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PubMed1996

Melatonin modulates cholinergic transmission by blocking nicotinic channels in the guinea-pig submucous plexus.

Melatonin, a hormone produced and released by the pineal gland is also synthesized by cells of the gastrointestinal wall, where it might be a local regulator of gut functions. In this study, we investigated the possible role of melatonin as a modulator of the enteric nervous system. Intracellular recordings were made in neurons of the submucosal plexus from the guinea-pig ileum to measure the melatonin effects on their electrophysiological properties. Melatonin did not alter the membrane potential, the membrane resistance and the noradrenergic inhibitory postsynaptic potentials. However, melatonin (30-3000 microM) reversibly decreased the amplitude of nicotinic excitatory postynaptic potentials (EPSPs) in a concentration-dependent manner (IC50 = 247 microM). These actions of melatonin were not modified by the presence of idazoxan and atropine indicating that they are not mediated by endogenous release of acetylcholine, noradrenaline, or by direct activation of alpha 2-adrenoceptors or muscarinic receptors. The superfusion of melatonin also blocked the nicotinic depolarizations induced by locally applied acetylcholine, indicating that at least part of its effects are postsynaptic. In voltage-clamp experiments, using the whole-cell configuration, melatonin also inhibited the nicotinic inward currents induced by acetylcholine (IACh) in a concentration-dependent manner (IC50 = 257 microM). Melatonin decreased the maximal IACh but did not affect the potency of acetylcholine to induce this current, indicating a noncompetitive antagonism. This effect was voltage-dependent. Our observations indicate that melatonin inhibits the fast EPSPs by directly and specifically blocking the nicotinic channels. The relative high concentrations of melatonin required to produce such an effect rules this out as one of its humoral actions. Such an effect, however, might be of physiological significance close to the cells that release melatonin in the gastrointestinal wall or in other organs.

Acetylcholine↗

PubMed1986

Response properties of the non-pyramidal tract neuron in the kitten motor cortex during early postnatal development: an intracellular HRP study.

Response properties of the non-pyramidal tract neurons (non-PTNs) of the kitten motor cortex were examined with intracellular horseradish peroxidase (HRP) staining under Nembutal anesthesia. Thirty-one neurons were identified as non-PTNs and their responses were analyzed with stimulation of the cerebellar nuclei (CN) and/or the medullary pyramid (Py). Excitatory postsynaptic potentials (EPSPs) were induced both by CN and Py stimulation even at birth, whereas inhibitory postsynaptic potentials (IPSPs) were first detected during the third postnatal week in layers II-III pyramidal neurons, which is much later than in PTNs. This indicates that the intracortical circuits responsible for IPSPs in the superficial cortical layers develop later than in layer V.

Animals↗

PubMed1990

Epileptiform activity in hippocampal slice cultures with normal inhibitory synaptic drive.

The synaptic events responsible for epileptiform burst discharge are often difficult to define. Blockade of inhibition has been used to produce epileptiform events, but it is unclear whether increased excitatory activity in the presence of normal inhibition can also result in burst discharge. In the hippocampal slice culture preparation, a small percentage of cultures exhibit spontaneous bursts. To determine whether the absence of inhibitory postsynaptic potentials (IPSPs) is responsible for these spontaneous bursts, we applied the glutamate antagonist, kynurenic acid (KYN) to block burst activity, and unmask any underlying IPSPs. KYN (10 mM) quickly reduced synaptic activity with concomitant loss of burst discharge. Washout of KYN resulted in a gradual return of synaptic activity, during which time both fast and slow IPSPs were clearly observed. As burst activity returned to control levels, excitatory postsynaptic potentials (EPSPs) were increasingly superimposed within the inhibitory events, obscuring (but not eliminating) the IPSPs. In these hippocampal slice cultures, therefore, epileptiform bursts appear to be the result of an abnormally high level of excitatory synaptic drive, not a reduction in inhibition.

Action Potentials↗

PubMed1997

Phospholipases and arachidonic acid contribute independently to sensory transduction and associative neuronal facilitation in Hermissenda type B photoreceptors.

