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PubMed1987

Epileptiform burst activity induced by potassium in the hippocampus and its regulation by GABA-mediated inhibition.

Intracellular and extracellular recordings were made from pyramidal neurons in hippocampal slices in order to study spontaneous paroxysmal bursting induced by raising the extracellular potassium concentration from 3.5 to 8.5 mM. Extracellular recordings from all hippocampal subfields indicated that spontaneous bursts appeared to originate in region CA3c or CA3b as judged by burst onset. Burst intensity was also greatest in regions CA3b and CA3c and became progressively less toward region CA2. Intracellular recordings indicated that in 8.5 mM potassium, large spontaneous excitatory postsynaptic potentials (EPSPs), large burst afterhyperpolarizations, and rhythmic hyperpolarizing-depolarizing waves of membrane potential were invariably present in CA3c neurons. High potassium (8.5 mM) induced a positive shift (+9 mV) in the reversal potential of GABAergic inhibitory postsynaptic potentials (IPSPs) in CA3c neurons without changing input resistance or resting potential. This resulted in a drastic reduction in amplitude of the IPSP. Reduction of IPSP amplitude occurred before the onset of spontaneous bursting and was reversible upon return to normal potassium. A new technique to quantify the relative intensity of interictal-like burst discharges is described. Pentobarbital, diazepam, and GABA uptake inhibitors, which enhance GABA-mediated synaptic inhibition, reduced the intensity of potassium-induced bursts, whereas the GABA antagonist bicuculline increased burst intensity. Diphenylhydantoin and phenobarbital, anticonvulsants that have little effect on GABAergic inhibition, were without effect on spontaneous bursts. Burst frequency was reduced by bicuculline and 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol but was unaffected by other drugs. Reduction of slice temperature from 35 to 19 degrees C dramatically reduced burst intensity but did not markedly affect burst frequency. We hypothesize that high potassium induces a rise in intracellular chloride concentration, possibly by activating an inward KCl pump or by a passive Donnan effect, which results in a decreased IPSP amplitude. With inhibition suppressed, the large spontaneous EPSPs that appear in high potassium cause individual CA3c neurons to fire. A combination of synaptic and electrical interactions among CA3c cells then synchronizes discharges into interictal spike bursts.

Action Potentials↗

PubMed1959

Functional organization in the terminal segments of the spinal cord with a consideration of central excitatory and inhibitory latencies in monosynaptic reflex systems.

Prominent monosynaptic and disynaptic reflex discharges characterize ipsilateral reflex transmission in the third sacral segment. Convergence upon the motoneurons from the two sides of the body is inhibitory, that through disynaptic paths excitatory. The relative latencies of excitation and inhibition of reflex responses, of excitatory and inhibitory synaptic potentials, and of various aspects of impulse discharge in motoneurons are considered. It is concluded: (1) that a direct (i.e. monosynaptic) action of primary afferent collaterals upon motoneurons is responsible for inhibition of monosynaptic reflex discharge of antagonist motoneurons within a myotatic unit; (2) that the inhibitory postsynaptic potential as described is not the primary agency for monosynaptic reflex inhibition of monosynaptic reflex discharge; (3) that, however, a common causal agent may be responsible for inhibition of reflex discharge and for generation of an inhibitory postsynaptic potential; and (4) that the inhibitory post-synaptic potential may be linked with, or be the agent for, inhibition of soma response.

Motor Neurons↗

PubMed1978

Durations of unitary synaptic potentials help time a behavioral sequence.

Recordings in identified neurons and muscles that mediate crayfish tailflips reveal inhibitory postsynaptic potentials of two distinct durations. Those of long duration are recorded in five classes of cells in the flexion circuit, while those of short duration are recorded in three classes of cells in the extension circuit. The durations of the inhibitory postsynaptic potentials are matched to the durations of inhibition required by the different phases of the behavior.

Animals↗

PubMed1994

Interleukin-1 beta inhibits synaptic transmission and induces membrane hyperpolarization in amygdala neurons.

