在体大鼠海马CA1区侧枝/联合纤维通路和TA通路的不同EPSP空间整合特性

在麻醉Wistar大鼠上,结合脑室给药,应用双电极刺激技术刺激海马独立的两条侧枝／联合纤维通路、TA通路,并在CA1区放射层记录兴奋性突触后电位（EPSP）,对海马CA1区锥体细胞近、远端树突EPSP的空间整合进行了初步探讨。结果表明,海马CA1区锥体细胞近、远端树突的空间整合都是亚线性的;近端树突的空间整合不受期望值大小的影响,但远端树突的空间整合随期望值增加而减小（更趋于亚线性）。此外,荷包牡丹碱没有影响EPSP的空间整合;但瞬时A型钾通道（IAK^＋）的拮抗剂氨基吡啶-4却使得近端树突的空间整合趋于线性发展。本研究表明,海马CA1锥体细胞近、远端树突不同的被动、主动特征使它们具有了不同的空间整合特性。由于近端树突接受海马内部侧枝／联合纤维投射的信息,远端树突通过TA通路接受内嗅皮层投射的信息,由此提示,CA1区锥体细胞对来自海马内部和直接来自皮层的信息输入采用了不同的整合方式。     

Long-lasting synaptic potentials and the modulation of synaptic transmission.

Long-lasting postsynaptic potentials (PSPs) generated by decreases in membrane conductance (permeability) have been reported in many types of neurons. We investigated the possible role of such long-lasting decreases in membrane conductance in the modulation of synaptic transmission in the sympathetic ganglion of the bullfrog. The molecular basis by which such conductance-decrease PSPs are generated was also investigated. Synaptic activation of muscarinic cholinergic receptors on these sympathetic neurons results in the generation of a slow EPSP (excitatory postsynaptic potential), which is accompanied by a decrease in membrane conductance. We found that the conventional "fast" EPSPs were increased in amplitude and duration during the iontophoretic application of methacholine, which activates the muscarinic postsynaptic receptors. A similar result was obtained when a noncholinergic conductance-decrease PSP--the late-slow EPSP--was elicited by stimulation of a separate synaptic pathway. The enhancement of fast EPSP amplitude increased the probability of postsynaptic action potential generation, thus increasing the efficacy of impulse transmission across the synapse. Stimulation of one synaptic pathway is therefore capable of increasing the efficacy of synaptic transmission in a second synaptic pathway by a postsynaptic mechanism. Furthermore, this enhancement of synaptic efficacy is long-lasting by virtue of the long duration of the slow PSP. Biochemical and electrophysiological techniques were used to investigate whether cyclic nucleotides are intracellular second messengers mediating the membrane permeability changes underlying slow-PSP generation. Stimulation of the synaptic inputs, which lead to the generation of the slow-PSPs, increased the ganglionic content of both cyclic AMP and cyclic GMP. However, electrophysiological analysis of the actions of these cyclic nucleotides and the actions of agents that affect their metabolism does not provide support for such a second messenger role for either cyclic nucleotide.     

Modulation of transmitter release from the locust forewing stretch receptor neuron by GABAergic interneurons activated via muscarinic receptors.

The role of muscarinic receptors in the down-regulation of acetylcholine (ACh) release from the locust forewing stretch receptor neuron (fSR) terminals has been investigated. Electrical stimulation of the fSR evokes monosynaptic excitatory postsynaptic potentials (EPSPs) in the first basalar motoneuron (BA1), produced mainly by the activation of postsynaptic nicotinic cholinergic receptors. The general muscarinic antagonists scopolamine (10(-6) M) and atropine (10(-8) to 10(-6) M) caused a reversible increase in the amplitude of electrically evoked EPSPs. However, scopolamine (10(-6) M) caused a slight depression in the amplitude of responses to ACh pressure-applied to the soma of BA1. These observations indicate that the EPSP amplitude enhancement is due to the blockade of muscarinic receptors on neurons presynaptic to BA1. The muscarinic receptors may be located on the fSR itself and act as autoreceptors, and/or they may be located on GABAergic interneurons which inhibit ACh release from the fSR. Electron microscopical immunocytochemistry has revealed that GABA-immunoreactive neurons make presynaptic inputs to the fSR. The GABA antagonist picrotoxin (10(-6) M) caused a reversible increase in the EPSP amplitude, which does not appear to be due to an increase in sensitivity of BA1 to ACh, as picrotoxin (10(-6) M) slightly decreased ACh responses recorded from BA1. Application of scopolamine (10(-6) M) to a preparation preincubated with picrotoxin did not cause the EPSP amplitude enhancement normally seen in control experiments; in fact, it caused a slight depression. This indicates that at least some of the presynaptic muscarinic receptors are located on GABAergic interneurons that modulate transmission at the fSR/BA1 synapse.     