During contiguous pairings of light and rotation, B photoreceptors in the Hermissenda eye undergo an increase in excitability that contributes to a modification of several light-elicited behaviors. This excitability increase requires a light-induced rise in intracellular Ca2+ in the photoreceptor concomitant with transmitter binding to G protein-coupled receptors as a result of presynaptic vestibular hair cell stimulation. Phospholipases and arachidonic acid (ArA) are here reported to be involved in independent signal transduction pathways that underlie both receptor function and activity-dependent facilitation of the B photoreceptor. 4-Bromophenacyl bromide (BPB), an inhibitor of phospholipases A2 (PLA2) and C (PLC), blocked the generation of light-induced depolarizing generator potentials, but had no affect on the inhibitory postsynaptic potential (IPSP) in the B cell that results from hair cell stimulation. Quinacrine, which predominantly blocks the activity of PLA2 in neurons, had no affect on either the light response or the IPSP, but did block increases in excitability (i.e. increased input resistance and elicited spike rate) of the B cell that results from pairings of light and presynaptic vestibular stimulation (i.e., in vitro associative conditioning). Neither nordihydroquararetic acid (NDGA), which inhibits metabolism of ArA by cyclooxygenase, nor indomethacin, which inhibits lipoxygenase metabolism of ArA, affected the light response or IPSP, but both blocked the increases in excitability in the B cell that accompanied in vitro conditioning. In combination with earlier results, these data suggest that ArA activates PKC in a synergistic fashion with Ca2+ and diacylglycerol in the B cell, and suggest that PLA2-induced ArA release, though not necessary for transduction of light or the hair cell-induced IPSP in the B cell, is a critical component of the convergence of signals that precipitates associative facilitation in this system.

Acetophenones↗

PubMedDate not supplied

High potency of the orally-active NMDA-receptor antagonist CGP 40 116 in inhibiting excitatory postsynaptic potentials of rat basolateral amygdala neurones in vitro.

Conventional intracellular recordings were used to monitor postsynaptic potentials of basolateral amygdala neurones (BLA) in brain slices comprising the BLA, the entorhinal cortex (EC) and the hippocampus, in which the EC-BLA connections were preserved. Stimulation of the BLA with a bipolar electrode elicited complex postsynaptic potentials consisting of alpha-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid (AMPA) receptor-mediated fast excitatory postsynaptic potentials (fast EPSPs), gamma-amino-butyric acid [GABA(A)] receptor-mediated fast inhibitory postsynaptic potentials (fast IPSPs) and GABAB receptor-mediated slow IPSPs. Bath application of 10 microM of the AMPA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and of 10 microM of the GABA(A) receptor antagonist bicuculline methiodide (BMI) revealed a N-methyl-D-aspartate (NMDA) receptor-mediated slow EPSPs, which was occasionally followed by a GABAB receptor-mediated slow IPSPs. Under these conditions, the log concentration-response curve for D-(E)-2-amino-4-methyl-5-phosphono-3-pentanoic acid (CGP 40 116), a newly developed drug with proposed NMDA-receptor antagonist properties, was compared to that obtained with the 'classic' antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) in inhibiting the NMDA-mediated postsynaptic potentials. CGP 40 116 (IC50: 130 nM) was over 30 times more potent than D-AP5 (IC50: 4100 nM) in reducing NMDA-mediated slow EPSP. In conclusion, the present study indicates that CGP 40 116, a new orally-active NMDA antagonist, shows a very high potency on NMDA receptors in the amygdala and may therefore be a valuable tool for studying the behavioural effect of NMDA-receptor mediated transmission in this structure.

2-Amino-5-phosphonovalerate↗

PubMed1994

Noradrenaline mediates paradoxical effects on rat neocortical neurons after GABA withdrawal.

