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PubMed1967

A direct synaptic connection mediating both excitation and inhibition.

Neurons have generally been thought to produce only one synaptic action on any particular cell which they innervate. An identified interneuron in the abdominal ganglion of Aplysia mediates both direct excitation and inhibition to an identified follower cell. At low firing rates the interneuron produces excitatory postsynaptic potentials; however at higher firing rates these gradually diminish in size and eventually invert to inhibitory postsynaptic potentials. Electrophysiological and pharmacological evidence indicates that the connection between these cells is monosynaptic, and that a single transmitter, acetylcholine, mediates both actions. These opposite synaptic responses appear to result from the transmitter's acting on two types of postsynaptic receptors having different thresholds for activation and different susceptibilities for desensitization.

Acetylcholine↗

PubMed1996

Ionic mechanisms underlying synchronized oscillations and propagating waves in a model of ferret thalamic slices.

1. A network model of thalamocortical (TC) and thalamic reticular (RE) neurons was developed based on electrophysiological measurements in ferret thalamic slices. Single-compartment TC and RE cells included voltage- and calcium-sensitive currents described by Hodgkin-Huxley type of kinetics. Synaptic currents were modeled by kinetic models of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), gamma-aminobutyric acid-A (GABAA) and GABAB receptors. 2. The model reproduced successfully the characteristics of spindle and slow bicuculline-induced oscillations observed in vitro. The characteristics of these two types of oscillations depended on both the intrinsic properties of TC and RE cells and their pattern of interconnectivity. 3. The oscillations were organized by the reciprocal recruitment between TC and RE cells, due to their manual connectivity and bursting properties. TC cells elicited AMPA-mediated excitatory postsynaptic potentials (EPSPs) in RE cells, whereas RE cells elicited a mixture of GABAA and GABAB inhibitory postsynaptic potentials (IPSPs) in TC cells. Because of the presence of a T current, sufficiently strong EPSPs could elicit a burst in RE cells, and TC cells could generate a rebound burst following GABAergic IPSPs. Under these conditions, interaction between the TC and RE cells produced sustained oscillations. 4. In the absence of spontaneous oscillation in any cell, the TC-RE network remained quiescent. Spindle oscillations with a frequency of 9-11 Hz could be initiated by stimulation of either TC or RE neurons. A few spontaneously oscillating TC neurons recruited the entire network model into a "waxing-and waning" oscillation. These "initiator" cells could be an extremely small proportion of TC cells. 5. In intracellular recordings, TC cells display a reduced ability for burst firing after a sequence of bursts. The "waning" phase of spindles was reproduced in the network model by assuming an activity-dependent upregulation of Ih operating via a calcium-binding protein in TC cells, as shown previously in a two-cell model. 6. Following the global suppression of GABAA inhibition, the disinhibited RE cells produced prolonged burst discharges that elicited strong GABAB-mediated currents in TC cells. The enhancement of slow IPSPs in TC cells was also due to cooperativity in the activation of GABAB-mediated current. These slow IPSPs recruited TC and RE cells into slower waxing-and-waning oscillations (3-4 HZ) that were even more highly synchronized. 7. Local axonal arborization of the TC to RE and RE to TC projections allowed oscillations to propagate through the network. An oscillation starting at a single focus induced a propagating wavefront as more cells were recruited progressively. The waning of the oscillation also propagated due to upregulation of Ih in TC cells, leading to waves of spindle activity as observed in experiments. 8. The spatiotemporal properties of propagating waves in the model were highly dependent on the intrinsic properties of TC cells. The spatial pattern of spiking activity was markedly different for spindles compared with bicuculline-induced oscillations and depended on the rebound burst behavior of TC cells. The upregulation of Ih produced a refractory period so that colliding spindle waves merged into a single oscillation and extinguished. Finally, reducing the Ih conductance led to sustained oscillations. 9. Two key properties of cells in the thalamic network may account for the initiation, propagation, and termination of spindle oscillations, the activity-dependent upregulation of Ih in TC cells, and the localized axonal projections between TC and RE cells. In addition, the model predicts that a nonlinear stimulus dependency of GABAB responses accounts for the genesis of prolonged synchronized discharges following block of GABAA receptors.

