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PubMed1988

Buspirone attenuates synaptic activation of hippocampal pyramidal cells.

The actions of 5-hydroxytryptamine (5-HT) and buspirone, an anxiolytic agent that displays high and selective affinity for 5-HT1A receptor sites, on synaptic activation of hippocampal CA1 pyramidal cells were studied in vitro. Whereas 5-HT application leads to a rapid hyperpolarization and decreased input resistance in pyramidal cells, buspirone has no measurable effects on membrane potential and input resistance. However, unlike 5-HT, buspirone application leads to a gradual and reversible reduction in excitatory postsynaptic potentials (EPSPs) elicited by stimulation of afferents in the stratum radiatum. Concurrent with this attenuation of the EPSP, buspirone decreases the excitability of afferent fibers in the stratum radiatum as evidenced by conduction slowing, increased refractory period, and decreased ability to generate repetitive impulses. 5-HT has no measurable effect on the afferent fibers. The attenuation of the EPSPs and the decrease in afferent fiber excitability appear to be independent of 5-HT receptors as 5-HT neither shares nor antagonizes the effects of buspirone. Thus, both 5-HT and buspirone can contribute to reduced spike activity in pyramidal cells, but they do so via different mechanisms: 5-HT hyperpolarizes pyramidal cells whereas buspirone attenuates their synaptic activation, possibly via action on the presynaptic fibers in the stratum radiatum.

Afferent Pathways↗
PubMed1996

Synaptic interactions between primate precentral cortex neurons revealed by spike-triggered averaging of intracellular membrane potentials in vivo.

To document synaptic interactions between neurons in the precentral cortex of macaque monkeys, we recorded in vivo the intracellular (IC) membrane potentials of cortical neurons simultaneously with extracellular (EC) action potentials of neighboring cells. The synaptic potentials correlated with EC spikes were obtained by spike-triggered averages (STA) of the IC membrane potentials for 373 cell pairs recorded in anesthetized and awake behaving monkeys. Sixty-three STAs (17%) showed excitatory postsynaptic potentials (EPSPs), beginning after the trigger spike. Pure EPSPs had onset latencies of 0.9 +/- 0.7 msec (mean +/- SD) and amplitudes of 226 +/- 130 microV. Sixteen STAs (4%) showed postspike inhibitory postsynaptic potentials (IPSPs), with onset latencies of 0.4 +/- 0.4 msec and amplitudes of -274 +/- 188 microV. The most common waveform, observed in 82% of the STAs with features, was a broad depolarization straddling the trigger spikes, reflecting synchronized synaptic input to both IC and EC neurons. These average synchronous excitation potentials (ASEPs) began 14.3 +/- 6.6 msec before the trigger spike and had amplitudes of 1064 +/- 867 microV. Twenty-three STAs (6%) showed an average synchronous inhibitory potential (ASIP): a hyperpolarization beginning before the trigger spike and reflecting IPSPs produced by a group of local inhibitory cells synchronized with the trigger cell. ASIPs had an onset latency of -5.5 +/- 2.7 msec and amplitude of -589 +/- 502 microV. Combinations of synchronous and postspike potentials were also observed. Successive recordings provided examples of convergent and divergent connections between EC and IC cells. Neuron pairs with depolarizing postsynaptic potentials (PSPs) in the STA yielded peaks in the cross-correlograms of the IC and EC action potentials; the peak area was proportional to the amplitude of the PSP. These data suggest that a significantly larger proportion of cortical neurons interact through synchronous activity than through simple serial interactions; moreover, synchronous excitation affected more widely separated cell pairs than EPSPs and IPSPs, which were seen most often among the closest cells.

Action Potentials↗
PubMed1983

Structure of the piriform cortex of the opossum. III. Ultrastructural characterization of synaptic terminals of association and olfactory bulb afferent fibers.