1. The aim of the present study was to determine the role of noradrenergic neurotransmission in neuronal activities intracellularly recorded in neocortical slices obtained from rats presenting the gamma-aminobutyric acid (GABA) withdrawal syndrome (GWS), a focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion into the somatomotor cortex. Neurons recorded in the epileptic focus area (n = 52) were bursting or nonbursting cells. Intrinsic bursting (IB, n = 20) cells presented bursts of action potentials (APs) to an intracellular depolarizing current injection and paroxysmal depolarization shifts (PDSs) to white matter stimulation. Synaptic bursting (SB, n = 22) cells presented only PDSs. Nonbursting (NB, n = 10) cells presented no burst after either synaptic stimulation or depolarizing current injection. Results were compared with those obtained from NB neurons (n = 4) recorded in slices from saline-infused rats. 2. In all of the recorded neurons, bath application of norepinephrine (NE, 10 and 100 microM) provoked a depolarization (1-5 mV) associated with a decrease in input K+ conductance having a mean reversal potential at -90 to -102 mV, not significantly different for bursting and nonbursting cells. This reversal potential differed from that of Cl(-)-mediated inhibitory postsynaptic potentials (-70 mV) elicited in NB cells by electrical stimulation of the white matter. 3. In IB cells, the NE-induced depolarization replaced the intrinsic bursts by a sustained repetitive discharge of single APs and caused intrinsic bursts to appear during previously subthreshold depolarizing current pulses. These NE-increased activities were abolished by dihydropyridine nitrendipine (1 microM) and by Cd2+ (0.5 mM) or Co2+ (2 mM), thus confirming that Ca2+ currents contribute to burst generation in IB cells. 4. In both NB and SB cells recorded in slices from GWS rats, NE provoked the appearance of intrinsic bursts of APs during steps of depolarizing current injections. In addition, in NB cells, NE caused synaptic bursts to appear after white matter stimulation. These NE-induced bursts were dihydropyridine (nitrendipine, 1 microM)- and Cd2+ (0.5 mM)- or Co2+ (2 mM)-sensitive and were related to an increased AP-afterdepolarization. The fast AP-afterhyperpolarization was not affected by NE. In NB cells recorded in slices from saline-infused rats (n = 4) NE did not provoke the appearance of bursts even when stimulation intensity was increased up to three times.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1999

Role of GABAB receptor-mediated inhibition in reciprocal interareal pathways of rat visual cortex.

In neocortex, synaptic inhibition is mediated by gamma-aminobutyric acid-A (GABAA) and GABAB receptors. By using intracellular and patch-clamp recordings in slices of rat visual cortex we studied the balance of excitation and inhibition in different intracortical pathways. The study was focused on the strength of fast GABAA- and slow GABAB-mediated inhibition in interareal forward and feedback connections between area 17 and the secondary, latero-medial visual area (LM). Our results demonstrate that in most layer 2/3 neurons forward inputs elicited excitatory postsynaptic potentials (EPSPs) that were followed by fast GABAA- and slow GABAB-mediated hyperpolarizing inhibitory postsynaptic potentials (IPSPs). These responses resembled those elicited by horizontal connections within area 17 and those evoked by stimulation of the layer 6/white matter border. In contrast, in the feedback pathway hyperpolarizing fast and slow IPSPs were rare. However weak fast and slow IPSPs were unmasked by bath application of GABAB receptor antagonists. Because in the feedback pathway disynaptic fast and slow IPSPs were rare, polysynaptic EPSPs were more frequent than in forward, horizontal, and interlaminar circuits and were activated over a broader stimulus range. In addition, in the feedback pathway large-amplitude polysynaptic EPSPs were longer lasting and showed a late component whose onset coincided with that of slow IPSPs. In the forward pathway these late EPSPs were only seen with stimulus intensities that were below the activation threshold of slow IPSPs. Unlike strong forward inputs, feedback stimuli of a wide range of intensities increased the rate of ongoing neuronal firing. Thus, when forward and feedback inputs are simultaneously active, feedback inputs may provide late polysynaptic excitation that can offset slow IPSPs evoked by forward inputs and in turn may promote recurrent excitation through local intracolumnar circuits. This may provide a mechanism by which feedback inputs from higher cortical areas can amplify afferent signals in lower areas.

Animals↗

PubMed1990

[Suppression of the "fast" IPSP when superimposed on the "slow" IPSP as a possible cause of priming in the mouse hippocampus].

Extra- and intracellular responses of the mouse hippocampus were recorded at CA1 region after stimulation of two independent inputs from the Schaffer collateral/commissural fibres: conditioning or priming input (C1) and testing or primed one (C2). Duration and amplitude of primed field potentials (FP) and excitatory postsynaptic potentials (EPSP) as well as amplitudes of early (IPSPa) and late (IPSPb) components of inhibitory postsynaptic potentials (IPSP) were measured with variation of C1-C2 intervals from 0 to 1 s. An increase in the FP duration as well as EPSP duration and amplitude and suppression of the IPSP amplitude occurred after conditioning with intervals of 50-500 ms, maximal effect was at 200 ms ("priming" effect). These changes correlated with the amplitude of priming IPSPb. The most prominent effect was observed in cells with hyperpolarizing IPSPa. It is assumed that primed FP and EPSP increase due to suppression of the primed IPSPa, when it is superimposed on the priming IPSPb.

