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PubMed2006

Functional significance of passive and active dendritic properties in the synaptic integration by an identified nonspiking interneuron of crayfish.

Nonspiking interneurons control their synaptic output directly by membrane potential changes caused by synaptic activities. Although these interneurons do not generate spikes, their dendritic membrane is endowed with a variety of voltage-dependent conductances whose functional significance in synaptic integration remains unknown. We quantitatively investigated how the passive and active dendritic properties affect the synaptic integration in an identified nonspiking interneuron of crayfish by computer simulation using its multicompartment model based on electrophysiological measurements and three-dimensional morphometry. At the resting potential level, the attenuation factor (V(s)/V(t)) of a unitary synaptic potential in the course of its spread from a dendritic terminal (V(s)) to other terminals (V(t)) ranged from 4.42 to 6.30 with no substantial difference between hyperpolarizing and depolarizing potentials. The compound synaptic responses to strong mechanosensory stimulation could be reproduced in calculation only as the result of spatial summation of attenuated potentials, not as any single large potential. The characteristic response could be reproduced by assuming that the active conductances were distributed only in the dendritic region where the synaptic summation was carried out. The active conductances in other parts of the cell affected neither the shape of the compound synaptic response nor the dendritic spread of synaptic potentials. These findings suggest that the active membrane conductances do not affect the spatial distribution of synaptic potentials over dendrites but function in sculpting the summed synaptic potential to enhance temporal resolution in the synaptic output of the nonspiking interneuron.

Algorithms↗
PubMed2003

Distinct local circuits between neocortical pyramidal cells and fast-spiking interneurons in young adult rats.

Connections between layer V pyramidal cells and GABAergic fast-spiking interneurons (pyramidal-FS) were studied by paired recordings combined with morphological analyses in acute neocortical slices from 28- to 52-day-old rats. Pairs of spikes elicited in pyramidal cells at a stimulation rate of 0.2 Hz induced unitary excitatory postsynaptic currents (EPSCs) in FS interneurons that displayed facilitation (48%), depression (38.5%), or neither depression nor facilitation (13.5%). Analyses of the EPSC amplitude distributions indicate that depressing connections always showed multiple functional release sites. On the contrary, facilitating connections consisted either of one or several release sites. At a holding potential of -72 mV, the quantal size (q) and the release probability (p) of facilitating connections with a single release site were -21.9 +/- 7.5 pA and 0.49 +/- 0.19 (SD), respectively. The mean q and the estimated number of release sites (n) at connections showing multiple sites were obtained by decreasing the release probability and did not differ between depressing and facilitating synapses (depressing connections: q = -15.3 +/- 2.5 pA, n = 5.1 +/- 3, facilitating connections: q = -23.9 +/- 9.8 pA, n = 7.8 +/- 5.4). However, the quantal content at facilitating synapses with multiple sites (1.9 +/- 1.5) was significantly different from that at depressing connections (4.1 +/- 3.9). Finally, quantitative morphological analyses revealed that most of the pyramidal cells displaying facilitation can be differentiated from those displaying depression by a more densely branched apical dendritic tree. Therefore two types of morphologically distinct pyramidal cells form excitatory connections with FS interneurons that differ in their short-term plasticity characteristics. Facilitating and depressing connections may provide a differential control of the temporal information processing of FS cells and thus finely regulate the inhibitory effect of these interneurons in neocortical networks of young adult rats.

Action Potentials↗
PubMed2003

Quantitative relationship between Kv4.2 mRNA and A-type K+ current in rat striatal cholinergic interneurons during development.

Channel density is a fundamental factor in determining neuronal firing and is primarily regulated during development through transcriptional and translational regulation. In adult rats, striatal cholinergic interneurons have a prominent A-type current and co-express Kv4.1 and Kv4.2 mRNAs. There is evidence that Kv4.2 plays a primary role in producing the current in adult neurons. The contribution of Kv4.2 and Kv4.1 to the A-type current in cholinergic interneurons during development, however, is not known. Here, using patch-clamp recording and semi-quantitative single-cell reverse transcription-polymerase chain reaction (RT-PCR) techniques, we have examined the postnatal development of A-type current and the expression of Kv4.2 and Kv4.1 in rat striatal cholinergic interneurons. A-type current was detectable at birth, and its amplitude was up-regulated with age, reaching a plateau at about 3 wk after birth. At all ages, the current inactivated with two time constants: one ranging from 15 to 27 ms and the other ranging from 99 to 142 ms. Kv4.2 mRNA was detectable at birth, and the expression level increased exponentially with age, reaching a plateau by 3 wk postnatal. In contrast, Kv4.1 mRNA was not detectable during the first week after birth, and the expression level did not show a clear tendency with age. Taken together, our results suggest that Kv4.2 plays an essential role in producing the A-type current in striatal cholinergic interneurons during the entire course of postnatal development.