Terminals of olfactory bulb afferent (OB) and association (ASSN) fibers within the piriform cortex were characterized ultrastructurally. Identification was by electron microscopic (EM) autoradiography following injections of tritiated amino acids into the olfactory bulb and anterior piriform cortex. The results show that terminals of both fiber systems contain round vesicles and make asymmetrical synaptic contacts predominantly onto dendritic spines. Profiles with pleomorphic vesicles do not appear to be labeled from either site. Since there is strong evidence that both fiber systems generate excitatory postsynaptic potentials (EPSPs) in pyramidal cells, these results provide additional examples in the mammalian CNS of terminals with round vesicles and asymmetrical contacts that mediate an excitatory effect. Percentage density analysis and quantitative study of a large number of heavily labeled terminals revealed that while OB and ASSN terminals are similar in terms of vesicle shape and contact type, they differ in many morphological details including pre- and postsynaptic profile size, the packing density and distribution of synaptic vesicles, synaptic contact shape, and the presence of overlying neuroglial lamellae. However, large variations in appearance of different terminals of the same type are also present so that a small percentage of OB and ASSN terminals are indistinguishable morphologically in the absence of label. An important finding of the quantitative analysis is that spines contacted by lateral olfactory tract (LOT) terminals appear to be of two types based on a bimodal distribution in size and differences in morphology, while spines contacted by ASSN terminals appear to be of a single type. Comparison of these data with results from Golgi analysis indicates that ASSN terminals predominantly contact pyramidal cell spines while OB terminals contact both pyramidal and semilunar cell spines. Quantitative analysis of synaptic vesicles revealed that histograms of vesicle size for OB and ASSN terminals are virtually identical in shape, but peaks are slightly displaced (ASSN vesicles are 5% larger; significant with P less than .002). An analysis of the laminar distribution of OB and ASSN synaptic terminals revealed that while most OB terminals are segregated in layer Ia and most ASSN terminals in layer Ib, occasional OB terminals are observed up to approximately 50 micro deep to the Ia-Ib boundary and occasional ASSN terminals up to approximately 50 micro superficial to this boundary.

Afferent Pathways↗
PubMed1991

Excitatory and inhibitory effects of norepinephrine on myenteric neurons of the guinea-pig gastric corpus.

The effects of norepinephrine on the electrical and synaptic behaviour of gastric myenteric neurons were investigated in vitro by using conventional intracellular recording methods. Application of norepinephrine (0.1-10 microM) evoked an excitatory effect in 40% of all cells tested. Excitation consisted of a depolarization of the membrane potential associated with increased spike discharge. Phentolamine or prazosin reversibly abolished and (-)phenylephrine mimicked the excitatory norepinephrine response. Yohimbine and clonidine had no effect. Focal electrical stimulation of interganglionic fibre tracts evoked fast excitatory postsynaptic potentials (fEPSPs) in all neurons. Only a minority of these fEPSPs were blocked by norepinephrine. However, fEPSPs evoked by stimulating presumably extrinsic nerves were always totally blocked by norepinephrine. The inhibitory effect of norepinephrine on fEPSPs could be reversed by phentolamine and yohimbine and mimicked by clonidine. Prazosin and phenylephrine had no effect. Isoproterenol and propranolol modified neither the excitatory nor the inhibitory effects. The results indicate that the excitatory effects of norepinephrine on gastric myenteric neurons are mediated by postsynaptic alpha 1 receptors, whereas the inhibitory effects are mediated by presynaptic alpha 2 receptors, which are located presumably on vagal extrinsic nerves. There was no evidence for beta-receptor-mediated effects in gastric myenteric neurons.

Animals↗
PubMed1979

Orthodromic activation of hippocampal CA1 region of the rat.

(1) The posterior alveus (PA), the anterior alveus (AA) and the Schaffer collaterals (SCH) evoked field potential components which were organized as parasagittal strips of various widths. Spatially continuous and interactive lamellae are suggested. (2) By correlation with unit activities, the early postsynaptic components evoked by PA, AA and SCH were inferred to be extracellular excitatory postsynaptic potentials (EPSPs) and the late, long-duration components, the inhibitory postsynaptic potentials (IPSPs). The hypothesis that interneurons as well as pyramidal cells generate the field is proposed and discussed. (3) One- and two-dimensional profiles of deep evoked potentials and current source-sink analysis revealed excitatory synapses in stratum oriens for the PA and AA inputs and in stratum radiatum for the SCH input. The late dipole field evoked by PA and AA possessed current sources in strata radiatum and pyramidale, the sites of the inhibitory synapses. The late dipole field evoked by SCH had another component possibly generated by recurrent activity, afterpotentials or relayed activity through CA3.

