular study of excitability in the seizure-prone neocortex in vivo.

The excitability of neocortical neurons from cat association areas 5-7 was investigated during spontaneously occurring seizures with spike-wave (SW) complexes at 2-3 Hz. We tested the antidromic and orthodromic responsiveness of neocortical neurons during the "spike" and "wave" components of SW complexes, and we placed emphasis on the dynamics of excitability changes from sleeplike patterns to seizures. At the resting membrane potential, an overwhelming majority of neurons displayed seizures over a depolarizing envelope. Cortical as well as thalamic stimuli triggered isolated paroxysmal depolarizing shifts (PDSs) that eventually developed into SW seizures. PDSs could also be elicited by cortical or thalamic volleys during the wave-related hyperpolarization of neurons, but not during the spike-related depolarization. The latencies of evoked excitatory postsynaptic potentials (EPSPs) progressively decreased, and their slope and depolarization surface increased, from the control period preceding the seizure to the climax of paroxysm. Before the occurrence of full-blown seizures, thalamic stimuli evoked PDSs arising from the postinhibitory rebound excitation, whereas cortical stimuli triggered PDSs immediately after the early EPSP. These data shed light on the differential excitability of cortical neurons during the spike and wave components of SW seizures, and on the differential effects of cortical and thalamic volleys leading to such paroxysms. We conclude that the wave-related hyperpolarization does not represent GABA-mediated inhibitory postsynaptic potentials (IPSPs), and we suggest that it is a mixture of disfacilitation and Ca(2+)-dependent K(+) currents, similar to the prolonged hyperpolarization of the slow sleep oscillation.

Animals↗

PubMed1987

Morphological and physiological properties of caudal medullary expiratory neurons of the cat.

The activity of respiratory neurons in the caudal part of the nucleus retroambigualis (NRA) was recorded intracellularly in decerebrated, spontaneously breathing cats. Spinal projections of these neurons were determined by antidromic stimulation at the C3 segment. A high concentration of bulbospinal expiratory (BS-E) neurons was identified in the caudal NRA, whereas the inspiratory (I) neurons, not activated antidromically, were also found to be intermingled in the same region. The BS-E neurons had ramp-like depolarizing potentials during expiration, and repolarized rapidly at the onset of phrenic nerve discharge. The I neurons depolarized abruptly in the early I phase, and repolarized gradually thereafter, namely, they were early-I neurons. Intracellular current injections revealed postsynaptic inhibition of the BS-E neurons during inspiration, as evidenced by inhibitory postsynaptic potential reversal. Using the technique of intracellular labeling with horseradish peroxidase, seven well-stained expiratory cells located in the caudal NRA revealed detailed information about axonal morphology: the axon projected rostrally and dorsomedially for the first 2 mm after emerging from the soma, then turned caudally and ventrally along two different courses, and crossed the midline of the medulla almost at the same rostrocaudal level as the soma. No axon collaterals were observed along the length of the stained portion, indicating that the BS-E neurons cannot influence other respiratory neurons in the brainstem. It has been concluded that the NRA expiratory neurons are involved only in spinal action, and that they receive a postsynaptic inhibition during inspiration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Comparison of the actions of phencyclidine and sigma ligands on CA1 hippocampal pyramidal neurons in the rat.

To compare the actions of prototypic drugs which are selective for phencyclidine and sigma receptors, the electrophysiological effects of phencyclidine (PCP),3-[3-hydroxyphenyl]-N-(1-propyl)piperidine [+)3-PPP), and 1,3-di(2-tolyl)guanidine (DTG) on CA1 hippocampal pyramidal neurons were examined. A wide range of concentrations of drug was tested to differentiate specific, receptor-mediated effects from nonselective, anesthetic-like actions. At relatively large concentrations (0.1-1 mM), each compound reversibly increased the threshold of action potentials driven by Schaffer collaterals, the duration of action potentials and membrane resistance. The low potencies and rank order of potency suggested that phencyclidine, (+)3-PPP, and DTG were not acting through either high affinity sigma or phencyclidine receptors. These compounds did have receptor-mediated effects at smaller concentrations. Since none of the compounds affected evoked excitatory or inhibitory postsynaptic potentials (EPSP or IPSP) or driven action potentials at subanesthetic concentrations (less than 100 microM), no evidence was found to support the hypothesis that the actions of phencyclidine result from enhanced release of transmitter, caused by the inhibition of a presynaptic potassium conductance. As observed in other neurons, phencyclidine blocked excitations in CA1 pyramidal cells mediated by N-methyl-D-aspartic acid (NMDA) at behaviorally relevant concentrations (1-10 microM). However, (+)3-PPP (1 microM-1 mM) enhanced the pyramidal cell response to NMDA. Alone, DTG did not effect the NMDA-induced response but did inhibit the enhancement induced by (+)3-PPP. The agonist and antagonist actions of the sigma-selective ligands, (+)3-PPP and DTG, suggests that they modify NMDA-induced responses by acting at the sigma receptor.