Electrical advantages of dendritic spines

Many neurons receive excitatory glutamatergic input almost exclusively onto dendritic spines. In the absence of spines, the amplitudes and kinetics of excitatory postsynaptic potentials (EPSPs) at the site of synaptic input are highly variable and depend on dendritic location. We hypothesized that dendritic spines standardize the local geometry at the site of synaptic input, thereby reducing location-dependent variability of local EPSP properties. We tested this hypothesis using computational models of simplified and morphologically realistic spiny neurons that allow direct comparison of EPSPs generated on spine heads with EPSPs generated on dendritic shafts at the same dendritic locations. In all morphologies tested, spines greatly reduced location-dependent variability of local EPSP amplitude and kinetics, while having minimal impact on EPSPs measured at the soma. Spine-dependent standardization of local EPSP properties persisted across a range of physiologically relevant spine neck resistances, and in models with variable neck resistances. By reducing the variability of local EPSPs, spines standardized synaptic activation of NMDA receptors and voltage-gated calcium channels. Furthermore, spines enhanced activation of NMDA receptors and facilitated the generation of NMDA spikes and axonal action potentials in response to synaptic input. Finally, we show that dynamic regulation of spine neck geometry can preserve local EPSP properties following plasticity-driven changes in synaptic strength, but is inefficient in modifying the amplitude of EPSPs in other cellular compartments. These observations suggest that one function of dendritic spines is to standardize local EPSP properties throughout the dendritic tree, thereby allowing neurons to use similar voltage-sensitive postsynaptic mechanisms at all dendritic locations.     

Input integration around the dendritic branches in hippocampal dentate granule cells

Recent studies have shown that the dendrites of several neurons are not simple translators but are crucial facilitators of excitatory postsynaptic potential (EPSP) propagation and summation of synaptic inputs to compensate for inherent voltage attenuation. Granule cells (GCs)are located at the gateway for valuable information arriving at the hippocampus from the entorhinal cortex. However, the underlying mechanisms of information integration along the dendrites of GCs in the hippocampus are still unclear. In this study, we investigated the input integration around dendritic branches of GCs in the rat hippocampus. We applied differential spatiotemporal stimulations to the dendrites using a high-speed glutamate-uncaging laser. Our results showed that when two sites close to and equidistant from a branching point were simultaneously stimulated, a nonlinear summation of EPSPs was observed at the soma. In addition, nonlinear summation (facilitation) depended on the stimulus location and was significantly blocked by the application of a voltage-dependent Ca²⁺ channel antagonist. These findings suggest that the nonlinear summation of EPSPs around the dendritic branches of hippocampal GCs is a result of voltage-dependent Ca²⁺ channel activation and may play a crucial role in the integration of input information.     