Animals↗
PubMed1991

Simulations of cortical pyramidal neurons synchronized by inhibitory interneurons.

1. The interaction between inhibitory interneurons and cortical pyramidal neurons was studied by use of computer simulations to test whether inhibitory interneurons could assist in phase-locking postsynaptic cells. Two models were used: a simplified model, which included only 3 membrane channels, and a detailed 11-channel model. 2. The 11-channel model included most of the ion channels known to be present in neocortical pyramidal neurons as well as calcium diffusion and other membrane mechanisms. The kinetics for the channels were obtained from voltage-clamp studies in a variety of preparations. The parameters were then adjusted to produce repetitive bursting similar to that seen in some cortical pyramidal cells entrained during visual stimulation. 3. Phase-locking to a train of inhibitory postsynaptic potentials (IPSPs) located on or near the soma was observed in the 3-channel model cell subjected to random synaptic bombardment. In the 11-channel model, phase-locking due to multiple IPSPs was compared with phase-locking due to multiple excitatory postsynaptic potentials (EPSPs). Phase-locking began to occur when 20% of the IPSPs (20/100) or 40% of the EPSPs (4,000/10,000) were synchronized. The exact percentages differed with different 11-channel models, but either EPSPs or IPSPs would generally produce entrainment with approximately 40% synchronization. Thus 40 inhibitory boutons had an effect equivalent to 4,000 excitatory boutons in producing phase-locking. 4. Phase-locking with IPSPs in these models was possible because the IPSPs could cause either an increase or a decrease in firing rate over a limited range. The IPSPs served a modulatory role, increasing the rate of firing in some cases and decreasing it in others, depending on the state of the cell. 5. We examined frequency entrainment by IPSPs. In the 3-channel model, frequency entrainment of a postsynaptic cell was observed with a rapid train of strong (20-100 nS), brief, compound IPSPs. A 40-Hz compound IPSP train of 60 nS entrained cells having initial firing rates between 32 and 47 Hz. Below this range, cells could be partially entrained. Above the range, entrainment would fail. Frequency entrainment in the 3-channel model generally occurred on the first cycle after onset of the IPSPs. 6. Phase-locking and frequency entrainment were less robust in the 11-channel model. This was partly because bursts rather than individual spikes were being entrained. A 40-Hz, 90-nS compound IPSP train entrained a model cell upward from 34 Hz. Downward frequency entrainment also occurred.(ABSTRACT TRUNCATED AT 400 WORDS)

Calcium Channels↗
PubMedDate not supplied

[Mechanism of action of protirelin tartrate (TRH-T) on spinal motor neurons].

Thyrotropin releasing hormone (TRH), an endogenous tripeptide of the spinal cord, is being used in clinical trials for the treatment of neurological disorders involving the spinal function. Experiments have been carried out on rat lumbar motoneurons identified by their action potentials evoked by antidromic ventral root stimulation. Glass microelectrodes containing a concentrated KCl solution were used for intracellular electrophysiological findings while the specimen was continuously perfused with oxygenated saline solution. Previous experiments conducted in our laboratory had shown that TRH (50 mumol) has an intense depolarizing activity on frog motoneurons and that it is capable of considerably increasing excitatory postsynaptic potentials. In an ongoing trial in rat neurons we have observed how TRH produces slowly developing but persisting motoneuron depolarization characterized by steady action potential discharges. This phenomenon is different from the much more rapid and shorter effect of glutamate which is thought to be the excitatory neurotransmitter of these neurons. The capacity of TRH to generate a series of action potentials without any apparent "fatigue" is an interesting and unusual property. In order to explain this property we pharmacologically isolated the neurons by means of tetrodotoxin treatment and recorded their ionic conductance. While TRH was acting the conductance decreased considerably, indicating that synaptic signals are amplified in this new condition of the postsynaptic membrane. Voltage clamp studies have suggested that this decrease in conductance occurs within a range of relatively negative membrane potentials and probably consists in the blocking of voltage-dependent, tendentially repolarizing ion channels (perhaps potassium).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Quantal components of the synaptic potential induced in hippocampal neurons by activation of granule cells, and the effect of 2-amino-4-phosphonobutyric acid.