Action Potentials↗

PubMed1994

Intracellular analysis of cutaneous afferent-induced excitation and inhibition in rat dorsal horn neurones in vitro.

The mechanoreceptive fields of 54 dorsal horn neurones were mapped intracellularly in the rat spinal cord-hindlimb preparation. A quantitative analysis of the parameters of excitation and inhibition was undertaken and a comparison was made between data obtained for innocuous versus noxious cutaneous stimulation. Neurones were classified as wide dynamic range (WDR), nociceptive specific (NS) or low threshold (LT) on the basis of their response to cutaneous stimuli. In WDR neurones, which responded differentially to both types of cutaneous stimuli, the EPSP produced by noxious pinch had a significantly larger amplitude and a longer duration (P < 0.01) compared to the excitatory postsynaptic potentials (EPSPs) produced by touch. A higher total number of spikes was also associated with the postsynaptic response to pinch in WDR neurones. A population of neurones which responded to mechanical stimuli with non-spiking excitation only were identified; their possible relevance to mechanisms of altered central sensitivity is discussed. Inhibitory components to the mechanoreceptive fields were identified; these were complex in form and co-incidental generation of EPSPs and inhibitory postsynaptic potentials (IPSPs) was common. Inhibition of spontaneous firing by cutaneous stimulation was also observed. This technique allows a quantitative intracellular analysis of naturally evoked postsynaptic excitation in physiologically classified dorsal horn neurones in vitro.

Animals↗

PubMed1992

Computer simulation of carbachol-driven rhythmic population oscillations in the CA3 region of the in vitro rat hippocampus.

1. We used simulations of the in vitro CA3 region of the hippocampus to analyse the 5 Hz population oscillations recorded experimentally in carbachol. 2. A simulation model of the in vitro CA3 region was constructed with 1000 pyramidal neurones and 200 inhibitory neurones (100 producing fast inhibitory postsynaptic potentials (IPSPs) and 100 producing slow IPSPs of delayed onset). Each neurone contained nineteen soma-dendritic compartments. Pyramidal neurones contained six voltage- and/or calcium-dependent ionic currents, whose kinetics were consistent with voltage-clamp data. The connectivity and waveform of unitary synaptic events for excitatory and fast inhibitory synapses were consistent with dual intracellular recordings. This network was shown to generate previously described network oscillations, including synchronized bursts recorded in the presence of GABAA blockers, and synchronized synaptic potentials observed during partial blockade of GABAA inhibition. 3. The model generated 5 Hz oscillations as recorded in carbachol under the following conditions: (a) excitatory synaptic conductance was within a limited range; (b) there was blockade of fast and slow IPSPs (consistent with the experimental lack of effect of bicuculline and phaclofen on carbachol oscillations and the known depression of IPSPs by acetylcholine); (c) the after hyperpolarization (AHP) conductance was reduced (consistent with the known pharmacology of carbachol); (d) the apical dendrites of the pyramidal cells were depolarized, as suggested by the carbachol-induced depolarization of pyramidal neurones. Each oscillation was associated in pyramidal cells with a burst of action potentials riding on a depolarizing wave. The N-methyl-D-aspartate (NMDA) type of excitatory synapse was not necessary for the oscillations to occur. 4. Progressive reduction of excitatory synaptic strength led to an oscillation of the same frequency, with bursts riding on smaller EPSPs (consistent with the experiment). Further reduction of excitatory synaptic strength abolished the population oscillation by uncoupling the neurones. When excitatory synaptic conductance was too large, population oscillations were attenuated as the cells switched from a bursting mode to a repetitively firing mode. 5. Increasing the AHP conductance prolonged the interburst interval as expected. Inclusion of slow IPSPs exerted a similar effect. 6. When fast IPSPs were included, an oscillation with different characteristics emerged: a 10 Hz oscillation that was gated by compound GABAA IPSPs. On any oscillatory wave, few pyramidal neurones fired, and the firing of individual neurones was irregular.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Physiology and pharmacology of corticothalamic stimulation-evoked responses in rat somatosensory thalamic neurons in vitro.