Interleukin-1 beta (IL-1 beta), a mediator of immune response, is found in the brain and IL-1 binding sites are located in the basolateral amygdala (BLA). Superfusion of IL-1 beta (118 pM) hyperpolarized the membrane and decreased input resistance in most BLA neurons in brain slice preparations. The hyperpolarization was dose dependent, reversible, persisted in tetrodotoxin and had an estimated EC50 of 15.3 pM. Reversal potentials for the hyperpolarization recorded with potassium acetate and KCl electrodes were -74 and -40 mV, respectively. These data suggest involvement of a chloride conductance. The hyperpolarization was not observed in bicuculline or in acutely dissociated BLA neurons, which implicates an indirect mediation through enhancement of endogenous gamma-aminobutyric acid (GABA). Superfusion of IL-1 beta (118 pM) inhibited excitatory and fast and slow inhibitory postsynaptic potentials evoked by stimulating either the stria terminalis or the lateral amygdala. Fast and slow inhibitory postsynaptic potentials elicited by direct stimulation of GABA interneurons in the lateral amygdala were also depressed by IL-1 beta. IL-1 beta did not depress responses to GABA or glutamate receptor agonists in slices or currents induced by glutamate agonists in acutely dissociated BLA neurons. These findings indicate that inhibition of synaptic transmission is presynaptic. The results show that IL-1 beta inhibits excitatory and inhibitory transmission at a presynaptic site and hyperpolarizes the membrane through an indirect action, possibly by enhancing the action of endogenous GABA in the BLA nucleus. The inhibitory effect of IL-1 beta suggests that factors in the immune system play a role in modulating neuronal function in the BLA.

Amino Acid Sequence↗

PubMed2000

Seizures induce simultaneous GABAergic and glutamatergic transmission in the dentate gyrus-CA3 system.

Monosynaptic and polysynaptic responses of CA3 pyramidal cells (PC) to stimulation of the dentate gyrus (DG) are normally blocked by glutamate receptor antagonists (GluRAs). However, after kindled seizures, GluRAs block the monosynaptic excitatory postsynaptic potential (EPSP) and isolate a monosynaptic inhibitory postsynaptic potential (IPSP), suggesting that mossy fibers release GABA. However, kindling epilepsy induces neuronal sprouting, which can underlie this fast inhibitory response. To explore this possibility, the synaptic responses of PC to DG stimulation were analyzed in kindled epileptic rats, with and without seizures, and in nonepileptic rats, immediately after a single pentylenetetrazol (PTZ)-induced seizure, in which sprouting is unlikely to have occurred. Excitatory and inhibitory synaptic responses of PC to DG stimulation were blocked by GluRAs in control cells and in cells from kindled nonseizing rats, confirming that inhibitory potentials are disynaptically mediated. However, a fast IPSP could be evoked in kindled epileptic rats and in nonepileptic rats after a single PTZ-induced seizure. The same response was induced after rekindling the epileptic nonseizing rats. This IPSP has an onset latency that parallels that of the control EPSP and is not altered under low Ca(2+) medium or halothane perfusion. In addition, it was reversibly depressed by L(+)-2-amino-4-phosphonobutyric acid (L-AP4), which is known to inhibit transmitter release from mossy fibers. These results demonstrate that seizures, and not the synaptic rearrangement due to an underlying epileptic state, induce the emergence of fast inhibition in the DG-CA3 system, and suggest that the mossy fibers underlie this plastic change.

Amygdala↗

PubMed2006

Differential sensitivity of excitatory and inhibitory synaptic transmission to modulation by nitric oxide in rat nucleus tractus solitarii.