Acetylcholine↗
PubMed2004

Characterization of neocortical principal cells and interneurons by network interactions and extracellular features.

Most neuronal interactions in the cortex occur within local circuits. Because principal cells and GABAergic interneurons contribute differently to cortical operations, their experimental identification and separation is of utmost important. We used 64-site two-dimensional silicon probes for high-density recording of local neurons in layer 5 of the somatosensory and prefrontal cortices of the rat. Multiple-site monitoring of units allowed for the determination of their two-dimensional spatial position in the brain. Of the approximately 60,000 cell pairs recorded, 0.2% showed robust short-term interactions. Units with significant, short-latency (<3 ms) peaks following their action potentials in their cross-correlograms were characterized as putative excitatory (pyramidal) cells. Units with significant suppression of spiking of their partners were regarded as putative GABAergic interneurons. A portion of the putative interneurons was reciprocally connected with pyramidal cells. Neurons physiologically identified as inhibitory and excitatory cells were used as templates for classification of all recorded neurons. Of the several parameters tested, the duration of the unfiltered (1 Hz to 5 kHz) spike provided the most reliable clustering of the population. High-density parallel recordings of neuronal activity, determination of their physical location and their classification into pyramidal and interneuron classes provide the necessary tools for local circuit analysis.

Action Potentials↗
PubMed1977

Physiological and kinetic properties of cholinergic receptors activated by multiaction interneurons in buccal ganglia of Aplysia.

1. Neurons of Aplysia buccal ganglia contain three types of acetylcholine (ACh) receptors, each of which has been characterized by its sensitivity to inhibitors and kinetics of desensitization and by the properties of the conductance change it controls, including reversal potential, major ion, and functional consequence. The receptors are classified as depolarizing, slowly decrementing hyperpolarizing, and rapidly decrementing hyperpolarizing. Identified neurons are innervated by identified cholinergic multiaction interneurons; the form of the postsynaptic potential produced depends on the number and class of receptor found on each cell. 2. Interneuronal action potentials produce monosynaptic IPSPs by activating slowly decrementing hyperpolarizing receptors on seven cells in each ganglion. The IPSP reversal potential of 75 mV is shifted 42 mV in a depolarizing direction in Cl = free seawater. The ACh response has a reversal potential identical to that of the PSP; the PSP is blocked by 10(-4) g/ml curare but unaffected by hexamethonium. Interneuronal action potentials also produce monosynaptic EPSPs with a -14 mV extrapolated reversal potential by activating depolarizing receptors on one cell in each ganglion. This PSP is blocked by 10(-4) g/ml hexamethonium and mimicked by a Na-dependent ACh response. 3. Each interneuronal action potential also produces a diphasic depolarizing-hyperpolarizing synaptic potential in one cell in each ganglion as a result of released ACh acting on two classes of postsynaptic receptor on the same cell. One of these receptors is depolarizing; the other is a rapidly decrementing hyperpolarizing receptor. The two differ in their sensitivity to inhibitors, and the conductance changes they produce differ in their reversal potential, duration, and functional consequences. Both components can be mimicked by iontophoretic application of ACh. 4. Although the hyperpolarizing receptors on the inhibitory and diphasic follower cells have similar sensitivity to inhibitors and control similar conductance changes, they differ in their kinetics of desensitization. The hyperpolarizing receptor on the diphasic cell shows marked decrement to repeated presynaptic action potentials and to repeated iontophoretic application of ACh. This decrement is greater than that seen in either the hyperpolarizing receptor on the inhibitory follower cell or the depolarizing receptor on the dual follower cell. The shape of the PSP in the diphasic follower and its effect on firing of the cell are thus functions of both membrane potential and the degree of desensitization of the receptor. 5. Rate of desensitization is, therefore, an additional criterion for characterizing otherwise similar receptors for neurotransmitters.

Acetylcholine↗
PubMed1980

Loss of inhibitory synaptic input to cricket sensory interneurons as a consequence of partial deafferentation.