The probabilistic nature of excitatory postsynaptic potentials (EPSPs) induced monosynaptically in CA3 neurons by impulses of granule cells was studied in thin transverse sections of the guinea pig hippocampus. More than 600 EPSPs were recorded under several conditions, their amplitudes were measured, and histograms representing the EPSP amplitude distribution were constructed. Quantal parameters were estimated by the method of maximum likelihood. Of 9 neurons examined in the control solution, one neuron showed an exceptionally large number of transmission failures. The amplitude distribution of EPSPs recorded from this neuron could be described by Pascal statistics, but not by binomial or Poisson statistics. The EPSP amplitude distribution from the other neurons could be described by either binomial, Poisson, or Pascal predictions with a minor preference for the last statistic. When an apparently homogeneous group of data was divided into two subgroups and parameters were estimated separately, inconsistent values were obtained in some neurons with no failures. 2-Amino-4-phosphonobutyric acid (APB) suppressed the EPSPs reversibly at relatively low concentrations. Theoretical curves calculated according to the Pascal statistics fit quite well to the entire amplitude distribution of EPSPs recorded under the action of APB. The suppression of EPSPs by APB was accompanied by a marked decrease in mean quantal content (m) with no significant reduction in mean quantal amplitude (q). A quantum induced an increase in membrane conductance of about 150 pS. These results suggest that the release probability of the mossy fiber terminal fluctuates temporally according to a gamma distribution, and that APB reduces the liberation of the transmitter from mossy fiber terminals, thereby suppressing transmission between mossy fibers and CA3 neurons.

Aminobutyrates↗
PubMed1998

Modulation by substance P of synaptic transmission in the mouse hippocampal slice.

The modulatory action of substance P on synaptic transmission of CA1 neurons was studied using intra- or extracellular recording from the mouse hippocampal slice preparation. Bath-applied substance P (2-4 microM) or the selective NK1 receptor agonist substance P methylester (SPME, 10 nM-5 microM) depressed field potentials (recorded from stratum pyramidale) evoked by focal stimulation of Schaffer collaterals. This effect was apparently mediated via NK1 receptors since it was completely blocked by the selective NK1 antagonist SR 140333. The field potential depression by SPME was significantly reduced in the presence of bicuculline. Intracellular recording from CA1 pyramidal neurons showed that evoked excitatory postsynaptic potentials (EPSPs) and evoked inhibitory postsynaptic potentials (IPSPs) were similarly depressed by SPME, which at the same time increased the frequency of spontaneous GABAergic events and reduced that of spontaneous glutamatergic events. The effects of SPME on spontaneous and evoked IPSPs were prevented by the ionotropic glutamate receptor blocker kynurenic acid. In tetrodotoxin (TTX) solution, no change in either the frequency of spontaneous GABAergic and glutamatergic events or in the amplitude of responses of pyramidal neurons to 4 microM alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) or 10 microM N-methyl-D-aspartate (NMDA) was observed. On the same cells, SPME produced minimal changes in passive membrane properties unable to account for the main effects on synaptic transmission. The present data indicate that SPME exerted its action on CA1 pyramidal neurons via a complex network mechanism, which is hypothesized to involve facilitation of a subset of GABAergic neurons with widely distributed connections to excitatory and inhibitory cells in the CA1 area.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1992

Cyclic adenosine 3'5'-monophosphate potentiates excitatory amino acid and synaptic responses of rat spinal dorsal horn neurons.