The nucleus tractus solitarii (NTS) is a key central link in control of multiple homeostatic reflexes. A number of studies have demonstrated that exogenous and endogenous nitric oxide (NO) within NTS regulates visceral function, but further understanding of the role of NO in the NTS is hampered by the lack of information about its intracellular actions. We studied effects of NO in acute rat brainstem slices. Aqueous NO solution (NO(aq)) potentiated electrically evoked excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs, respectively) in different neuronal subpopulations and, in some neurones, caused a depolarization. Similar effects were observed using the NO donor diethylamine NONOate (DEA/NO). The threshold NO concentration as determined using an NO electrochemical sensor was estimated as approximately 0.4 nm (EC(50) approximately 0.9 nm) for potentiating glutamatergic EPSPs but approximately 3 nm for monosynaptic GABAergic IPSPs. Bath application of the soluble guanylate cyclase (sGC) inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) abolished NO(aq)- and DEA/NO-induced potentiation of evoked EPSPs, IPSPs and depolarization. All NO actions were mimicked by the non-NO-dependent guanylate cyclase activator Bay 41-2272. The effects of NO on EPSPs and IPSPs persisted in cells where postsynaptic sGC was blocked by ODQ and therefore were presynaptic, owing to a direct modulation of transmitter release combined with depolarization of presynaptic neurones. Therefore, while lower concentrations of NO may be important for fine tuning of glutamatergic transmission, higher concentrations are required to directly engage GABAergic inhibition. This differential sensitivity of excitatory and inhibitory connections to NO may be important for determining the specificity of the effects of this freely diffusible gaseous messenger.

Animals↗

PubMed1993

The behavior of mossy cells of the rat dentate gyrus during theta oscillations in vivo.

Intracellular current clamp recordings were obtained from mossy cells (n = 6, identified by intracellular injection of biocytin) of the dorsal dentate gyrus from rats under ketamine-xylazine anesthesia. During electroencephalographic theta rhythm (4-6 Hz), recorded with a macroelectrode placed in the contralateral dorsal hippocampus near the fissure, mossy cells displayed intracellular membrane potential oscillations at low frequencies (4-6 Hz) which appeared to be phase locked to the electroencephalographic theta rhythm. The frequency of the intracellular theta rhythm was independent of the membrane potential. However, the phase difference between the intracellular and the electroencephalographic theta rhythms as well as the amplitude of the intracellular theta oscillations were voltage-dependent. These findings are consistent with the hypothesis that rhythmic GABAA receptor-mediated inhibitory postsynaptic potentials contribute to the genesis of the intracellular theta rhythm. Indeed, mossy cells displayed an early, fast inhibitory postsynaptic potential in response to electrical stimulation of the entorhinal cortex, which most likely represents a GABAA receptor-mediated event, indicating that mossy cells possess functional GABAA receptors. At the resting membrane potential, mossy cells did not fire at each cycle of the electroencephalographic theta rhythm but fired only rarely (< 1 Hz). However, when they did fire they did so preferentially in phase with the peak positivity of the electroencephalographic theta rhythm. Reconstruction of two mossy cells with axonal projections to the inner molecular layer showed that the spatial extent of the influence such weakly discharging mossy cells may have on other dentate gyrus neurons during theta oscillations can be several millimeters in the septotemporal direction. In conclusion, these findings show that mossy cells of the rat hilus during ketamine-xylazine anesthesia participate in theta oscillations of the hippocampal formation, during which their low-frequency firing may contribute to the phase-locking of a large number of spatially distributed postsynaptic neurons with postsynaptic sites in the inner molecular layer of the dentate gyrus.

Animals↗

PubMed1989

Evidence that glycine mediates the postsynaptic potentials that inhibit lumbar motoneurons during the atonia of active sleep.

Postsynaptic inhibition of somatic motoneurons underlies the atonia of active sleep. This inhibitory control depends, in large measure, on the bombardment of motoneurons during active sleep by a unique class of large-amplitude inhibitory postsynaptic potentials (IPSPs). These potentials are present only during this behavioral state and have therefore been designated as active sleep-specific IPSPs (AS-IPSPs). The present study was concerned with determining the neurotransmitter that mediates these AS-IPSPs. Lumbar motoneurons were recorded intracellularly during quiet and active sleep in intact, undrugged, normally respiring cats. The frequency and waveform parameters of the inhibitory postsynaptic potentials recorded from these motoneurons were examined following the microiontophoretic juxta-cellular administration of strychnine (a glycine receptor antagonist) and picrotoxin and bicuculline (GABA receptor antagonists). Microiontophoretically applied strychnine abolished the AS-IPSPs and a majority of smaller-amplitude IPSPs. Neither picrotoxin nor bicuculline modified the frequency, amplitude, or rising phase of the AS-IPSPs or the smaller-amplitude IPSPs. We conclude that the postsynaptic inhibitory drive that impinges on motoneurons during active sleep is principally mediated by glycine or a glycinergic substance.