1. In a companion paper (5) we suggested that the enhanced ability of excitatory pathways to drive deafferented interneurons in crickets could be attributed to a reduction in the effectiveness of remaining inhibitory pathways impinging on these neurons. 2. In order to test this idea more directly, we examined a sensory interneuron in the cricket known as sensory interneuron 10-3 (SI 10-3). We first demonstrated that SI 10-3 was more sensitive to remaining excitatory inputs after partial deafferentation. 3. We then tested the ability of inhibitory inputs to suppress a train of current-evoked action potentials. Brief (100 ms) depolarizing current pulses were injected into the soma of SI 10-3 and the number of action potentials counted. Next, an identical depolarizing pulse was injected into the interneuron coincident with activation of the inhibitory pathway by a tone (75 dB at 450 Hz). Activation of the inhibition decreased the number of current-evoked action potentials. In order to quantify this effect, current-tone pairs were presented at four current intensities. Over the range of current intensities used, the relationship between current intensity and number of action potentials (AP/I curve), elicited with or without tones, was linear (Fig. 7A). 4. In control preparations, tones always lowered the calculated slope of the observed curve and its y intercept. In treated specimens inhibiting tones decreased the slope of the AP/I curve less than in control specimens. Based on this evidence, we concluded that the inhibitory pathway had been disrupted by partial deafferentation. This releases the giant neuron from inhibition, allowing it to respond more strongly to remaining excitatory inputs.

Animals↗
PubMed1983

Neuronal pathways for activation of inhibitory interneurons in pyriform cortex of the rabbit.

The neuronal pathways responsible for the fast inhibitory postsynaptic potentials (IPSPs) elicited in principal cells in the pyriform cortex (PC) by volleys from the olfactory bulb (OB), the lateral olfactory tract (LOT), the anterior commissure (AC), and the deep-lying structures of the PC (DPC) were studied in the rabbit. The central latencies of the fast IPSPs (measured from the onset of the monosynaptic excitatory postsynaptic potential (EPSP) elicited by volleys through the LOT) ranged between 3.0 and 9.3 ms (5.5 +/- 1.3 (SD) ms; n = 54) in the case of OB shocks and between 4.5 and 6.5 ms (5.1 +/- 0.7 (SD) ms; n = 7) in the case of LOT shocks. The onset latencies of the fast IPSPs were between 2.5 and 11.8 ms (5.1 +/- 1.8 (SD) ms; n = 66) in the case of DPC shocks and between 3.5 and 10.1 ms (5.8 +/- 1.5 (SD) ms; n = 61) in the case of AC shocks. The conditioning OB or LOT shocks almost completely eliminated the LOT-evoked fast IPSP when the testing shock was applied at the peak period of the conditioning slow IPSP. The conditioning OB shocks also eliminated the initial part of the OB-evoked fast IPSP, leaving the later part of the fast IPSP almost unchanged. Thus, the onset latency of the OB-evoked fast IPSP was lengthened by 7.1 +/- 2.9 (SD) ms (n = 35) by the conditioning OB shock. The conditioning OB or DPC shocks left the peak amplitude of the DPC-evoked fast IPSP almost unaffected. Similarly, the conditioning OB or AC shocks left the peak amplitude of the AC-evoked fast IPSP almost unaffected. The conditioning OB, DPC, or AC shocks had only a slight influence on the onset latency of the DPC- or AC-evoked fast IPSPs. Rhythmical steps at intervals of 3-5 ms were observed in the rising phase of the OB-evoked fast IPSP. This was interpreted as a result of a repetitive impingement of interneuronal discharges on the impaled cells. Spatial facilitation was observed among the fast IPSPs evoked by volleys from the OB, DPC, and AC when shocks were applied at suitable intervals. A slight facilitation was also seen between the LOT-evoked fast IPSP and the DPC- or AC-evoked fast IPSP. These results were interpreted as a result of the convergence of excitatory synaptic inputs onto the presumed inhibitory interneurons from the four structures of the brain. A temporal facilitation of the fast IPSPs was observed when the OB, DPC, or AC shocks were applied repetitively at short intervals. This suggests a temporal facilitation of the spike discharges of the presumed inhibitory interneurons under similar conditions. From these results, criteria were determined for identifying the inhibitory interneurons.

Animals↗
PubMed1984

Sensory, interneuronal, and motor interactions within Hermissenda visual pathway.