Animals↗

PubMed1997

Effects of adenosine on cholinergic transmission in mammalian vesical parasympathetic ganglia.

Intracellular recordings were made from mammalian vesical parasympathetic ganglia. A fast excitatory postsynaptic potential (EPSP) was abolished by hexamethonium (200 microM) in rabbit and feline ganglia. A slow inhibitory postsynaptic potential (IPSP) and a following slow EPSP were abolished by atropine (1 microM) in the feline ganglia. Bath application of adenosine (300 microM) depressed the amplitude of nicotinic fast EPSP by 48 +/- 4% in the rabbit ganglia. The action of adenosine was dose-dependent. An antagonist of A1-purinoceptors, 8-cyclopentyltheophylline (1-10 microM), inhibited the adenosine-induced depression but not the amplitude of fast EPSP. Adenosine (2-3 mM) did not significantly affect either the muscarinic slow IPSP, or the slow EPSP, in the feline ganglia. Adenosine also caused a hyperpolarization (1-5 mV) in 40% of the rabbit neurons and 66% of the feline neurons. However a purinergic IPSP was not recorded from either species. These data suggest diverse actions of adenosine in modulating cholinergic transmission in rabbit and feline vesical ganglia.

Adenosine↗

PubMed1999

Triggering action potentials in an axo-dendritic inhibitory synaptic terminal.

Intracellular activity of the slow adapting neurone (SAN) was recorded together with extracellular action potentials (APs) of SAN, fast adapting neurone and inhibitory fibre in the isolated stretch receptor of the moulting crayfish. Following strychnine application, spontaneous APs and seizure-like AP trains were observed. A delay of the inhibitory fibre APs relative to SAN inhibitory postsynaptic potential, their waveforms and their initiation by intracellular SAN hyperpolarization indicate that their generation was close to the inhibitory nerve terminal. Such antidromic (ectopic) APs assert their postsynaptic action on both receptor neurones via the axon reflex. The findings provide first evidence of antidromic APs generated in the vicinity of inhibitory terminals, their direct and axon reflex-mediated action on target neurones and support a hypothesis that increased terminal excitability contributes to seizure activity.

Action Potentials↗

PubMed1992

Persistent hyperexcitability in isolated hippocampal CA1 of kainate-lesioned rats.

1. Subcutaneous kainate injection in rats evoked acute seizures and led to cell loss in the hilus and areas CA1 and CA3, which resembled the pattern of hippocampal sclerosis often associated with temporal lobe epilepsy in humans. 2. Simultaneous intra- and extracellular recordings were performed in the stratum pyramidale of area CA1 while stimulating in the stratum radiatum close to the recording electrodes. Responses from control slices consisted of a brief excitatory postsynaptic potential (EPSP) with only one action potential, corresponding to a single extracellular population spike, followed by a clear biphasic inhibitory postsynaptic potential (IPSP). In slices from kainate-treated animals, however, stimulation evoked a prolonged EPSP, which often triggered multiple action potentials corresponding to multiple extracellular population spikes. 3. In slices from kainate-treated animals, the mean amplitude but not the duration of the stimulation-evoked IPSP was reduced. The extent of the kainate-induced loss of inhibition in area CA1 was highly variable. 4. Low concentrations of bicuculline in control slices led to a moderate hyperexcitability, which consisted of multiple population spikes and mirrored the responses observed in slices from kainate-treated animals in normal ACSF. Prolonged application of 10-30 microM bicuculline for > or = 30 min led to a much higher level of hyperexcitability, which was similar in slices from controls and kainate-treated rats. These findings are consistent with the hypothesis that the hyperexcitability of CA1 pyramidal neurons following kainate treatment is mainly due to decreased GABAA-receptor-mediated inhibition and that the loss of inhibition is only partial.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2006

Opposing inward and outward conductances regulate rebound discharges in olfactory mitral cells.