Animals↗

PubMed1983

Summation of excitatory postsynaptic potentials in hippocampal pyramidal cells.

The summation of excitatory postsynaptic potentials (EPSPs) generated in separate parts of the dendritic tree of hippocampal pyramidal cells has been investigated using the in vitro slice preparation. Two separate inputs with known synaptic location were used. The EPSP produced by simultaneous activation of the two inputs (observed sum) was compared to the algebraic sum of the individual EPSPs. Small-amplitude EPSPs (0.5-1.5 mV) added linearly. The shortest distance between the two synaptic groups was 75 micron. With larger amplitudes (greater than 2.5 mV), the EPSP summated nonlinearly. The nonlinear summation was reduced by moderate hyperpolarizations (2-10 mV) of the soma membrane. Also, large EPSPs (greater than 2.5 mV) summated linearly when the peak of the summed EPSP was brought close to the equilibrium potential for the inhibitory postsynaptic potential (IPSP) (EIPSP). When the EPSP peak was made more negative than the EIPSP, summation was again nonlinear but the algebraic sum was now smaller than the observed EPSP sum, i.e., the direction of the nonlinearity was reversed. EPSP summation was linear after the IPSP had been blocked by benzyl penicillin application. We conclude that separate EPSPs in hippocampal pyramids (minimal separation, 75 micron) add linearly but that the addition of an IPSP may complicate this picture. No evidence was found for interaction between the different populations of excitatory synapses.

Animals↗

PubMed2004

Effects of cortical stimulation on auditory-responsive thalamic neurones in anaesthetized guinea pigs.

In the present study, we investigated neuronal responses to acoustic stimuli and cortical stimulation in the medial geniculate body (MGB) through in vivo intracellular recordings in anaesthetized guinea pigs. Of the 54 neurones examined with acoustic stimuli, 36 showed excitatory postsynaptic potential (EPSP) responses and 19 showed inhibitory postsynaptic potential (IPSP) responses to acoustic stimuli. Of the 36 EPSP neurones examined with corticofugal modulation, 29 received corticofugal depolarization, 3 corticofugal inhibition, and 4 showed no effect. Of the 19 IPSP neurones, 17 received corticofugal inhibition and 2 were not affected. The mean amplitude of the EPSPs evoked by acoustic stimuli was similar to that evoked by the electrical cortical stimulation (9.19 +/- 5.55 mV versus 9.22 +/- 5.16 mV). There was a significant correlation between the parameters of the EPSPs evoked by an acoustic stimulus and those evoked by cortical stimulation. The mean amplitude of the IPSP evoked by electrical cortical stimulation was significantly greater than that evoked by acoustic stimuli (11.6 +/- 3.8 mV versus 9.1 +/- 3.7 ms, P < 0.05). Seven auditory EPSP and 7 IPSP neurones were examined with corticofugal modulation and labelled with Neurobiotin. Of the 7 EPSP neurones, 5 showed excitatory responses to cortical stimulation and 2 demonstrated no effects. Four of the 5 neurones that received corticofugal depolarization were located in the lemniscal MGB and 1 in the non-lemniscal MGB; of the remaining 2, 1 was located in the lemniscal and the other in the non-lemniscal MGB. Of the 7 IPSP neurones, 1 received an excitatory corticofugal input followed by an inhibitory input and 4 received only an inhibitory corticofugal input, while the remainder demonstrated no corticofugal effects. All 7 neurones were located in the non-lemniscal MGB. The result that both ascending and descending inputs caused similarly shaped EPSPs reflects a neuronal endogenous characteristic irrespective of the physical locations of the synapses. The IPSP responses to both acoustic stimuli and electrical cortical stimulation are likely to be caused by feedback from the thalamic reticular nucleus.