The visual pathway of Hermissenda was identified by means of intracellular recordings and iontophoretic injection of the fluorescent dye lucifer yellow. This pathway consisted of five neuron types, namely, type B photoreceptors and the medial type A photoreceptor within each of the two eyes, hair cells in the two statocysts, a group of interneurons in the cerebropleural ganglia, and a putative motor neuron (MN1) in each pedal ganglion. The MN1 cells responded during illumination of the eye with increased impulse and excitatory postsynaptic potential (EPSP) activity. This response was often followed by bursting activity for higher light intensities. The medial type A photoreceptor, which was found to be inhibited by medial and intermediate type B photoreceptors, was demonstrated to excite the MN1 cell indirectly via a group of identified interneurons. Hair cells were also found to excite the MN1 cell indirectly via these interneurons. Among the ipsilateral hair cells, cephalic hair cells were least frequently found to excite the MN1 cell. Among the contralateral hair cells, on the other hand, lateral hair cells were most often found to excite the MN1 cell. Interneurons that were shown to excite the MN1 cell received excitatory input from the medial type A photoreceptor and hair cells. Our observations are consistent with the interpretation that these interactions are mediated by monosynaptic chemical synapses. Electrical stimulation of the MN1 cell with positive-current injection produced turning of the posterior half of the animal's foot to the ipsilateral direction consistent with the animal's turning behavior toward light. The visual pathway identified in this experiment was considered to have some significance in explaining, at least in part, a causal role for changes within type B photoreceptors in producing Hermissenda's modified behavior following associative conditioning.

Animals↗
PubMed1988

Connectivity pattern of the cercal-to-giant interneuron system of the American cockroach.

1. The pattern of connectivity between identified cercal afferents and the three largest giant interneurons (GIs 1, 2, and 3) of the American cockroach was investigated by intracellular methods. These three GIs all have different directional response sensitivities and appear to be especially important in initiating the short latency escape behavior of the American cockroach. 2. One of the interneurons, GI 1 responds to wind from all four quadrants of space about the animal. However, it clearly shows a greater ipsilateral versus contralateral (relative to the GI's axon within the nerve cord) wind sensitivity. In contrast, the directional sensitivity of GI 2 is more nearly bilaterally symmetrical. Both of these interneurons receive excitatory synaptic input from the sensory cells of the nine most prominent columns (a, d, g, f, h, i, k, l, and m) of filiform hairs of the ipsilateral cercus. 3. The nine ipsilateral inputs all made roughly equivalent strength excitatory connections with GI 1. The connectivity pattern to GI 2 was the same as that to GI 1 except that the connection strength for two of the nine columns, h and i, was substantially stronger to GI 2 than to GI 1. The remaining seven sensory columns all make equivalent strength connection with GI 2. 4. Only select columns of contralateral sensory cells made synaptic connection with GIs 1 and 2. All detectable connections produced subthreshold depolarizations. 5. The response curve of GI 3 is more sharply restricted in space than that of either GI 1 or 2 and this interneuron only responds to wind stimuli originating from in front of the animal. GI 3 received excitatory synaptic input only from ipsilateral columns d, f, g, i, and k, all of which have their best excitatory directions well within the boundaries of the response curve of GI 3. Columns a and l with best excitatory directions near the edges of the response curve of GI 3 made no detectable connection. The remaining two columns (h and m) with best excitatory directions well outside the boundaries of the response curve of GI 3 provided inhibitory input. 6. GI 3 received synaptic input from contralateral columns d, f, g, h, i, k, and m.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1989

Chemically and electrically coupled interneurons mediate respiratory pumping in Aplysia.