Intracellular recordings were made from rat dorsal horn neurons in the in vitro slice preparation to study the actions of cyclic adenosine 3',5'-monophosphate (cyclic AMP). In the presence of TTX, bath application of the membrane permeable analogue of cyclic AMP, 8-Br cyclic AMP (25-100 microM) caused a small depolarization of the resting membrane potential accompanied by a variable change in membrane input resistance. In addition, 8-Br cyclic AMP caused a long-lasting increase in the spontaneous synaptic activity and the amplitude of presumed monosynaptic excitatory postsynaptic potentials evoked in the substantia gelatinosa neurons by orthodromic stimulation of a lumbar dorsal root. When the fast voltage-sensitive Na conductance was blocked by TTX, 8-Br cyclic AMP enhanced in a reversible manner, the depolarizing responses of a proportion of dorsal horn neurons to N-methyl-D-aspartic acid (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), quisqualic acid (QA) and kainic acid (KA). The effects of 8-Br cyclic AMP on the resting membrane potential and the NMDA response of dorsal horn neurons were mimicked by reducing phosphodiesterase activity with bath application of 3-isobutyl-1-methylxanthine, but not by cyclic AMP applied extracellularly. Moreover, we have found that intracellular application of a protein inhibitor of cyclic AMP-dependent protein kinase (PKI) into dorsal horn neurons prevents the 8-Br cyclic AMP-induced potentiation of the NMDA response of these cells. These results suggest that in the rat spinal dorsal horn the activation of the adenylate cyclase-cyclic AMP-dependent protein kinase system may be involved in the enhancement of the sensitivity of postsynaptic excitatory amino acid (NMDA, AMPA, KA) receptors and modulation of primary afferent neurotransmission, including nociception.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1993

Giant cells of the dorsal cochlear nucleus of mice: intracellular recordings in slices.

1. In slices of the murine cochlear nuclear complex, intracellular recordings were made from five giant cells that were identified by intracellular labeling with biocytin. Giant cells form one of the two output pathways of the dorsal cochlear nucleus (DCN). Understanding how neuronal circuits and intrinsic electrical properties interact to control the firing of giant cells is a step toward understanding what acoustic information is conveyed through these cells. 2. Cell bodies of the labeled giant cells lay in the deep layer of the DCN. Dendrites, widespread both along the isofrequency axis and along the tonotopic axis, occupied mainly the deep layer, but some distal ends strayed into the molecular layer. Axons of giant cells were large, varying between 1 and 2 microns diam, and left through the dorsal acoustic stria. They were not observed to branch in the cochlear nuclei. 3. Giant cells fired large, overshooting action potentials that were followed by two afterhyperpolarizations. The first brought the membrane potential below rest, independent of the strength of injected current. The more variable second one produced either an undershoot or an inflection in the membrane potential between action potentials. 4. In each of the five labeled giant cells, shocks to the nerve root or to the anteroventral cochlear nucleus (AVCN) evoked a monosynaptic excitatory postsynaptic potential and two tandem inhibitory postsynaptic potentials (IPSPs) in the first 10 ms. Later IPSPs followed after latencies of between 10 and 50 ms. Monosynaptic excitation was usually cut short by the inhibition. 5. Strychnine, at 1 microM, blocked all IPSPs in the one giant cell tested, indicating that inhibitory input to this giant cell from circuits intrinsic to the cochlear nuclear complex was glycinergic. 6. The location of afferents was mapped for two giant cells. Both excitatory and inhibitory inputs to giant cells could be driven by the local application of glutamate to many loci in the AVCN and posteroventral cochlear nucleus, indicating that the ventral cochlear nucleus VCN contains interneurons that are monosynaptically or polysynaptically connected to giant cells. 7. An interpretation consistent with the results is that giant cells are excited by auditory nerve fibers and are inhibited by tuberculoventral cells. Giant cells may also be excited by granule or T stellate cells.

Animals↗
PubMed2001

Zinc co-localizes with GABA and glycine in synapses in the lamprey spinal cord.