M-channels modulate the intrinsic excitability and synaptic responses of layer 2/3 pyramidal neurons in auditory cortex

Neurons in the auditory cortex are believed to utilize temporal patterns of neural activity to accurately process auditory information but the intrinsic neuronal mechanism underlying the control of auditory neural activity is not known. The slowly activating, persistent K⁺ channel, also called M-channel that belongs to the Kv7 family, is already known to be important in regulating subthreshold neural excitability and synaptic summation in neocortical and hippocampal pyramidal neurons. However, its functional role in the primary auditory cortex (A1) has never been characterized. In this study, we investigated the roles of M-channels on neuronal excitability, short-term plasticity, and synaptic summation of A1 layer 2/3 regular spiking pyramidal neurons with whole-cell current-clamp recordings in vitro. We found that blocking M-channels with a selective M-channel blocker, XE991, significantly increased neural excitability of A1 layer 2/3 pyramidal neurons. Furthermore, M-channels controled synaptic responses of intralaminar-evoked excitatory postsynaptic potentials (EPSPs); XE991 significantly increased EPSP amplitude, decreased the rate of short-term depression, and increased the synaptic summation. These results suggest that M-channels are involved in controlling spike output patterns and synaptic responses of A1 layer 2/3 pyramidal neurons, which would have important implications in auditory information processing.     

Synaptic responses of medullary neurons of turtles to stimulation of the locomotor region

Responses of medullary neurons to microstimulation of the locomotor region by a current of up to 30 µA were studied by intracellular recording in turtles. The resting potential recorded in these neurons was from 22 to 42 mV. Depolarization PSPs (EPSPs) were recorded in 43 neurons, hyperpolarization PSPs (IPSPs) in 12, and mixed in 36. Synaptic discharges were observed in 29 neurons. Of these cells 11 generated action potentials without visible PSPs. The latent period of the PSPs was most frequently between 2 and 8 msec. The time from the beginning of the EPSP to the beginning of the action potential was 1–3 msec if the response index was high, but in the case of weaker stimulation, it began to fluctuate strongly and lengthened. Unitary EPSPs were recorded in 15 neurons and IPSPs in three. Their amplitude was 0.6–0.8 mV, from 2 to 12 times less than the depolarization threshold (1–7 mV). These results, together with those obtained previously by extracellular recording of medullary unit activity in turtles and cats, are used to discuss the possible mechanism of spread of locomotor activity.Institute for Problems in Information Transmission, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 14, No. 2, pp. 122–129, March–April, 1982.     

Modulation of transmitter release from the locust forewing stretch receptor neuron by GABAergic interneurons activated via muscarinic receptors

The role of muscarinic receptors in the down‐regulation of acetylcholine (ACh) release from the locust forewing stretch receptor neuron (fSR) terminals has been investigated. Electrical stimulation of the fSR evokes monosynaptic excitatory postsynaptic potentials (EPSPs) in the first basalar motoneuron (BA1), produced mainly by the activation of postsynaptic nicotinic cholinergic receptors. The general muscarinic antagonists scopolamine (10⁻⁶ M) and atropine (10⁻⁸ to 10⁻⁶ M) caused a reversible increase in the amplitude of electrically evoked EPSPs. However, scopolamine (10⁻⁶ M) caused a slight depression in the amplitude of responses to ACh pressure‐applied to the soma of BA1. These observations indicate that the EPSP amplitude enhancement is due to the blockade of muscarinic receptors on neurons presynaptic to BA1. The muscarinic receptors may be located on the fSR itself and act as autoreceptors, and/or they may be located on GABAergic interneurons which inhibit ACh release from the fSR. Electron microscopical immunocytochemistry has revealed that GABA‐immunoreactive neurons make presynaptic inputs to the fSR. The GABA antagonist picrotoxin (10⁻⁶ M) caused a reversible increase in the EPSP amplitude, which does not appear to be due to an increase in sensitivity of BA1 to ACh, as picrotoxin (10⁻⁶ M) slightly decreased ACh responses recorded from BA1. Application of scopolamine (10⁻⁶ M) to a preparation preincubated with picrotoxin did not cause the EPSP amplitude enhancement normally seen in control experiments; in fact, it caused a slight depression. This indicates that at least some of the presynaptic muscarinic receptors are located on GABAergic interneurons that modulate transmission at the fSR/BA1 synapse. © 1999 John Wiley & Sons, Inc. J Neurobiol 40: 420–431, 1999     