Animals↗

PubMed1984

[Inhibitory responses of neurons of an isolated strip of auditory cortex to intracortical stimulation in the cat].

Neuronal reactions to intracortical stimulation at a depth of 1.2-1.4 mm have been investigated in an acutely isolated auditory cortex slab from the cat brain (A-1). It is shown that among neuronal reactions to such stimulation primary inhibitory postsynaptical potentials (IPSPs) prevailed. Latent periods of the inhibitory reactions did not exceed 10 ms. Amplitude and duration of IPSPs did not differ from those of inhibitory responses of neurons in the intact auditory cortex. Some peculiarities in the development of inhibitory responses were found in different layers. The distribution of neurons reacting by IPSP was analyzed according to the slab depth, the duration of primary IPSPs and their latent periods, depending on the distance between the recording microelectrode and stimulating electrode. The mechanisms of inhibitory process spreading in an isolated slab and the mechanisms providing prolongation of cortical inhibitory responses are discussed.

Animals↗

PubMed2006

Acute injury to superficial cortex leads to a decrease in synaptic inhibition and increase in excitation in neocortical layer V pyramidal cells.

Injury to the superficial layers of cerebral cortex produces alterations in the synaptic responses of local circuits that promote the development of seizures. To further delineate the specific changes in synaptic strength that are induced by this type of cortical injury, whole cell voltage-clamp recordings were used to examine evoked and spontaneous synaptic events from layer V pyramidal cells in coronal slices prepared from surgically traumatized rat neocortices in which the superficial third of the cortex (layers I, II, and part of III) was removed. Slices from intact neocortices were used as controls. Examinations of fast inhibitory postsynaptic currents (IPSCs) indicated that traumatized slices were disinhibited, exhibiting evoked IPSCs (eIPSCs) with lower peak amplitudes. Measurements of spontaneous IPSCs (sIPSCs) revealed no difference in the mean amplitudes of sIPSCs recorded in traumatized versus control slices. However, the mean sIPSC frequency was lower in traumatized slices, indicative of a decrease in GABA release at these inhibitory synapses. Traumatized slices also displayed an increase in synaptic excitation, exhibiting spontaneous EPSCs (sESPCs) with larger peak amplitudes and higher frequencies. Peak-scaled nonstationary fluctuation analysis of sEPSCs and sIPSCs was used to obtain estimates of the unit conductance and number of functional receptor channels. EPSC and IPSC channel numbers and IPSC unit conductance did not differ between traumatized and intact slices. However, the mean unit conductance of EPSCs was higher (+25%) in traumatized slices. These findings suggest that acute injury to the superficial neocortical layers results in a disinhibition of cortical circuits that stems from a decline in GABA release likely due to the loss of superficial inhibitory interneurons and an enhancement of synaptic excitation consequent to an increase in the AMPA receptor unit conductance.

Acute Disease↗

PubMed2000

Reversal of the activity-dependent suppression of GABA-mediated inhibition in hippocampal slices from gamma-vinyl GABA (vigabatrin)-pretreated rats.