The presence of zinc in synaptic terminals in the lamprey spinal cord was examined utilizing a modification of the Timm's sulfide silver method and with the fluorescent marker 6-methoxy-8-quinolyl-p-toluenesulfonamide (TSQ). Axons labeled with a Timm's staining method were predominantly located in the lateral region of the dorsal column. This correlated with a maximum of TSQ fluorescence in this region of the spinal cord. Single labeled terminals accumulating Timm reaction product were also found throughout the gray matter and fiber tracts. At the ultrastructural level, zinc was located in a population of synaptic terminals that co-localized gamma-aminobutyric acid (GABA) and glycine. Possible effects of Zn2+ on neuronal activity were examined. In spinobulbar interneurons, which receive GABAergic input in the dorsal column, zinc potentiated responses to GABA application, but it did not affect responses to GABA in motoneurons. Responses in motoneurons to pressure application of glycine were also not affected by Zn2+. Zinc, however, potentiated monosynaptic glycinergic inhibitory postsynaptic potentials (IPSPs) evoked in motoneurons by inhibitory locomotor network interneurons and increased frequency, but not amplitude of spontaneous miniature IPSPs recorded in the presence of tetrodotoxin (TTX), suggesting presynaptic effects. Glutamate responses and the amplitude of monosynaptic excitatory postsynaptic potentials (EPSPs) in motoneurons were reduced by zinc. These effects appeared to be mediated largely postsynaptically through an effect on the N-methyl-D-aspartate (NMDA) component of the glutamatergic input. Our results thus show that free zinc is present in inhibitory synaptic terminals in the lamprey spinal cord, and that it may function as a modulator of inhibitory synaptic transmission.

Aminoquinolines↗
PubMed1993

CA3 neuron excitation and epileptiform discharge are sensitive to osmolality.

1. The clinical signs of rapidly developing overhydration commonly include generalized tonic-clonic seizure, which can be combatted by raising plasma osmolality. How cortical neurons respond to osmotic imbalance has been addressed only recently. In the CA3 cell region of hippocampal slices, lowered osmolality (-40 mOsm) rapidly swelled cells, increasing field potential amplitude over a period of 8 min and thereby elevating field effects and associated neuronal synchronization. 2. Over a longer time course (10-30 min), spontaneous excitatory postsynaptic potential (EPSP) amplitude gradually increased in 7 of 10 CA3 neurons recorded intracellularly. In nine additional CA3 cells, hyposmolality gradually induced combinations of action potential discharge, endogenous bursting, and increased synchronized synaptic input. All of these effects reversed in normosmotic ACSF. 3. Hyperosmotic artificial cerebrospinal fluid (ACSF) using mannitol reduced field potentials and dramatically lowered CA3 excitability by reducing spontaneous EPSP amplitude and associated bursting. Again, the gradual onset (10-30 min) of changes in spontaneous EPSP amplitude appeared independent of field potential changes, which were already maximal by 8 min. 4. Cutting mossy fibers did not affect the excitability changes induced by osmotic stress noted above. The EPSP/inhibitory postsynaptic potential (IPSP) sequence evoked from mossy fibers or stratum oriens was unaltered by osmotic change and so did not represent osmosensitive afferent input to CA3 neurons. Furthermore, as measured at the soma, resting membrane potential, cell input resistance, and the action potential threshold were unchanged in all cells. It followed that, because the CA3 neurons themselves were not responsive, a recurrent excitatory pathway could not represent the osmosensitive input.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Long-term depression but not potentiation is induced in Ca(2+)-chelated visual cortex neurons.

An entry of Ca2+ into postsynaptic sites may play a role in the induction of long-term potentiation (LTP) of synaptic transmission in the visual cortex. To test this hypothesis, a Ca(2+)-chelator was injected into layer II/III neurons of sliced visual cortex obtained from young rats, and excitatory postsynaptic potentials (EPSPs) of these cells to test stimulation of the white matter were observed before and after tetanic stimulation of the same site. To confirm the effectiveness of the tetanus, field potentials reflecting the activities of many cells were recorded with another extracellular electrode. The chelator injection led to long-term depression (LTD) of EPSPs following tetanic stimuli which simultaneously induced LTP of field potentials derived from unchelated cells in most of the slices tested. This suggests that a low concentration of post-synaptic, free Ca2+, when associated with tetanic inputs, may lead to LTD while a rise of Ca2+ may lead to LTP.

Animals↗
PubMed1989

Responses of rat lateral hypothalamic neuronal activity to fastigial nucleus stimulation.