A presynaptic locus of the action of Met-enkephalin demonstrated in mouse spinal cord cultures

Monosynaptic excitatory post-synaptic potentials (EPSPs) evoked in spinal cord (SC) neurons by stimulation of dorsal root ganglion (DRG) neurons in cell cultures were reduced by perfusion application of the opiate peptide, Met-enkephalin (2-4 microM). In about 2/3 of cases examined, EPSPs evoked by stimulation of spinal cord cells were also reduced by Met-enkephalin. The effects were antagonized by concomitant perfusion with naloxone (1-2 microM) and recovered when perfusion with Met-enkephalin was stopped. Statistical analysis of synaptic responses indicated that the reduction of EPSP amplitude was due, at least to a major extent, to a decrease in presynaptic transmitter release.     

Role of GABA<Subscript>B</Subscript> receptor in the regulation of excitatory synaptic transmission in trigeminal motoneurons

The aim of the present study was to determine if excitatory synaptic transmission onto trigeminal motoneurons is subject to a presynaptic modulation by gamma-aminobutyric acid (GABA) via GABA(B) receptor in this system. Whole cell recordings were made from trigeminal motoneurons in longitudinal brain stem slices taken from 8-day-old rats. Monosynaptic excitatory postsynaptic potential (EPSP) activity was evoked by placing bipolar stainless steel electrodes dorsal-caudal to the trigeminal motor nucleus. Bath application of the GABA(B) receptor agonist, baclofen, produced a marked reduction in the mean amplitude and variance of evoked EPSPs and also increased the portion of transmission failures. It also produced a decrease in the frequency, but not in the mean amplitude, of spontaneous miniature EPSPs. Bath application of GABA(B) receptor antagonists 6-hydroxy-saclofen and CGP35348 increased both the amplitude and frequency of miniature EPSP activity. Taken together the above results suggest that the excitatory synaptic inputs onto trigeminal motoneurons are controlled by tonic presynaptic modulation by GABA(B) receptor.     

Propofol suppresses synaptic responsiveness of somatosensory relay neurons to excitatory input by potentiating GABAA receptor chloride channels

Propofol is a widely used intravenous general anesthetic. Propofol-induced unconsciousness in humans is associated with inhibition of thalamic activity evoked by somatosensory stimuli. However, the cellular mechanisms underlying the effects of propofol in thalamic circuits are largely unknown. We investigated the influence of propofol on synaptic responsiveness of thalamocortical relay neurons in the ventrobasal complex (VB) to excitatory input in mouse brain slices, using both current- and voltage-clamp recording techniques. Excitatory responses including EPSP temporal summation and action potential firing were evoked in VB neurons by electrical stimulation of corticothalamic fibers or pharmacological activation of glutamate receptors. Propofol (0.6 – 3 μM) suppressed temporal summation and spike firing in a concentration-dependent manner. The thalamocortical suppression was accompanied by a marked decrease in both EPSP amplitude and input resistance, indicating that a shunting mechanism was involved. The propofol-mediated thalamocortical suppression could be blocked by a GABA_A receptor antagonist or chloride channel blocker, suggesting that postsynaptic GABA_A receptors in VB neurons were involved in the shunting inhibition. GABA_A receptor-mediated inhibitory postsynaptic currents (IPSCs) were evoked in VB neurons by electrical stimulation of the reticular thalamic nucleus. Propofol markedly increased amplitude, decay time, and charge transfer of GABA_A IPSCs. The results demonstrated that shunting inhibition of thalamic somatosensory relay neurons by propofol at clinically relevant concentrations is primarily mediated through the potentiation of the GABA_A receptor chloride channel-mediated conductance, and such inhibition may contribute to the impaired thalamic responses to sensory stimuli seen during propofol-induced anesthesia.     