The antiepileptic drug, gamma-vinyl GABA (GVG, vigabatrin), is an irreversible inhibitor of GABA-transaminase, the enzyme responsible for the breakdown of GABA. In hippocampal slices prepared from rats pretreated with either an anticonvulsant dose of GVG (1500 mg/kg) or saline, electrophysiological recordings were performed in order to examine the effects of GVG pretreatment on GABAergic neurotransmission. Although GVG had no effect on the effectiveness of GABA-mediated inhibition when elicited by a single stimulus, it reversed the activity-dependent depression of inhibition which is typically observed when inhibitory pathways are activated repetitively by a train of stimuli delivered at low frequency. Similarly, GVG pretreatment prevented the progressive decline in the amplitude of monosynaptic inhibitory postsynaptic potentials (IPSPs) during low-frequency stimulation of inhibitory interneurons. Thus, in slices from GVG pretreated rats, the amplitudes of both the fast and slow components of the last of a series of IPSPs evoked by a 5 Hz, 4 s train were maintained at 91.5 +/- 6.6% and 87.7 +/- 6.5%, respectively, compared to 61.1 +/- 3.9% and 57.1 +/- 5.0% in control slices. Finally, in slices from GVG pretreated rats, we observed a reduction in the ability of the GABA(B) receptor agonist, baclofen, to decrease the amplitude of monosynaptic inhibitory postsynaptic currents. These results suggest that GVG may produce its frequency-dependent actions by reducing the function of release regulating presynaptic GABA(B) autoreceptors. The frequency-dependent reinforcement of inhibition by GVG may importantly contribute to the anticonvulsant effectiveness of this compound.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2003

Actions of galanin on neurotransmission in the submucous plexus of guinea pig small intestine.

Electrophysiologic recording methods were used to study the actions of galanin on synaptic transmission in the submucous plexus of guinea pig ileum. Exposure to galanin resulted in concentration-dependent suppression of slow noradrenergic inhibitory postsynaptic potentials and fast nicotinic excitatory postsynaptic potentials in the majority of neurons. Failure of galanin to suppress nicotinic depolarizing responses to micropressure pulses of acetylcholine and failure to suppress hyperpolarizing responses to micropressure pulses of norepinephrine suggested that galanin acted at presynaptic inhibitory receptors to suppress release of acetylcholine and norepinephrine. Galanin suppressed slow excitatory postsynaptic potentials in eight of eight neurons with AH (after-hyperpolarization) type electrical behavior and in none of 26 neurons with S (synaptic) type electrical behavior. Suppression of excitatory neurotransmission in AH neurons was always associated with membrane hyperpolarization. Excitatory responses caused by experimentally applied substance P were also inhibited by galanin. Galanin-(1-16) and galanin-like peptide mimicked the inhibitory actions of galanin on neurotransmission. The selective galanin GAL2 receptor agonist [D-Trp(2)]galanin was inactive. The chimeric peptides, galanin-(1-13)-spantide I, galantide, galanin-(1-13)-neuropeptide Y(25-36) amide, galanin-(1-13)-bradykinin-(2-9)amide and galanin-(1-13)-Pro-Pro-Ala-Leu-Ala-Leu-Ala amide all produced varying degrees of suppression of the synaptic potentials. The evidence suggests that the galanin GAL1 receptor, but not the galanin GAL2 receptor, mediated the presynaptic and postsynaptic inhibitory actions of galanin.

Animals↗

PubMed1985

Evidence that receptors mediating central synaptic potentials extend beyond the postsynaptic density.

Physiological recordings and computer simulations of unitary inhibitory postsynaptic potentials in the Mauthner cell of the goldfish central nervous system have been used to estimate the expected size of the postsynaptic receptor matrix at individual junctions. Simultaneous pre- and postsynaptic recordings were used to determine the kinetic parameters of the quantal responses under normal conditions and in the presence of strychnine, a competitive antagonist of glycine, which is the putative transmitter at these synapses. Calculations indicate that if the postsynaptic density, which has a radius of 0.1 micron, were to accommodate the population of channels estimated to be opened during a quantal response, the glycine binding site density in that region would be unrealistically high. Computer simulation of the quantal responses included transmitter diffusion, transmitter-receptor interactions, and channel activation under conditions including both normal and lowered binding site densities, the latter corresponding to the experimental data obtained with strychnine. The data indicate that the synaptic receptors involved in generating unitary responses are widely distributed to include regions located outside the junctional area, which directly faces the presynaptic release sites. We further suggest that the receptor matrix is surrounded by a restricted diffusional space; this geometrical organization may underlie the finding that response rise times are relatively independent of receptor binding site densities.

Action Potentials↗

PubMed1996

Kindling-induced epileptiform potentials in piriform cortex slices originate in the underlying endopiriform nucleus.