The olfactory bulb, a second-order sensory brain region, relays afferent input from olfactory receptor neurons to piriform cortex and other higher brain centers. Although large inhibitory postsynaptic potentials (IPSPs) are evident in in vivo intracellular recordings from mitral cells, the functional significance of these synaptic responses has not been defined. In many brain regions, IPSPs can function to either inhibit spiking by transiently suppressing activity or can evoke spiking directly by triggering rebound discharges. We used whole cell patch-clamp recordings from mitral cells in olfactory bulb slices to investigate the mechanisms by which IPSPs regulate mitral cell spike discharges. Mitral cells have unusual intrinsic membrane properties that support rebound spike generation in response to small-amplitude (3-5 mV) but not large-amplitude hyperpolarizing current injections or IPSPs. Rebound spiking occurring in mitral cells was dependent on recovery of subthreshold Na currents, and could be blocked by tetrodotoxin (TTX, 1 microM) or the subthreshold Na channel blocker riluzole (10 microM). Surprisingly, larger-amplitude hyperpolarizing stimuli impeded spike generation by recruiting a transient outward I(A)-like current that was sensitive to high concentrations of 4-aminopyridine and Ba. The interplay of voltage-gated subthreshold Na channels and transient outward current produces a narrow range of IPSP amplitudes that generates rebound spikes. We also found that subthreshold Na channels boost subthreshold excitatory stimuli to produce membrane voltages where granule-cell-mediated IPSPs can produce rebound spikes. These results demonstrate how the intrinsic membrane properties of mitral cells enable inhibitory inputs to bidirectionally control spike output from the olfactory bulb.

Animals↗

PubMed1991

Inhibitory substantia nigra inputs to the pedunculopontine neurons.

Responses of 43 pedunculopontine area (PPN area) neurons to electrical stimulation of the substantia nigra (SN) were studied in anesthetized rats. An intracellular recording technique was used to demonstrate that SN stimulation evoked hyperpolarizing potentials, which were identified by intracellular injections as inhibitory postsynaptic potentials (IPSPs). These IPSPs were often followed by a rebound depolarization that originates several spike potentials. These IPSPs were characterized as monosynaptic, with latencies varying from 1.0 to 8.5 ms. Similar results were observed in some animals with chronic unilateral coronal lesion just rostral to subthalamic nucleus (STH), which severed the rostral afferents. PPN are neurons were also antidromically activated by SN stimulation. Two PPN area projection neurons were clearly identified. Mean latency of one group was 0.71 ms; mean latency of the second group was 5.16 ms. The morphological analysis of a neuron inhibited by SN stimulation and labeled with horseradish peroxidase (HRP) demonstrated that the soma was fusiform in shape, with the axon originating in the soma and collaterals and a large dendritic field extending in the ventrodorsalis direction. The results indicate that the PPN area is reciprocally connected with the SN, which elicits an inhibitory effect on PPN area neurons.

Animals↗

PubMed2005

GABAB receptors in the medial septum/diagonal band slice from 16-25 day rat.