Acoustic Stimulation↗

PubMed1996

Cooperative interactions in the induction of long-term potentiation and depression of synaptic excitation between hippocampal CA3-CA1 cell pairs in vitro.

The requirement for cooperative interactions between multiple synaptic inputs in the induction of long-term potentiation (LTP) and long-term depression (LTD) has been tested at Schaffer collateral synapses with paired recordings from monosynaptically coupled CA3-CA1 cell pairs in rat hippocampal slice cultures. Tetanization of single presynaptic neurons at 50 Hz (repeated 5-7 times for 300-500 ms each) induced only a transient potentiation (< 3 min) of excitatory postsynaptic potentials (EPSPs). Persistent potentiation (> 15 min) was induced only when single presynaptic action potentials were synchronously paired with directly induced postsynaptic depolarizing pulses (repeated 50-100 times). Tetanus-induced potentiation of extracellularly evoked EPSPs lasting > 4 min could only be obtained if the EPSP was > 4 mV. Because unitary EPSP amplitudes average approximately 1 mV, we conclude that high-frequency discharge must occur synchronously] in 4-5 CA3 cells for LTP to be induced in a common postsynaptic CA1 cell. Asynchronous pairing of presynaptic action potentials with postsynaptic depolarizing current pulses (preceding each EPSP by 800 ms) depressed both naive and previously potentiated unitary EPSPs. Likewise, homosynaptic LTD of unitary EPSPs was induced when the presynaptic cell was tetanized at 3 Hz for 3 min, regardless of their amplitude (0.3-3.2 mV). Homosynaptic LTD of extracellularly evoked Schaffer collateral EPSPs < 4 mV could be induced if no inhibitory postsynaptic potential was apparent, but was prevented by eliciting a large inhibitory postsynaptic potential or by injection of hyperpolarizing current in the postsynaptic cell. We conclude that cooperative interactions among multiple excitatory inputs are not required for induction of homosynaptic LTD of unitary EPSPs.

Animals↗

PubMed1999

Physiology of electrosensory lateral line lobe neurons in Gnathonemus petersii.

In mormyrid electric fish, sensory signals from electroreceptors are relayed to secondary sensory neurons in a cerebellum-like structure known as the electrosensory lateral line lobe (ELL). Efferent neurons and interneurons of the ELL also receive inputs of central origin, including electric organ corollary discharge signals, via parallel fibers and via fibers from the juxtalobar nucleus. To understand the cellular mechanisms of the integration of sensory inputs and central inputs in the ELL, the intracellular activity and ionic properties of the efferent projection neurons and interneurons were examined in an in vitro slice preparation.We focus here on the electrophysiological properties of the efferent neurons of the ELL network, the large fusiform cells and large ganglion cells, and on a class of gamma-aminobutyric acid (GABA)-ergic interneurons known as medium ganglion (MG) cells. In response to current injection through a recording pipette, both types of efferent neuron fire a large narrow spike followed by a large hyperpolarizing afterpotential. The MG cells fire a complex spike which consists of small narrow spikes and a large broad spike. Although the forms of the action potentials in efferent neurons and in MG cells are different, all spikes are mediated by tetrodotoxin (TTX)-sensitive Na+ conductances and spike repolarization is mediated by tetraethylammonium (TEA+)-sensitive K+ conductances. In the presence of TEA+, substitution of Ba2+ for Ca2+ in the bath revealed the presence of a high-voltage-activated Ca2+ conductance. Stimulation of parallel fibers conveying descending input to the ELL molecular layer in vitro evokes an excitatory postsynaptic potential (EPSP), generally followed by an inhibitory postsynaptic potential (IPSP), in the efferent neurons. In MG cells, the same stimulation evokes an EPSP, often followed by a small IPSP. Synaptic transmission at parallel fiber synapses is glutamatergic and is mediated via both N-methyl-d-aspartate (NMDA)- and (AMPA)-type glutamate receptors. The inhibitory component of the parallel fiber response is GABAergic. It is probably mediated via the stellate neurons and the MG cells, which are themselves GABAergic interneurons intrinsic to the ELL network.A hypothetical neural circuit of the intrinsic connections of the ELL, based on the known morphology of projection neurons and medium ganglion interneurons, is presented. This circuit includes an excitatory and an inhibitory submodule. The excitatory submodule is centered on a large fusiform cell and appears to relay the sensory input as a positive 'ON' image of an object. The inhibitory submodule is centered on a large ganglion cell and relays a negative 'OFF' image to the next higher level. We suggest that MG cells exert an inhibitory bias on efferent neuron types and that the ELL network output is modulated by the dynamically plastic integration of central descending signals with sensory input.