A dendritic cable model for the amplification of synaptic potentials by an ensemble average of persistent sodium channels

The persistent sodium current density (I(NaP)) at the soma measured with the 'whole-cell' patch-clamp recording method is linearized about the resting state and used as a current source along the dendritic cable (depicting the spatial distribution of voltage-dependent persistent sodium ionic channels). This procedure allows time-dependent analytical solutions to be obtained for the membrane depolarization. Computer simulated response to a dendritic current injection in the form of synaptically-induced voltage change located at a distance from the recording site in a cable with unequally distributed persistent sodium ion channel densities per unit length of cable (the so-called 'hot-spots') is used to obtain conclusions on the density and distribution of persistent sodium ion channels. It is shown that the excitatory postsynaptic potentials (EPSPs) are amplified if hot-spots of persistent sodium ion channels are spatially distributed along the dendritic cable, with the local density of I(NaP) with respect to the recording site shown to specifically increase the peak amplitude of the EPSP for a proximally placed synaptic input, while the spatial distribution of I(NaP) serves to broaden the time course of the amplified EPSP. However, in the case of a distally positioned synaptic input, both local and nonlocal densities yield an approximately identical enhancement of EPSPs in contradiction to the computer simulations performed by Lipowsky et al. [J. Neurophysiol. 76 (1996) 2181]. The results indicate that persistent sodium channels produce EPSP amplification even when their distribution is relatively sparse (i.e. , approximately 1-2% of the transient sodium channels are found in dendrites of CA1 hippocampal pyramidal neurons). This gives a strong impetus for the use of the theory as a novel approach in the investigation of synaptic integration of signals in active dendrites represented as ionic cables.     

Activity-dependent induction of facilitation,depression, and post-tetanic potentiation at an insect central synapse

Summary In Manduca sexta larvae, sensory neurons innervating planta hairs on the tips of the prolegs make monosynaptic excitatory connections with motoneurons innervating proleg retractor muscles. Tactile stimulation of the hairs evokes reflex retraction of the proleg. In this study we examined activity-dependent changes in the amplitude of the excitatory postsynaptic potentials (EPSPs) evoked in a proleg motoneuron by stimulation of individual planta hair sensory neurons. Deflection of a planta hair caused a phasic-tonic response in the sensory neuron, with a mean peak instantaneous firing frequency of >300 Hz, and a tonic firing rate of 10–20 Hz. Direct electrical stimulation was used to activate individual sensory neurons to fire at a range of frequencies including those observed during natural stimulation of the hair. At relatively low firing rates (e.g., 1 Hz), EPSP amplitude was stable indefinitely. At higher instantaneous firing frequencies (>10 Hz), EPSPs were initially facilitated, but continuous stimulation led rapidly to synaptic depression. High-frequency activation of a sensory neuron could also produce post-tetanic potentiation, in which EPSP amplitude remained elevated for several min following a stimulus train. Facilitation, depression, and post-tetanic potentiation all appeared to be presynaptic phenomena. These activity-dependent changes in sensory transmission may contribute to the behavioral plasticity of the proleg withdrawal reflex observed in intact insects.Abbreviations ACh acetylcholine - AChE acetylcholine esterase - CNS central nervous system - EPSP excitatory postsynaptic potential - I _h injected hyperpolarizing current - LTP long-term potentiation - PPR principal planta retractor motoneuron - PTP post-tetanic potentiation - R _in input resistance - V _h hyperpolarized potential - V _m membrane potential - VN ventral nerve - VNA anterior branch of the ventral nerve - V _r resting potential.     

Age-associated synapse elimination in mouse parasympathetic ganglia

Little is known about the effects of aging on synapses in the mammalian nervous system. We examined the innervation of individual mouse submandibular ganglion (SMG) neurons for evidence of age-related changes in synapse efficacy and number. For approximately 85% of adult life expectancy (30 months) the efficacy of synaptic transmission, as determined by excitatory postsynaptic potential (EPSP) amplitudes, remains constant. Similarly, the number of synapses contacting individual SMG neurons is also unchanged. After 30 months of age, however, some neurons (23%) dramatically lose synaptic input exhibiting both smaller EPSP amplitude and fewer synaptic boutons. Attenuation of both the amplitude and frequency of miniature EPSPs was also observed in neurons from aged animals. Electron micrographs revealed that, although there were many vesicle-laden preganglionic axonal processes in the vicinity of the postsynaptic membrane, the number of synaptic contacts was significantly lower in old animals. These results demonstrate primary, age-associated synapse elimination with functional consequences that cannot be explained by pre- or postsynaptic cell death.     