1. Respiratory pumping in Aplysia consists of synchronous, brief contractions of the mantle organs that can occur spontaneously and also can be triggered by tactile or noxious stimulation. It has been shown previously to be driven in part by a cluster of electrically coupled interneurons, called the L25 cells, located in the left hemiabdominal ganglion. This paper describes a second class of interneurons, the R25 cells, that also plays an important role in the control of respiratory pumping. 2. The R25 cells are a cluster of approximately 14 interneurons located in the right hemiabdominal ganglion, roughly symmetrical to the L25 cells. The R25 cells are electrically coupled to each other and to the L25 cells. Some R25 and L25 cells also produce chemically mediated fast excitation and slow inhibition of other neurons in the R25/L25 network. 3. Three lines of evidence demonstrate that the R25 cells play a role in mediating respiratory pumping: 1) They fire in a synchronous burst each time the behavior occurs. 2) They make direct chemical synaptic connections to motoneurons that mediate the behavior; and 3) Firing a single R25 cell can trigger the entire behavior, by recruiting synchronous bursts of activity in all of the other R25 and L25 neurons. Individual R25 and L25 cells can act both as trigger cells (exciting the other interneurons) and as relay cells (projecting directly to motoneurons). 4. Burst initiation within the R25/L25 network appears to have two phases: 1) There is an initial phase when the R25 and L25 cells fire at a relatively low frequency. This phase can be driven either by endogenous pacemaker activity of the R25/L25 cells or by afferent synaptic input from sensory pathways; and 2) The late, high-frequency phase of the burst results largely from reverberation within the network, as activity in each cell contributes positive feedback via the excitatory chemical and electrical connections between R25 and L25 cells. 5. Synchronization of the different motor outputs that make up the pumping behavior is achieved by three mechanisms: 1) When pumping occurs spontaneously, the electrical coupling between the cells of the R25/L25 network ensures that these cells will all be near spike threshold at the end of each interburst period.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Synaptic connections between motor neurons and interneurons in the fourth thoracic ganglion of the crayfish, Procambarus clarkii.

1. A new preparation of the thoracic nervous system of the crayfish, Procambarus clarkii, has been developed, in which it is possible to work with identified members of motor neuronal pools. 2. In such a preparation, it is possible to dissect all specific proximal motor nerves (protractor, retractor, anterior elevator, posterior elevator, and depressor). Motor neurons innervating the four proximal muscles of the fourth walking leg have been identified both physiologically and anatomically by staining the recorded motor neuron with Lucifer yellow through the microelectrode. 3. By the use of cobalt chloride, we have mapped the distribution of somata of all motor neurons within the fourth thoracic ganglion that innervate the different groups of muscles controlling the movement of the fourth walking leg. 4. Most motor neurons innervating the same muscle seem to be electrically coupled, except some depressor motor neurons. 5. Motor neurons innervating antagonist muscles are linked by inhibitory connections. These connections are reciprocal for protractor and retractor motor neurons but usually not reciprocal between elevator and depressor motor neurons. 6. Walking interneurons were identified as neurons without axons in any motor nerve, which modified the motor neuronal activity. Some of them have been injected with Lucifer yellow. 7. Some interneurons make synaptic connections only with antagonist motor neurons that control the movement of one joint. Probably their functional role is to reinforce or to limit the antagonism between each pair of antagonist motor neurons. 8. Other interneurons make synaptic connections with motor neurons innervating muscles controlling different leg joints. These interneurons may play a role in generating the motor patterns that underlie forward and backward walking.

Action Potentials↗
PubMed1995

Hippocampal CA1 lacunosum-moleculare interneurons: comparison of effects of anoxia on excitatory and inhibitory postsynaptic currents.

1. The effects of anoxia on excitatory and inhibitory postsynaptic currents (EPSCs and IPSCs, respectively) evoked by electrical stimulation in the stratum radiatum were studied in morphologically and electrophysiologicaly identified lacunosum-moleculare (LM) interneurons of the CA1 region of rat hippocampal slices. The blind whole cell patch-clamp technique was used, and anoxia was induced by superfusion of the slice with an anoxic artificial cerebral spinal fluid saturated with 95% N2-5% CO2 for 4-6 min. 2. In LM interneurons, anoxia generated currents similar to those in pyramidal cells, the most prominent being anoxic and postanoxic outward currents. The adenosine A1 type receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, 200 nM) did not significantly affect anoxia-generated currents. 3. EPSCs and polysynaptic IPSCs (pIPSCs) evoked in LM interneurons by "distant" stimulation (> 1 mm) in the stratum radiatum were strongly depressed by anoxia and recovered upon reoxygenation. 4. Responses to pressure application of glutamate, alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and N-methyl-D-aspartate (NMDA) were not significantly affected by anoxia, suggesting that the suppression of EPSCs is due to presynaptic mechanisms. 5. DPCPX (200 nM) prevented anoxia-induced suppression of EPSCs, suggesting that this suppression was mediated by presynaptic A1 adenosine receptors. 6. Monosynaptic IPSCs evoked by "close" stimulation (< 0.5 mm) in the stratum radiatum, in the presence of glutamate-receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 20 microM) and D-2-amino-5-phosphopentanoate (APV; 50 microM), were reversibly depressed but not blocked by anoxia. 7. Anoxia depressed monosynaptic GABAA receptor-mediated IPSCs (monosynaptic IPSCAs) by inducing a positive shift in the reversal potential and a decrease in slope conductance. Responses to pressure-applied isoguvacine, a GABAA receptor agonist, were reversibly depressed by anoxia, again because of a positive shift in reversal potential and decrease in conductance. Anoxic effects on slope conductances and reversal potential of isoguvacine responses and monosynaptic IPSCA coincided, suggesting that evoked transmitter release from GABAergic terminals was not affected by anoxia. 8. Anoxic depression of monosynaptic GABAB receptor-mediated IPSCs (monosynaptic IPSCBs) was due to a decrease in the slope conductance of monosynaptic IPSCB. In contrast to EPSCs, DPCPX (200 nM) failed to prevent anoxia-induced depression of mIPSCA and mIPSCB. 9. Paired-pulse depression of monosynaptic IPSCs, partially mediated by presynaptic GABAB receptors, was not affected by anoxia. 10. These data provide direct evidence for the hypothesis that inhibitory interneurons of CA1 stratum LM are functionally disconnected from excitatory inputs by anoxia. This disconnection underlies the preferential block by anoxia of IPSCs recorded in pyramidal cells, and it may occult the postsynaptic modifications in GABAA and GABAB responses. This disconnection involves adenosine-dependent inhibition of glutamate release from excitatory terminals. GABA release and its modulation by presynaptic GABAB receptors, both known to be insensitive to adenosine, seems to be resistant to anoxia.