Animals↗

PubMed1990

Calcium-dependent potentials with different sensitivities to calcium agonists and antagonists in guinea-pig hippocampal neurons.

Effects of organic Ca channel blockers, Ca channel activators and omega-conotoxin on guinea-pig hippocampal CA1 neurons in vitro preparations were studied with intracellular recording methods. Most of the Ca channel blockers, such as prenylamine, D 600, flunarizine, nifedipine, cinnarizine and nicardipine (0.2-4 microM), raised the threshold for Na-dependent spike generation and decreased the amplitude of the spike afterhyperpolarization. Verapamil (5 microM) and diltiazem (5 microM) did not significantly alter the threshold and amplitude of the Na spike. Action potentials elicited in the presence of either tetrodotoxin (0.5 microM) and tetraethylammonium (20 mM) or tetrodotoxin (0.5 microM) and Ba (1.25 mM) consisted of an initial spike component followed by a long depolarization. Both responses were abolished by addition of Co (2 mM) or Cd (0.25-0.5 mM), or by superfusion with a low Ca (0.25 mM)-high Mg(15 mM) medium, indicating that the potentials resulted from Ca entry. The Ca-dependent slow depolarization was preferentially blocked by most of the organic Ca channel blockers at approximately one-third the concentrations (0.1-2 microM) which were required to shorten the Ca spike. When the cell in a solution containing tetrodotoxin (0.5 microM), Co (2 mM) and 4-aminopyridine (2 mM) was hyperpolarized and then depolarized by passing current pulses across the membrane, a transient depolarizing hump occurred on the decay phase of the electrotonic potential. This transient depolarization was abolished by Co (2 mM), Ni (2 mM) or most of the organic Ca channel blockers (0.2-5 microM). Diltiazem (5 microM) did not significantly change these Ca-dependent potentials. The evoked excitatory postsynaptic potential was very resistant to the Ca channel blockers. Approximately 2-10 times higher concentrations (0.5-3 microM) were necessary to decrease the excitatory postsynaptic potential amplitude than to shorten the Ca spike. On the other hand, the minimal concentrations and order of potencies of the Ca channel blockers for depressing the evoked inhibitory postsynaptic potential and for elevating the threshold for Na spike generation were almost the same. Dihydropyridine Ca channel activators, such as Bay K 8644, CGP 28 392 and YC 170 at low concentrations (0.1-1 microM), decreased the Ca spike, the Ca-dependent slow depolarization and the evoked synaptic potentials, while the substances augmented the Ca-dependent transient depolarization. On the other hand, omega-conotoxin (5 microM) reversibly depressed the Ca spike and slow depolarization to the same degree, without affecting the transient depolarization and the evoked excitatory or inhibitory postsynaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1992

Mono- and disynaptic pathways from Forel's field H to dorsal neck motoneurones in the cat.