GABA(B) receptors are believed to play a role in rhythmic activity in the mammalian brain. The aim of our study was to examine the presynaptic and postsynaptic locations of these receptors in the medial septal diagonal band area (MS/DB), an area known to pace the hippocampus theta rhythm. Whole-cell patch recordings were made from parasagittal MS/DB slices obtained from the 16-25 day rat. Neurons were classified into GABAergic and cholinergic subtypes according to previous electrophysiological criteria. Bath application of the GABA(B) receptor agonist baclofen in the presence of tetrodotoxin, and brief tetanic fiber stimulation in the presence of ionotropic receptor antagonists, provided evidence for the presence of postsynaptic GABA(B) receptor transmission to GABAergic but not cholinergic neurons. Bath application of baclofen, at concentrations too low to elicit postsynaptic activity in MS/DB neurons, significantly reduced the amplitudes of stimulus-evoked ionotropic receptor inhibitory postsynaptic potentials (IPSPs) and excitatory postsynaptic potentials (EPSPs) and the paired pulse depression of these evoked potentials. Baclofen also significantly reduced the frequencies but not the amplitudes of miniature inhibitory postsynaptic currents (IPSCs) and excitatory postsynaptic currents (EPSCs), indicating the presence of presynaptic GABA(B) receptors on GABAergic and glutamatergic terminals in the MS/DB. Baclofen, also at a concentration too low to elicit postsynaptic activity, reduced the frequencies and amplitudes of spontaneous IPSCs and EPSCs recorded in the presence of 200-400 nM kainate. Rhythmic compound IPSCs at theta frequencies were recorded under these conditions in some neurons, and these rhythmic compound IPSCs were disrupted by the activation but not by the inhibition of GABA(B) receptors. These results suggest that GABA(B) receptors modulate rather than generate rhythmic activity in the MS/DB, and that this modulatory effect occurs via receptors located on presynaptic terminals.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1988

Inhibitory action of serotonin in CA1 hippocampal neurons in vitro.

The ionic mechanism of the inhibitory effect of serotonin was investigated in vitro in the CA1 region of the rat hippocampus by extra- and intracellular recordings. Local or bath applications of serotonin induced a long-lasting reduction of extracellularly recorded synaptic potentials and orthodromic population spikes without affecting the afferent volley or the antidromic population spike. Serotonin can also reduce the frequency of occurrence of spontaneous excitatory and inhibitory postsynaptic potentials without any reduction of input resistance of the pyramidal neuron. During the response to serotonin, the conductance increase evoked by GABA, the inhibitory neurotransmitter, was not changed. A direct postsynaptic effect of serotonin was demonstrated: local or bath applications of serotonin induced a tetrodotoxin-resistant hyperpolarization and conductance increase. The conductance change was not reduced by manual clamp of the neurons to the control resting membrane potential; therefore, a possible involvement of the sodium-potassium electrogenic pump is unlikely. When neurons were loaded with chloride, serotonin could still induce a hyperpolarization with an apparent reversal more negative than the resting membrane potential. When neurons were loaded with caesium, the hyperpolarization and the conductance increase evoked by serotonin were blocked. It is therefore concluded that serotonin increases potassium permeability. Similar effects were induced by a 5-HT1A ligand. The slow after hyperpolarization was reduced by serotonin; the calcium spike was reduced at the same time. In caesium loaded neurons, the spike duration was not modified by serotonin. In the presence of extracellular caesium (4-5 mM), the serotonin-induced hyperpolarization and the conductance change were blocked, but the effect of serotonin on calcium spikes persisted. Tetraethylammonium (5-10 mM) or 4-aminopyridine (0.5 mM) had no effect on the response to serotonin. These data indicate that serotonin has a postsynaptic inhibitory action by an activating potassium conductance. The possibility of a regulation of calcium currents is discussed. The possible role of serotonin on intrinsic synaptic transmission is also discussed.

Action Potentials↗

PubMed1990

On the presynaptic action of baclofen at inhibitory synapses between cultured rat hippocampal neurones.

1. (-)Baclofen reduces inhibitory postsynaptic potentials (IPSPs) and the associated synaptic currents (IPSCs) at inhibitory GABAergic synapses between cultured rat hippocampal neurones. The reversal potential for the IPSC is unaltered. 2. The effect of (-)baclofen is concentration dependent; the EC50 for (-)baclofen is approximately 5 microM. 3. Statistical analyses of the amplitude fluctuations of the IPSC in the presence of (-)baclofen suggested a presynaptic location for the depression of synaptic transmission by (-)baclofen. In control experiments, lowering extracellular Ca2+ produced similar effects. (-)Baclofen has no detectable postsynaptic actions in these cultured neurones. 4. Phaclofen (0.2-0.5 mM) increases IPSC amplitude but does not significantly block the depressant effect of (-)baclofen on synaptic transmission. 5. The effect of (-)baclofen is not blocked by pertussis toxin pre-treatment. 6. It is concluded that (-)baclofen acts presynaptically to reduce the release of GABA. The mechanism by which release is reduced may involve a phaclofen-insensitive GABAB receptor.