1. Previous studies in vivo and in vitro have shown that kindling from several locations in the limbic system induces the onset of epileptiform activity in the piriform (olfactory) cortex in the rat. In the present study we tested the hypothesis that kindled epileptiform events in piriform cortex are initiated in the underlying endopiriform nucleus. The experiments were performed in slices taken from rats that were previously kindled by conventional means. 2. Both stimulus-evoked and spontaneous interictal-like epileptiform events were observed in most slices from the anterior piriform cortex, but in few slices from the posterior piriform cortex. These events resembled those described in unanesthetized and urethan-anesthetized rats in previous studies. 3. Findings in support of the hypothesis were as follows. Epileptiform events in the endopiriform nucleus preceded those in the piriform cortex. Epileptiform events could occur in endopiriform nucleus alone, but were only observed in the piriform cortex following occurrence in the endopiriform nucleus. A buildup in population activity preceded the onset of all-or-none epileptiform events in the endopiriform nucleus. Epileptiform events could be triggered by local application of glutamate in the endopiriform nucleus and adjacent claustrum, but not from the piriform cortex. Finally, local application of Co2+ in the endopiriform nucleus, but not in the piriform cortex or elsewhere in the slices, blocked the occurrence of epileptiform events. 4. Additional experiments were performed to further characterize the generation process. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) blocked epileptiform events and the preceding accelerating buildup in multiunit activity at a concentration below that required to block the monosynaptic excitatory postsynaptic potential (EPSP). This suggests that EPSPs mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors underlie epileptiform events in slices of piriform cortex, and that multisynaptic interactions within the endopiriform nucleus are required for generation of these epileptiform EPSPs. By contrast, block of N-methyl-D-aspartate (NMDA) receptors decreased the amplitude of epileptiform EPSPs but did not block their occurrence, indicating that NMDA receptors contribute to generation but are not required. When membrane potential was depolarized to increase driving force, fast inhibitory postsynaptic potentials were found to consistently accompany the buildup process and epileptiform EPSPs. This indicates that if initiation of epileptiform activity in the endopiriform nucleus results from a compromise in feedback inhibition, this compromise is partial rather than complete. 5. Epileptiform EPSPs in slices of piriform cortex from kindled rats displayed similarities in properties, locus of origin, and mechanism of generation to those previously studied in slices from normal rats in which epileptiform activity was induced by a brief period of bursting activity. These similarities suggest that study of bursting-induced epileptiform EPSPs may provide insight into certain aspects of kindling-induced epileptogenesis.

Amygdala↗

PubMed1991

Glutamate as a putative neurotransmitter in the buccal central pattern generator of Helisoma trivolvis.

1. The effects of L-glutamate superfusion over identified neurons within the buccal ganglia of Helisoma trivolvis were examined. Glutamate mirrored the effect of activity of subunit 2 (S2) of the tripartite feeding central pattern generator (CPG) on S2 postsynaptic neurons. Neurons that are excited by S2 are depolarized by glutamate, whereas neurons that are inhibited by S2 are hyperpolarized by glutamate. Glutamate also stimulated rhythmic S2 activity. 2. Different glutamate agonists could mimic specific components of the effects of glutamate on buccal neurons. Kainate produced depolarizations in neurons that receive S2 excitatory postsynaptic potentials (EPSPs) and activated rhythmic S2 activity. Quisqualate produced hyperpolarizations in neurons that receive S2 inhibitory postsynaptic potentials (IPSPs). 3. The non-N-methyl-D-aspartate glutamate receptor antagonist cyano-7-nitroquinoxaline-2,3-dione (CNQX) blocked the effects of S2 EPSPs and depolarizations produced by application of glutamate and kainate, but was ineffective in blocking S2 IPSPs or hyperpolarizations produced by application of glutamate and quisqualate. 4. These data support the hypothesis that glutamate is the transmitter of S2 of the feeding CPG in Helisoma, acting at CNQX-sensitive kainate-like receptors at excitatory synapses and CNQX-insensitive quisqualate-like receptors at inhibitory synapses.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed2007

Postsynaptic targets of somatostatin-containing interneurons in the rat basolateral amygdala.