Whole cell current- and voltage-clamp recording techniques were employed in a rat thalamocortical slice preparation to characterize corticothalamic stimulation-evoked responses in thalamic neurons. Three types of corticothalamic stimulation-evoked responses were observed in thalamic neurons. Of thalamic neurons, 57% responded to corticothalamic stimulation with purely excitatory synaptic responses, whereas 27% had inhibitory synaptic responses and 16% had mixed excitatory/inhibitory responses. This suggested corticothalamic activation of multiple distinct synaptic circuits, presumably involving both nucleus reticularis thalami (NRT) and thalamus, because the rat ventrobasal complex is virtually devoid of GABAergic interneurons. Corticothalamic-stimulation-evoked excitatory postsynaptic currents (EPSCs) were predominantly slow rising currents that showed nonlinear voltage dependence, characteristics of an N-methyl-D-aspartate (NMDA)-receptor-mediated synaptic current. These slow rising EPSCs were blocked by the NMDA antagonist 2-amino-5-phosphonovaleric acid (APV). A minority of corticothalamic EPSCs had faster kinetics, and were blocked by 6-cyano-7 nitroquinoxaline-2,3-dione (CNQX). Corticothalamic stimulation of varying frequency optimally activated burst responses in thalamic neurons at low frequencies (3-6 Hz). The optimal 3- to 6-Hz response was reduced by ethosuximide, by APV, and by detaching the neocortex from the thalamocortical slice, suggesting that T current, NMDA receptors, and neocortical properties all contributed to generation of this 3- to 6-Hz frequency preference. In contrast to corticothalamic EPSCs, medial-thalamic-stimulation-evoked responses consisted of fast CNQX-sensitive EPSCs that were predominantly voltage insensitive, with no 3- to 6-Hz frequency preference. In thalamic neurons in which corticothalamic stimulation evoked predominantly inhibitory synaptic responses, this inhibitory postsynaptic potential (IPSP) had early and late phases, often followed by a rebound burst. The early IPSP reversed at -95 mV and was bicuculline sensitive, whereas the late IPSP reversed at -113 mV and was blocked by the gamma-aminobutyric acid-B (GABA(B)) antagonist 3-N[1-(S)-(3,4-dichlorophenyl)ethyl]amino-2-(S)-hydroxypropyl-P-benzy lphoshinic acid (CGP-55845A). In thalamic neurons in which corticothalamic stimulation evoked a mixed excitatory postsynaptic potential (EPSP)/IPSP response, repetitive corticothalamic stimulation rapidly reduced IPSPs and enhanced EPSPs at higher frequencies. This resulted in burst firing being triggered in these mixed response neurons at frequencies >6 Hz. Corticothalamic feedback onto thalamic relay neurons activated diverse responses due to differing relative activation of NRT and "feedforward" inhibitory responses. These multiple in vitro corticothalamic responses differ from responses encountered in other in vitro thalamic preparations lacking a synaptically connected neocortex, but are similar to results evident in thalamic neurons in response to cortical stimulation in vivo. In addition, the thalamocortical 3- to 6-Hz frequency preference was conserved, suggesting that many factors critical for this emergent property of the thalamocortical system are maintained in vitro.

2-Amino-5-phosphonovalerate↗

PubMed1998

Inhibition evoked from primary afferents in the electrosensory lateral line lobe of the weakly electric fish (Apteronotus leptorhynchus).