Action Potentials↗

PubMed2006

Subiculum network excitability is increased in a rodent model of temporal lobe epilepsy.

In this study, we used in vitro electrophysiology along with immunohistochemistry and molecular techniques to study the subiculum--a limbic structure that gates the information flow from and to the hippocampus--in pilocarpine-treated epileptic rats. Comparative data were obtained from age-matched nonepileptic controls (NEC). Subicular neurons in hippocampal-entorhinal cortex (EC) slices of epileptic rats were: (i) hyperexcitable when activated by CA1 or EC inputs; and (ii) generated spontaneous postsynaptic potentials at higher frequencies than NEC cells. Analysis of pharmacologically isolated, GABA(A) receptor-mediated inhibitory postsynaptic potentials revealed more positive reversal potentials in epileptic tissue (-67.8 +/- 6.3 mV, n = 16 vs. -74.8 +/- 3.6 mV in NEC, n = 13; P < 0.001) combined with a reduction in peak conductance (17.6 +/- 11.3 nS vs. 41.1 +/- 26.7 nS in NEC; P < 0.003). These electrophysiological data correlated in the epileptic subiculum with (i) reduced levels of mRNA expression and immunoreactivity of the neuron-specific potassium-chloride cotransporter 2; (ii) decreased number of parvalbumin-positive cells; and (iii) increased synaptophysin (a putative marker of sprouting) immunoreactivity. These findings identify an increase in network excitability within the subiculum of pilocarpine-treated, epileptic rats and point at a reduction in inhibition as an underlying mechanism.

Action Potentials↗

PubMed1988

Neuronal pathways for the lingual reflex in the Japanese toad.

1. Anuran tongue is controlled by visual stimuli for releasing the prey-catching behavior ('snapping') and also by the intra-oral stimuli for eliciting the lingual reflex. To elucidate the neural mechanisms controlling tongue movements, we analyzed the neuronal pathways from the glossopharyngeal (IX) afferents to the hypoglossal (XII) tongue-muscle motoneurons. 2. Field potentials were recorded from the bulbar dorsal surface over the fasciculus solitarius (fsol) to the electrical stimulation of the ipsilateral IX nerve. They were composed of three successive negative waves: S1, S2 and N wave. The S1 and S2 waves followed successive stimuli applied at short intervals (10 ms or less), whereas the N wave was strongly suppressed at intervals shorter than 500 ms. Furthermore, the S1 wave had lower threshold than the S2 wave. 3. Orthodromic action potentials were intra-axonally recorded from IX afferent fibers in the fsol to the ipsilateral IX nerve stimuli. Two peaks found in the latency distribution histogram of these action potentials well coincided with the negative peaks of the S1 and the S2 waves of the simultaneously recorded field potentials. Therefore, the S1 and S2 waves should represent the compound action potentials of two groups of the IX afferent fibers with different conduction velocities. 4. Ipsilateral IX nerve stimuli elicited excitatory postsynaptic potentials (EPSPs) in the tongue-protractor motoneurons (PMNs) and the tongue-retractor motoneurons (RMNs). Inhibitory postsynaptic potentials were not observed. 5. The EPSPs recorded in PMNs had mean onset latencies of 6.4 ms measured from the negative peaks of the S1 wave. The EPSPs were facilitated when paired submaximal stimuli were applied at intervals shorter than 20 ms, but were suppressed at intervals longer than 30 ms. Furthermore, the EPSPs were spatially facilitated when peripherally split two bundles of the IX nerve were simultaneously stimulated. 6. On the other hand, the EPSPs recorded in RMNs had shorter onset latencies, averaging 2.5 ms. In 14 of 43 RMNs, early and late EPSP components could be reliably discriminated. The thresholds for the early EPSP components were as low as those for the S1 waves, whereas for the late EPSP components the thresholds were usually higher than those for the S2 waves.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed1987

Motor cortical epileptic foci in vivo: actions of a calcium channel blocker on paroxysmal neuronal depolarizations.