1. The aim of this study was investigation of neuronal mechanisms underlying inputs from the fastigial nucleus (FN) to the lateral hypothalamic area (LHA). 2. In male anesthetized rats, 295 extracellular and 82 intracellular recordings of LHA responses to electrical stimulation of the FN, which elicited stimulus-locked pressor responses, were examined. 3. Contralateral FN stimulation evoked three types of responses in 48% of spontaneously firing LHA neurons: inhibition with 11 +/- 6 (SD) ms latency followed by excitation (30%), excitation with 15 +/- 12.5 ms latency (14%), and excitation followed by inhibition with 6 +/- 4 ms latency (4%). 4. Contralateral FN stimulation after transection of the inferior cerebellar peduncle (ICP), which resulted in a substantial fall of the fastigial pressor response, also evoked the three types of responses. These responses were unaffected by transection of the ICP. 5. Neuronal activity was recorded intracellularly from 82 LHA neurons, of which 36 (44%) responded to FN stimulation. Of the 36 neurons, 24 showed inhibitory postsynaptic potentials (IPSPs) with a mean latency of 7.5 +/- 2 ms. Of the 24 neurons, 16 were checked for change in IPSP latency with stimulus intensity, and 11 were considered to be monosynaptically connected since their latencies were constant when FN stimulation intensity was changed. The remaining 12 exhibited excitatory postsynaptic potentials (EPSPs) with a longer latency of 10.5 +/- 3 ms, which indicated polysynaptic conduction. The reversal potentials of the IPSP and EPSP were estimated to be about -77 mV and -13 mV, respectively. 6. Most glucose-sensitive neurons (78%), which were identified by their inhibition in response to electrophoretically applied glucose, were inhibited by FN stimulation, whereas only 7% of the glucose-insensitive neurons responded to such stimulation. 7. From the results, it was concluded that LHA neurons receive inhibitory monosynaptic and excitatory polysynaptic inputs from the FN via the superior cerebellar peduncle. These connections may contribute to hypothalamic modulation of feeding behavior.

Animals↗
PubMed1988

Modulation of synaptic transmission in autonomic ganglia mediated via the activation of postganglionic muscarinic M1 receptors.

The facilitatory actions of muscarine on synaptic transmission were measured in rat superior cervical ganglia in vitro. Muscarine (300 nmol/l) induced increases in submaximal population action potentials, which were mimicked by the M1 receptor agonist McN-A-343 (1 mumol/l) and antagonized by the M1 receptor antagonist pirenzepine (100 nmol/l) and telenzepine (100 nmol/l), but not by the M2 receptor antagonist AF-DX 116 (1 mumol/l). Slow excitatory postsynaptic potentials recorded from curarized rabbit isolated superior cervical ganglia were also blocked by telenzepine (300 nmol/l) but not by AF-DX 116 (3 mumol/l). It is concluded that M1 receptors mediate the excitatory actions of muscarinic agonists in these sympathetic ganglia.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1993

Depression of glutamatergic and GABAergic synaptic responses in striatal spiny neurons by stimulation of presynaptic GABAB receptors.