The basolateral amygdala contains several subpopulations of inhibitory interneurons that can be distinguished on the basis of their content of calcium-binding proteins or peptides. Although previous studies have shown that interneuronal subpopulations containing parvalbumin (PV) or vasoactive intestinal peptide (VIP) innervate distinct postsynaptic domains of pyramidal cells as well as other interneurons, very little is known about the synaptic outputs of the interneuronal subpopulation that expresses somatostatin (SOM). The present study utilized dual-labeling immunocytochemical techniques at the light and electron microscopic levels to analyze the innervation of pyramidal cells, PV+ interneurons, and VIP+ interneurons in the anterior basolateral amygdalar nucleus (BLa) by SOM+ axon terminals. Pyramidal cell somata and dendrites were selectively labeled with antibodies to calcium/calmodulin-dependent protein kinase II (CaMK); previous studies have shown that the vast majority of dendritic spines, whether CAMK+ or not, arise from pyramidal cells. Almost all SOM+ axon terminals formed symmetrical synapses. The main postsynaptic targets of SOM+ terminals were small-caliber CaMK+ dendrites and dendritic spines, some of which were CaMK+. These SOM+ synapses with dendrites were often in close proximity to asymmetrical (excitatory) synapses to these same structures formed by unlabeled terminals. Few SOM+ terminals formed synapses with CaMK+ pyramidal cell somata or large-caliber (proximal) dendrites. Likewise, only 15% of SOM+ terminals formed synapses with PV+, VIP+, or SOM+ interneurons. These findings suggest that inhibitory inputs from SOM+ interneurons may interact with excitatory inputs to pyramidal cell distal dendrites in the BLa. These interactions might affect synaptic plasticity related to emotional learning.

Amygdala↗

PubMed2002

Intracellular activity of superior laryngeal nerve motoneurons during fictive swallowing in decerebrate rats.

We examined the swallowing-related intracellular activity of motoneurons of the superior laryngeal nerve (SLN) in decerebrate, paralyzed and artificially-ventilated rats, to elucidate the neuronal mechanism of the pharyngo-esophageal and laryngo-esophageal coordination during swallowing. The majority of the SLN motoneurons exhibited respiratory rhythm (n=16; 13 inspiratory, one expiratory and two non-respiratory neurons). During fictive swallowing evoked by electrical stimulation of the SLN, all these motoneurons showed a hyperpolarization-depolarization sequence in their membrane potentials. The hyperpolarization, which was shown to consist of inhibitory postsynaptic potentials, started at the onset of the hypoglossal swallowing burst, lasted during the burst, and was followed by a depolarization at the end of the burst. This hyperpolarization-depolarization pattern implies that the SLN motoneurons may be involved in the 'inhibitory chain' within the swallowing pattern generator, which may be cardinal in the sequential activation of different populations of motoneurons innervating the swallowing-related muscles.

Action Potentials↗

PubMed2001

Activation of metabotropic glutamate receptors inhibits GABAergic transmission in the rat subfornical organ.

Glutamate is known to increase neuronal excitability in the subfornical organ, a circumventricular organ devoid of the blood-brain barrier. To understand the synaptic mechanism of neuronal excitation by glutamate in this nucleus, we examined the effects of glutamate on GABAergic spontaneous inhibitory postsynaptic currents recorded from subfornical organ neurons in the rat brain slice. The baseline frequency, amplitude and decay time-constant of such spontaneous synaptic currents were 5.60 Hz, 119 pA and 17.3 ms, respectively. Glutamate (10-1000 microM) selectively inhibited the frequency of spontaneous GABAergic inhibitory postsynaptic currents (half-maximal effective concentration=47 microM) with little effects on their amplitudes and decay time constants. The inhibitory effect of glutamate on the frequency of spontaneous GABAergic postsynaptic currents was not blocked by tetrodotoxin (1 microM), or by the antagonists of ionotropic glutamate receptors. In contrast, such inhibitory effect of glutamate was mimicked by general or group II selective metabotropic glutamate receptor agonists such as DCGIV (2S,1'R,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (half-maximal effective concentration=112 nM), but not by the agonists for group I or group III metabotropic glutamate receptors. Under current clamp mode, glutamate reduced the frequencies of spontaneous inhibitory postsynaptic potentials and action potentials in subfornical organ neurons. Our data indicate that glutamate decreases the frequency of spontaneous inhibitory postsynaptic currents by acting on the group II metabotropic glutamate receptors on axonal terminals in the subfornical organ. From these results we suggest that the glutamate-induced modulation of tonic GABAergic inhibitory synaptic activity can influence the excitability of subfornical organ neurons.

Animals↗