Focal epileptiform activity was induced by local application of penicillin to the surface of the rat motor cortex. Neurons located within the epileptic focus displayed typical paroxysmal depolarization shifts (PDS). The participation of membrane calcium currents in the generation of PDS was examined by injecting the quaternized calcium entry blocker D890 into single neurons by iontophoresis or by pressure pulses. After intracellular injections of D890, PDS were depressed in amplitude by up to 55%. In a few cases the depression of PDS following intracellular application of D890 was preceded by a transient increase. Similar increases of PDS amplitude were obtained by injections of the calcium chelator EGTA. Control experiments in preparations without epileptic activity revealed that excitatory potentials elicited by thalamic stimulation and Cl(-)-dependent inhibitory postsynaptic potentials evoked by epicortical stimulation were not affected by intracellular D890. In these experiments successful intracellular drug application was verified by monitoring the transient shift of the Cl(-)-equilibrium potential induced by injection of KCl together with D890. It is concluded that in the penicillin-induced epileptic focus of the motor cortex Ca2+ inward currents participate in the generation of neuronal PDS.

Animals↗

PubMed1991

Origin of the secondary increase in firing probability of human motor neurons following transcranial magnetic stimulation. Studies in healthy subjects, type I hereditary motor and sensory neuropathy and multiple sclerosis.

In tonically active human motor neurons serving upper limb muscles there is a late rise in firing probability following transcranial magnetic stimulation termed the secondary peak (SP). The aim was to study the mechanism of SP and the pathway that mediates it. For this purpose, the response to transcranial magnetic stimulation of 62 repetitively firing low threshold single motor units from upper limb muscles was studied with peri-stimulus time histograms in 8 healthy subjects and in 13 patients with either Type I hereditary motor and sensory neuropathy (HMSN) or multiple sclerosis (MS). Separate peri-stimulus time histograms, constructed for trials in which the motor unit fired in the primary peak (PP) and those in which it fired in SP, showed that SP was not caused by a resumption of firing after the preceding PP. In the first dorsal interosseous muscle, the observed increase in the interval between PP and SP in patients with either HMSN or MS, when compared with healthy subjects, suggested that the pathway mediating SP had both peripheral and central components. Evidence for a peripheral component was substantiated by the observed slope of the line relating the latency of SP in different upper limb muscles to peripheral conduction distance, which was more than 3 times greater than that for PP, and by comparisons in the same motor unit made between the latency of responses to finger taps and to transcranial magnetic stimulation. Evidence for the origin of SP was consistent with a long loop reflex, or with collateral activation of gamma motor neurons and subsequent motor neuron firing from muscle afferent inputs. SP discharges were found to occur earlier than expected on the basis of the spontaneous motor unit firing rate, suggesting that SP was caused by the rising phase of an excitatory post-synaptic potential, rather than by the decay of an inhibitory postsynaptic potential.

Action Potentials↗

PubMed1990

Feed-forward inhibitory potentials and excitatory interactions in guinea-pig hippocampal pyramidal cells.