The influence of gamma-aminobutyric acidB (GABAB) receptor stimulation on the excitatory and inhibitory synaptic potentials and membrane properties of identified striatal spiny neurons was examined in a corticostriatal slice preparation. Stimulation of the subcortical white matter evoked a monosynaptic, excitatory postsynaptic potential (EPSP) and a polysynaptic, inhibitory postsynaptic potential (IPSP) in spiny neurons. The EPSP had two components: a large amplitude response which could be blocked by the kainate/quisqualate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), and a small amplitude, long-duration depolarization which could be blocked by the N-methyl-D-aspartate receptor antagonist, d-(-)-2-amino-5-phosphonovaleric acid (APV, 100 microM). The IPSP was observed as a membrane depolarization when recorded from neurons at resting membrane potential. However, when neurons were injected with the Na(+)-channel blocker, QX-314, allowing cells to be depolarized above their spike thresholds, a prominent hyperpolarizing IPSP was readily observed which could be blocked by the GABAA antagonist, bicuculline (10-50 microM). This bicuculline-sensitive IPSP was responsible for the inhibition of EPSP amplitude and probability of spike discharge revealed using paired stimulation of the subcortical white matter. The amplitude of both the EPSP and the IPSP were depressed by the GABAB receptor agonist, p-chlophenyl-GABA (baclofen, 0.5-100 microM) in a concentration-dependent manner. Baclofen also blocked paired stimulus inhibition of spike discharge. These effects of baclofen persisted in slices in which the cortex was removed and were reversed by the GABAB receptor antagonist, 3-amino-3-hydroxy-2-(4-chlorophenyl)-propanesulphonic acid (saclofen, 100-500 microM). In contrast to its profound influence on synaptic input, baclofen did not alter resting membrane potential, input resistance, membrane current-voltage relationship, or spike threshold of the cells recorded, and therefore did not appear to exert direct postsynaptic effects on the striatal spiny neurons. Taken together, these data indicate that the depressant effects of baclofen on EPSPs are mediated through GABAB receptors located on the terminals of glutamatergic afferents within the striatum. Moreover, the results suggest that the actions of baclofen on IPSPs and paired stimulus inhibition are produced by activation of GABAB receptors within the striatum at a site presynaptic to spiny neurons, either on the terminals of GABAergic afferents or on an interposed non-spiny GABAergic cell. Thus, GABAB hetero- and auto-receptors have the capacity to provide a negative feedback mechanism through which the major excitatory and inhibitory inputs to striatal spiny neurons are regulated.

2-Amino-5-phosphonovalerate↗
PubMed1996

Visual potentiation of vestibular responses in lamprey reticulospinal neurons.

The lamprey normally swims with the dorsal side up. Illumination of one eye shifts the set-point of the vestibular roll control system, however, so that the animal swims with a roll tilt towards the source of light (the dorsal light response). A tilted orientation is often maintained for up to 1 min after the stimulation. In present study, the basis for this behaviour was investigated at the neuronal level. The middle rhombencephalic reticular nucleus (MRRN) is considered a main nucleus for the control of roll orientation in lampreys. Practically all MRRN neurons receive vestibular and visual input and project to the spinal cord. Earlier extracellular experiments had shown that optic nerve stimulation potentiates the response to vestibular stimulation in the ipsilateral MRRN. This most likely represents a neural correlate of the dorsal light response. Experiments were carried out in vitro on the isolated brainstem of the silver lamprey (Ichthyomyzon unicuspis). MRRN cells were recorded intracellularly, and the overall activity of descending systems was monitored with bilateral extracellular electrodes. The responses to 10 Hz optic nerve stimulation and 1 Hz vestibular nerve stimulation, and the influence of optic nerve stimulation on the vestibular responses, were investigated. In most preparations, optic nerve stimulation excited practically all ipsilateral MRRN cells. After stimulation, the cell was typically depolarized and showed an increased level of synaptic noise for up to 80 s. In contralateral MRRN neurons, optic nerve stimulation usually evoked hyperpolarization or no response. Vestibular nerve stimulation evoked compound excitatory postsynaptic potentials (EPSPs) or spikes in approximately 90% of the cells, both ipsilaterally and contralaterally. A smaller subpopulation of MRRN cells (approximately 10%) received vestibular inhibition. In 26 of 48 recorded MRRN cells, the response to vestibular stimulation was potentiated after ipsilateral optic nerve stimulation. The potentiation was seen in cells receiving either excitatory or inhibitory vestibular input as an increase in EPSP amplitude/spiking (85%) and a decrease in inhibitory postsynaptic potential amplitude (15%) respectively. In most cases the vestibular responses did not return to control levels during the testing period (10-30 min), and thus the visual stimulation most likely induced long-lasting changes in the functional connectivity of the role control network, in addition to the short-lasting afteractivity. In four of the 11 cells recorded contralateral to the stimulated optic nerve, a depression of the vestibular response could be seen. In potentiated cells, single vestibular pulses often evoked longer episodes of large synaptic noise and sometimes spiking. In the latter case, the action potentials appeared with highly variable latency after each stimulation pulse. This indicates that an important mechanism underlying the potentiation may be a long-lasting increase in excitability in a pool of unidentified interneurons located either upstream of the MRRN cells, relaying vestibular and visual inputs, or downstream, providing positive feedback.

Animals↗

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