1. We analysed the synaptic actions produced by Forel's field H (FFH) neurones on dorsal neck motoneurones and the pathways mediating the effects. 2. Stimulation of ipsilateral FFH induced negative field potentials of several hundred microvolts with the latency of about 1.1 ms in the medial ponto-medullary reticular formation, being largest in the ventral part of the nucleus reticularis pontis caudalis (NRPC), and in the dorsal part of the nucleus reticularis gigantocellularis (NRG). 3. Stimulation of ipsilateral FFH induced excitatory postsynaptic potentials (EPSPs) in 90% (47/52) and inhibitory postsynaptic potentials (IPSPs) in 19% (10/52) of the reticulospinal neurones (RSNs) in the NRPC and the NRG. Latencies of the EPSPs and IPSPs were 0.7-3.0 ms, the majority of which were in the monosynaptic range. The monosynaptic connexions were confirmed by spike triggered averaging technique both in excitatory (n = 4) and inhibitory (n = 2) pathways. 4. Single stimulation of FFH induced EPSPs at the segmental latencies of 0.3-1.0 ms in neck motoneurones, which were clearly in the monosynaptic range. Repetitive stimulation of FFH produced marked temporal facilitation of EPSPs in neck motoneurones. The facilitated components of the EPSPs had a little longer latencies and their amplitude reached several times as large as that evoked by single stimulation in all the tested motoneurones. These facilitated excitations are assumed to be mediated by RSNs in the NRPC and NRG, since RSNs were mono- and polysynaptically fired by stimulation of FFH and they were previously shown to directly project to neck motoneurones. 5. EPSPs were induced in 91% (82/91) of motoneurones supplying m. biventer cervicis and complexus (BCC; head elevator), 10% (3/29) of motoneurones supplying m. splenius (SPL; lateral head flexor). Likewise, stimulation of FFH produced EMG responses in BCC muscles, while not in SPL muscle. Thus FFH neurones produce excitations preferentially in BCC motoneurones. 6. Systematic tracking in and around FFH revealed that the effective sites for evoking above effects were in FFH and extended caudally along their efferent axonal course. 7. These results suggested that FFH neurones connect with neck motoneurones (chiefly BCC, head elevator) mono-, di- and/or polysynaptically and are mainly concerned with the control of vertical head movements.

Animals↗

PubMed1989

The cellular mechanism of thalamic ponto-geniculo-occipital waves.

The cellular mechanisms underlying the genesis of thalamic ponto-geniculo-occipital waves were studied in reserpinized cats under urethane anaesthesia. Simultaneous field potential and intracellular recordings were performed in the lateral geniculate nucleus after acute lesions of retinal and visual cortical inputs. In most relay cells, reserpine-induced ponto-geniculo-occipital waves were associated with a transient depolarization that was often interrupted by a unitary inhibitory postsynaptic potential. The depolarization grew in size with membrane hyperpolarization and was accompanied by an increase in membrane conductance. The inhibitory postsynaptic potential is likely to have resulted from the activation of intrageniculate interneurons since perigeniculate cells were always inhibited during the occurrence of ponto-geniculo-occipital waves. Under reserpine, thalamic ponto-geniculo-occipital waves could also be triggered by peribrachial or auditory stimulation. These evoked ponto-geniculo-occipital waves were associated with intracellular events identical to those occurring spontaneously after reserpine administration. In addition, thalamic spindle oscillations were readily blocked by the occurrence of spontaneous or evoked ponto-geniculo-occipital waves. On the basis of the present results and those already published in the literature, the conclusion is reached that lateral geniculate ponto-geniculo-occipital waves result from a nicotinic activation of relay cells and from a parallel muscarinic inhibition of perigeniculate cells by peribrachial afferents. The functional significance of the ponto-geniculo-occipital activity is discussed on the basis of the antagonistic action of these signals on thalamic oscillations. It is proposed that these signals are the central correlates of orienting reactions elicited by sensory stimuli during waking (the so-called eye movement potentials) and by internally generated drives during paradoxical sleep.

Action Potentials↗

PubMed1989

Activity-dependent disinhibition. I. Repetitive stimulation reduces IPSP driving force and conductance in the hippocampus in vitro.