1. The patterns of inhibition in the CA1 region of the rat hippocampus were evaluated by focal proximal and distal stratum radiatum stimulation, during intracellular recording. The characteristics of isolated inhibitory responses and the interactions of excitatory and inhibitory potentials were analysed. 2. The amplitude of minimal inhibitory postsynaptic potentials (IPSPs) evoked by both proximal and distal stimulation averaged -0.51 +/- 0.24 mV (mean +/- S.D.; n = 32). These responses demonstrated little variability from trial to trial and showed no net trends in amplitude at a stimulation rate of 1 Hz. 3. Minimal IPSPs demonstrated a short latency to onset (2.90 +/- 1.58 ms for proximal and 3.64 +/- 1.39 ms for distal) at stimulation levels which were insufficient to evoke an extracellular field potential. Thus, minimal IPSPs were recruited through feed-forward circuitry, based on the rapid onset and the lack of activation of recurrent collaterals. 4. The minimal IPSPs showed a similar 10-90% rise time for proximal and distal responses. However, the half-width and decay time constant (from the peak) were more prolonged for the distal stimulation, indicating that a late IPSP component was evoked primarily by the distal stimulation. This late component was not observed in isolation at low stimulation intensities. 5. The conductance transient underlying the IPSPs was calculated using a neurone cable model. The proximal IPSP responses were simulated by an alpha input function (at the soma) with a peak conductance in the range of 2.5-45 nS (alpha = 1.75; reversal potential -1.0 to -10 mV). The distal IPSP shape was only partially reproduced by a longer single transient (alpha = 1.25), suggesting the presence of a second, slower component. However, insufficient data on this slower component precluded a more exact simulation of the distal IPSP response. 6. Analysis of interactions between minimal excitatory postsynaptic potentials (EPSPs) and IPSPs showed that often the rising as well as the falling phase of the EPSP could be affected by the IPSP. At small stimulation levels, minimal EPSPs and IPSPs were closely overlapping, but the IPSPs were of significantly longer duration than EPSP responses. 7. The composite EPSP waveform shape became progressively truncated with increasing afferent stimulation. Feed-forward inhibition limited the time course of excitation to a narrow window, approximately 3-5 ms wide. Feed-forward postsynaptic inhibition significantly limited both the duration and the overall efficacy of small EPSPs in CA1 pyramidal neurones.

Action Potentials↗

PubMed1988

Modulation of carotid sinus afferent input to nucleus tractus solitarius by parabrachial nucleus stimulation.

There is increasing evidence that the parabrachial nucleus (PBN) may be integrally involved in cardiovascular reflex regulation. In cats in which anesthesia was induced with pentobarbital and maintained with alpha-chloralose, we studied the effects of PBN stimulation on cardiovascular afferent inputs to nucleus tractus solitarius (NTS), the site of first central termination for cardiovascular afferent fibers. Electrical stimulation of PBN resulted in an initial excitation followed by prolonged inhibition of the spontaneous activity of NTS neurons activated by ipsilateral carotid sinus nerve (CSN) stimulation. In 53 units recorded extracellularly in and around NTS, the number of action potential responses to ipsilateral CSN stimulation was reduced 73 +/- 3% by a prior conditioning stimulus to PBN at an interval of 30-60 msec. CSN input to 10 units excited by selective baroreceptor stimulation was inhibited by the PBN conditioning stimulus, as were convergent inputs from contralateral CSN, vagus, and renal nerves. The inhibitory influence of the PBN stimulus lasted as long as 450 msec. We examined the mechanism for these phenomena in additional intracellular recording experiments. In 57 units, PBN stimulation evoked a long lasting (65-359 msec) membrane potential hyperpolarization. In 42 cells, the PBN evoked inhibitory postsynaptic potential (IPSP) was preceded by an excitatory postsynaptic potential (EPSP). CSN and convergent inputs were inhibited when timed to occur during the PBN induced IPSP. Conversely, CSN and convergent afferent nerves inhibited PBN input to NTS neurons with no associated change in membrane potential (n = 9 of 14). These data demonstrate for the first time a potent modulatory influence of PBN on NTS neurons processing cardiovascular afferent input.

Afferent Pathways↗

PubMed1997

A monosynaptic GABAergic input from the inferior colliculus to the medial geniculate body in rat.