Long-term potentiation in the neurons of the edible snail

A brief high-frequency stimulation of the anal nerve of the isolated nerve ring of snail Helix induced a pronounced increase in the amplitude of EPSPs, evoked in identified neurons of left parietal and visceral ganglions by low frequency (once in 5 min) stimulation of the same nerve. The amplitude of EPSP returned to the control level 30-120 min after tetanization. We called this effect long-term potentiation. A brief application of serotonin (10 microM) in the majority of neurons also induced lasting either 15-30 min or more than 2 hours facilitation of EPSP, evoked by anal nerve stimulation. Intracellular cAMP injections, being without effect on EPSP amplitude in many neurons, in certain neurons caused an increase in EPSP amplitude, lasting up to 30 min. It is suggested that the 3 factors shown to increase synaptic efficiency in molluscan neurons may have common mechanisms of action.     

Analysis of function of the glutamatergic and GABAergic mediator systems in the olfactory cortex of spontaneously hipertensive rats in vitro

The effect of persistent hypertension on neuronal activity and synaptic transmission has been studied on olfactory cortex slices of SHR rats. The profilies of focal potentials in hypertensive rats demonstrated a short duration of the 2-amino-3-(5-methyl-3-hydroxyisoxazol-4-yl)-propanoic acid (AMPA) component of excitatory postsynaptic potential (EPSP), a small amplitude and long duration of the N-methyl D-aspartate (NMDA) component of EPSP, and a large amplitude of the GABA_B-dependent slow inhibitory postsynaptic potentials. The sensitivity of glutamate receptors responsible for the generation of AMPA- and NMDA-mediated EPSPs was low after the exposure to 1 mM L-glutamate. The amplitudes of the AMPA- and NMDA-mediated EPSPs decreased. Tetanization of slices from hypertensive rats induced a short-term potentiation followed by a depression. The data obtained indicate that persistent hypertension has depressive effects on the basic glutamatergic and GABAergic parameters of synaptic activity of neurons as well as on learning and memory. Apparently, these processes were evoked by glutamate excitotoxicity in the brain of hypertensive rats.     

Analysis of the processes of summation of postsynaptic potentials on the membrane of motoneurons upon realization of the stretch reflex

Stretching of the m. triceps surae (TS) of decerebrated cats evokes reflex shifts of the membrane potential (MP) in spinal motoneurons resulting from summation of EPSPs. We carried out model analysis of summation of a great number of EPSPs and compared the respective results with changes in the MP observed in real experiments using intrasomatic microelectrode recording. Simulation was based on the supposition of the proximity of the time course of an excitatory postsynaptic current to the positive part of the EPSP derivative. Transformation of EPSPs was performed using low-frequency filtration with two values of the time constant, 7 and 20 msec, (models M1 and M2, respectively). The models obtained provided sufficiently adequate reflection of the ascending phase of the real EPSP but inadequately reflected the rate of its decline and slow components of the MP changes. The disagreement of simulations with the real MP shifts shows that, most probably, final postsynaptic effects are to a considerable extent provided by summation of a great number of EPSPs generated in distal dendrites, and EPSPs immediately recorded in trasomatically cannot provide one with adequate information on the entire pattern of natural synaptic activation of the neuron. In addition, simulation analysis demonstrated a high probability of the contribution of active inhibitory processes to the formation of resulting MP changes under conditions of the stretch reflex. Neirofiziologiya/Neurophysiology, Vol. 40, No. 3, pp. 260–263, May–June, 2008.     