1. Intracellular recording techniques were used to investigate the mechanisms underlying the activity-dependent lability of inhibitory synaptic potentials indirectly evoked in CA3 pyramidal neurons by stimulation of the mossy fiber afferent pathway in organotypic slice cultures of hippocampus. 2. Repetitive stimulation (3-10 Hz, 30-60 s) was found to reduce the amplitude of the inhibitory postsynaptic potential (IPSP) and occasionally lead to repetitive, epileptiform discharge. 3. Under single-electrode voltage-clamp, the current underlying the inhibitory postsynaptic potential (IPSC) was found to have the same reversal potential (EIPSC) as the response to iontophoretically applied gamma-aminobutyric acid (EGABA), and both were blocked by bicuculline. Reducing the extracellular Cl- concentration from 153 to 89 mM shifted EGABA in the depolarizing direction by 9 mV from -64.7 to -55.6 mV, an amount close to that predicted by the Nernst equation. We therefore presume that the IPSC is mediated by GABA and that the reversal potentials of both are equal to ECl-. 4. Under single-electrode voltage-clamp, repetitive stimulation (3-10 Hz, 30-60 s) was found to cause a mean decrease in the conductance underlying the IPSC (gIPSC) of 22%. This decrease was independent of the membrane potential at which stimuli were delivered. 5. Under single-electrode voltage-clamp, repetitive stimulation (3-10 Hz, 30-60 s) was found to cause a 2-8 mV depolarizing shift in EIPSC when the membrane potential was held constant 5-15 mV depolarized from EIPSC. The mean decrease in IPSC driving force was 49%. If membrane potential was held 10-20 mV hyperpolarized from EIPSC, there was no change in driving force. 6. Currents activated by iontophoretically applied GABA were decreased in amplitude following repetitive stimulation at depolarized, but not hyperpolarized, holding potentials. 7. The decrease in IPSC driving force following repetitive stimulation at depolarized holding potentials was less after decreasing the extracellular K+ concentration from 5.8 to 1 mM. 8. We conclude that the decrease in driving force following repetitive stimulation results from an increase in the intracellular Cl- concentration, and that the activity-dependent decrease in gIPSC results from a decrease in presynaptic release rather than from postsynaptic receptor desensitization.

Action Potentials↗

PubMed1997

Is activation of the metabotropic glutamate receptors impaired in the hippocampal CA1 area of the aged rat?

The effects of aging on activation of metabotropic glutamate (mGlu) receptors were studied in the CA1 field of hippocampal slices from young (3- to 4-month-old) and aged (24- to 27-month-old) Sprague-Dawley rats with the use of ex vivo electrophysiological recording techniques. The depolarization of membrane potential, the increase in input resistance, and the blockade of the afterhyperpolarization induced in pyramidal cells of young rats by bath application of the mGlu receptor agonist (+/-)-trans-1-aminocyclopentate-1,3-dicarboxylic acid were not altered in aged animals. No age-related changes of the depressive effects of the mGlu receptor agonist were found on either the excitatory glutamatergic postsynaptic potential or the GABA-mediated inhibitory postsynaptic potentials induced by the stimulation of the stratum radiatum. The magnitude of synaptic plasticity involving mGlu receptor activation, although weaker, was not significantly altered in aged rats. This absence of age-related effects on activation of mGlu receptors may be important in understanding the possible origins of the alterations in neuronal plasticity which occur in brain aging.

2-Amino-5-phosphonovalerate↗

PubMed1986

Electrophysiology of rat thalamo-cortical relay neurons: an in vivo intracellular recording and labeling study.

Membrane properties and responses to frontal cortical stimulation were studied on electrophysiologically and morphologically identified thalamo-cortical neurons in anesthetized rats. Those neurons generated membrane responses resembling the low-threshold Ca-spike, gK(Ca) and IA that have been previously demonstrated in in vitro studies of thalamic neurons. Stimulation of the frontal cortex evoked a sequence of responses; antidromic spike, initial depolarization, long duration hyperpolarization and a short period of depolarization. The initial depolarization was considered to be a monosynaptic excitatory postsynaptic potential (EPSP) which overlapped with an inhibitory postsynaptic potential (IPSP). Major constituents of the long duration hyperpolarization were considered to be short duration IPSPs and long duration disfacilitations of cortical inputs.

Animals↗