The goal was to investigate possible monosynaptic GABAergic projections from the inferior colliculus (IC) to thalamocortical neurons of the medial geniculate body (MGB) in the rat. Although there is little evidence for such a projection in other sensory thalamic nuclei, a GABAergic, ascending auditory projection was reported recently in the cat. In the present study, immunohistochemical and tract-tracing methods were used to identify neurons in the IC that contain GABA and project to the MGB. GABA-positive projection neurons were most numerous in the central nucleus and less so in the dorsal and lateral cortex. They were rare in the lateral tegmental system and brachium of the IC. The dorsal nucleus of the lateral lemniscus also contained GABA-positive projection neurons. In brain slices, stimulation of the brachium produced monosynaptic inhibitory postsynaptic potentials in morphologically identified thalamocortical relay neurons. The inhibitory potentials cannot originate locally, because they persisted when ionotropic glutamatergic transmission was blocked. Typically, brachium stimulation elicited a GABAA-mediated inhibitory potential followed by an excitatory potential and a longer latency GABAB-mediated inhibitory potential. We conclude that the GABA-containing neurons of the IC make short-latency, monosynaptic inputs to the thalamocortical projection neurons in the MGB. Such inputs may distinguish the main auditory pathway from indirect or tegmental auditory pathways as well as from other sensory systems. Monosynaptic inhibitory inputs to the medial geniculate may be important for the regulation of firing patterns in thalamocortical neurons.

Animals↗

PubMed1991

Depression of the fast IPSP underlies paired-pulse facilitation in area CA1 of the rat hippocampus.

1. Intracellular recordings from CA1 pyramidal neurons in the rat hippocampal slice have been used to study synaptic transmission after maximal orthodromic stimulation of the Schaffer collateral-commissural fibers. Paired-pulse stimulation was used to investigate how the first (conditioning) stimulation influenced the response to the second (test) stimulation. 2. When the test stimulation was delivered up to approximately 4 s after the conditioning stimulation, the late phase of the excitatory postsynaptic synaptic potential (EPSP) was increased ("late-phase facilitation") whereas the fast (f-) and the slow (s-) inhibitory postsynaptic potentials (IPSPs) were depressed. 3. In terms of appearance and time course, facilitation of the intracellularly recorded EPSP was similar to that of the extracellularly recorded field EPSP in stratum radiatum. 4. The s-IPSP is not involved in facilitation of the EPSP. To show this, we counteracted the s-IPSP either by repolarizing the membrane potential to the resting level or by intracellularly injecting the quaternary lignocaine derivative QX 314. Facilitation of the late phase of the EPSP was unaffected by either procedure. 5. The conditioned response was modified in two ways when the stimulation was delivered at the equilibrium potential for the f-IPSP (Ef-IPSP) and the s-IPSP had been blocked by intracellular injection of QX 314. The amplitude of the EPSP was increased, and the repolarizing phase was delayed with an apparent depolarizing shift of Ef-IPSP. This effect was present at pulse intervals greater than 20 ms and was maximal after 150 ms. Facilitation could be detected at interpulse intervals of up to 4 s. 6. The gamma-aminobutyric acid-B (GABAB) agonist baclofen (1 microM) reduced late-phase facilitation by preferentially increasing the unconditioned response, such that this came to resemble a conditioned response in control medium. 7. The f-IPSP was isolated pharmacologically to investigate its role in the facilitation of the EPSP. This was done by blocking the s-IPSP with QX314 and the EPSP with a mixture of the N-methyl-D-aspartate (NMDA) receptor blocker, 2-amino-5-phosphonovaleric acid (APV, 50 microM), and the non-NMDA receptor blocker 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM). An f-IPSP was then evoked by stimulating the interneurons directly. This potential could be blocked by the GABAA receptor antagonist bicuculline (20 microM), thereby confirming the successful isolation of GABAAergic transmission. 8. With paired-pulse stimulation, the amplitude of the conditioned f-IPSP was depressed.(ABSTRACT TRUNCATED AT 400 WORDS)

2-Amino-5-phosphonovalerate↗