Age‐associated synapse elimination in mouse parasympathetic ganglia

Little is known about the effects of aging on synapses in the mammalian nervous system. We examined the innervation of individual mouse submandibular ganglion (SMG) neurons for evidence of age‐related changes in synapse efficacy and number. For approximately 85% of adult life expectancy (30 months) the efficacy of synaptic transmission, as determined by excitatory postsynaptic potential (EPSP) amplitudes, remains constant. Similarly, the number of synapses contacting individual SMG neurons is also unchanged. After 30 months of age, however, some neurons (23%) dramatically lose synaptic input exhibiting both smaller EPSP amplitude and fewer synaptic boutons. Attenuation of both the amplitude and frequency of miniature EPSPs was also observed in neurons from aged animals. Electron micrographs revealed that, although there were many vesicle‐laden preganglionic axonal processes in the vicinity of the postsynaptic membrane, the number of synaptic contacts was significantly lower in old animals. These results demonstrate primary, age‐associated synapse elimination with functional consequences that cannot be explained by pre‐ or postsynaptic cell death. © 2004 Wiley Periodicals, Inc. J Neurobiol 60: 214–226, 2004     

Central nervous sensitization and dishabituation of reflex action in an insect by the neuromodulator octopamine

Habituation of excitatory synaptic inputs onto identified motor neurons of the locust metathoracic ganglion, driven electrically and by natural stimuli, was examined using intracellular recording. Rapid progressive reduction in amplitude of EPSPs from a variety of inputs onto fast-type motor neurons occurred. The habituated EPSPs were quickly dishabituated by iontophoretic release of octopamine from a microelectrode into the neuropilar region of presumed synaptic action. The zone within which release was effective for a given neuron was narrowly-defined. With larger amounts of octopamine applied at a sensitive site the EPSP became larger than normal, and in many instances action potentials were initiated by the sensitized response. Very small EPSPs onto a motor neuron, which were associated with proprioceptive feedback, and which were originally too small to be detected above the noise, were potentiated to a level of several mV by the iontophoresed octopamine. A DUM neuron (presumed to be octopaminergic) was found, whose direct stimulation was followed by a strong dishabituating and sensitizing action leading to spikes, of inputs to an identified flexor tibiae motor neuron. The action and its time course were closely similar to those evoked by octopamine iontophoresed into the neuropil in the region of synaptic inputs to the motor neuron. It is concluded that DUM (octopaminergic) neurons exert large potentiating actions on central neuronal excitatory synaptic transmission in locusts.     

Dissociation of μ- and δ-opioid inhibition of glutamatergic synaptic transmission in superficial dorsal horn

Background

Although it has been widely accepted that the primary somatosensory (SI) cortex plays an important role in pain perception, it still remains unclear how the nociceptive mechanisms of synaptic transmission occur at the single neuron level. The aim of the present study was to examine whether noxious stimulation applied to the orofacial area evokes the synaptic response of SI neurons in urethane-anesthetized rats using an in vivo patch-clamp technique.

Results

In vivo whole-cell current-clamp recordings were performed in rat SI neurons (layers III-IV). Twenty-seven out of 63 neurons were identified in the mechanical receptive field of the orofacial area (36 neurons showed no receptive field) and they were classified as non-nociceptive (low-threshold mechanoreceptive; 6/27, 22%) and nociceptive neurons. Nociceptive neurons were further divided into wide-dynamic range neurons (3/27, 11%) and nociceptive-specific neurons (18/27, 67%). In the majority of these neurons, a proportion of the excitatory postsynaptic potentials (EPSPs) reached the threshold, and then generated random discharges of action potentials. Noxious mechanical stimuli applied to the receptive field elicited a discharge of action potentials on the barrage of EPSPs. In the case of noxious chemical stimulation applied as mustard oil to the orofacial area, the membrane potential shifted depolarization and the rate of spontaneous discharges gradually increased as did the noxious pinch-evoked discharge rates, which were usually associated with potentiated EPSP amplitudes.

Conclusions

The present study provides evidence that SI neurons in deep layers III-V respond to the temporal summation of EPSPs due to noxious mechanical and chemical stimulation applied to the orofacial area and that these neurons may contribute to the processing of nociceptive information, including hyperalgesia.