Inhibition evoked from primary afferents in the electrosensory lateral line lobe of the weakly electric fish (Apteronotus leptorhynchus). J. Neurophysiol. 80: 3173-3196, 1998. The responses of two types of projection neurons of the electrosensory lateral line lobe, basilar (BP) and nonbasilar (NBP) pyramidal cells, to stimulation of primary electrosensory afferents were determined in the weakly electric fish, Apteronotus leptorhynchus. Using dyes to identify cell type, the response of NBP cells to stimulation of primary afferents was inhibitory, whereas the response of BP cells was excitation followed by inhibition. gamma-Aminobutyric acid (GABA) applications produced biphasic (depolarization then hyperpolarization) responses in most cells. GABAA antagonists blocked the depolarizing effect of GABA and reduced the hyperpolarizing effect. The GABAB antagonists weakly antagonized the hyperpolarizing effect. The early depolarization had a larger increase in cell conductance than the late hyperpolarization. The conductance changes were voltage dependent, increasing with depolarization. In both cell types, baclofen produced a slow small hyperpolarization and reduced the inhibitory postsynaptic potentials (IPSPs) evoked by primary afferent stimulation. Tetanic stimulation of primary afferents at physiological rates (100-200 Hz) produced strongly summating compound IPSPs (approximately 500-ms duration) in NBP cells, which were usually sensitive to GABAA but not GABAB antagonists; in some cells there remained a slow IPSP that was unaffected by GABAB antagonists. BP cells responded with excitatory or mixed excitatory + inhibitory responses. The inhibitory response had both a fast (approximately 30 ms, GABAA) and long-lasting slow phase (approximately 800 ms, mostly blocked by GABAA antagonists). In some cells there was a GABAA antagonist-insensitive slow IPSP (approximately 500 ms) that was sensitive to GABAB antagonists. Application of glutamate ionotropic receptor antagonists blocked the inhibitory response of NBP cells to primary afferent stimulation and the excitatory response of BP cells but enhanced the BP cell slow IPSP; this remaining slow IPSP was reduced by GABAB antagonists. Unit recordings in the granule cell layer and computer simulations of pyramidal cell inhibition suggested that the duration of the slow GABAA inhibition reflects the prolonged firing of GABAergic granule cell interneurons to primary afferent input. Correlation of the results with known GABAergic circuitry in the electrosensory lobe suggests that the GABAergic type 2 granule cell input to both pyramidal cell types is via GABAA receptors. The properties of the GC2 GABAA input are well suited to their putative role in gain control, regulation of phasicness, and coincidence detection. The slow GABAB IPSP evoked in BP cells is likely due to ovoid cell input to their basal dendrites.

Animals↗

PubMed1994

Electrophysiology of globus pallidus neurons in vitro.

1. We investigated the electrical properties of globus pallidus neurons intracellularly using brain slices from adult guinea pigs. Three types of neurons were identified according to their intrinsic electrophysiological properties. 2. Type I neurons (59%) were silent at the resting membrane level (-65 +/- 10 mV, mean +/- SD) and generated a burst of spikes, with strong accommodation, to depolarizing current injection. Calcium-dependent low-frequency (1-8 Hz) membrane oscillations were often elicited by membrane depolarization (-53 +/- 8 mV). A low-threshold calcium conductance and an A-current were also identified. The mean input resistance of this neuronal type was 70 +/- 22 M omega. 3. Type II neurons (37%) fired spontaneously at the resting membrane level (-59 +/- 9 mV). Their repetitive firing (< or = 200 Hz) was very sensitive to the amplitude of injected current and showed weak accommodation. Sodium-dependent high-frequency (20-100 Hz) subthreshold membrane oscillations were often elicited by membrane depolarization. This neuronal type demonstrated a low-threshold calcium spike and had the highest input resistance (134 +/- 62 M omega) of the three neuron types. 4. Type III neurons (4%) did not fire spontaneously at the resting membrane level (-73 +/- 5 mV). Their action potentials were characterized by a long duration (2.3 +/- 0.6 ms). Repetitive firing elicited by depolarizing current injection showed weak or no accommodation. This neuronal type had an A-current and showed the lowest input resistance (52 +/- 35 M omega) of the three neuron types. 5. Stimulation of the caudoputamen evoked inhibitory postsynaptic potentials (IPSPs) in Type I and II neurons. In Type II neurons the IPSPs were usually followed by rebound firing. Excitatory postsynaptic potentials and antidromic responses were also elicited in some Type I and II neurons. The estimated conduction velocity of the striopallidal projection was < 1 m/s (Type I neurons, 0.49 +/- 0.37 m/s; Type II neurons, 0.33 +/- 0.13 m/s).

Animals↗