Animals↗
PubMed1996

Two temporally overlapping "delayed-rectifiers" determine the voltage-dependent potassium current phenotype in cultured hippocampal interneurons.

1. Whole cell voltage-clamp recordings were used to characterize the calcium-independent "delayed-rectifier" potassium currents of gamma-aminobutyric acid (GABA)-positive stratum radiatum-lacunosum-moleculare (st. L-M) interneurons in primary culture derived from neonate rats [postnatal day 5-7 (P5-P7)]. 2. Two distinct current phenotypes were observed, which we termed "sustained" and "slowly inactivating." Despite possessing similar voltage-dependent activation properties, current differed in their time-dependent inactivation properties and their kinetics of activation and deactivation. The phenotypes of the observed currents did not change during the time in vitro. The total current phenotype observed in any cell likely resulted from the temporal overlap of the two current components expressed in different relative proportions. 3. Externally applied 4-aminopyridine (4-AP) selectively blocked the slowly inactivating current component, by a use-dependent, but voltage-independent mechanism, suggesting that channel activation is required for 4-AP to interact with its binding site. In contrast, the sustained current component was unaffected by 4-AP. 4. Both the slowly inactivating and sustained current phenotypes were sensitive to externally applied tetraethylammonium (TEA). The IC50 of block by TEA was lower in cells expressing predominantly the sustained current components. 5. Currents recorded in the presence of internally applied TEA were of a slowly inactivating phenotype, suggesting that [TEA]i preferentially blocked the sustained current component. 6. When test pulses were preceded by a prepulse to -100 mV, a transient A-type current component was observed, but in contrast to pyramidal neurons and other interneuron types, this transient current contributed only a minor component to the total initial peak current. 7. In conclusion, two distinct, temporally overlapping potassium current phenotypes were observed on st. L-M interneurons. The overall phenotype was determined by the relative proportion of each current component. The absence of a prominent transient current suggests that the two delayed-rectifier currents play a critical role in determining the firing characteristics of these interneurons.

4-Aminopyridine↗
PubMed1997

In vitro investigation of synaptic relations between interneurons surrounding the trigeminal motor nucleus and masseteric motoneurons.

Because of their many inputs and bilateral projections, interneurons surrounding the trigeminal motor nucleus (MotV) are thought to be very important in control of jaw movements and reflexes. However, their interactions with the trigeminal motoneurons are almost unknown. In the present study an in vitro slice preparation was used to investigate this relationship in rat. The zone bordering MotV has been subdivided into four regions: the supra-, juxta-, and intertrigeminal areas (SupV, JuxtV, and IntV, respectively) and the parvocellular reticular formation ventral and caudal to MotV. Stimulation of all areas evoked short-latency excitatory postsynaptic potentials (EPSPs) in masseteric motoneurons. Frequently the EPSPs masked inhibitory postsynaptic potentials (IPSPs) or were followed by long-lasting inhibitory potentials. Only responses obtained from stimulation of JuxtV and IntV seemed devoid of inhibitory components. The EPSPs were mediated through kainate/alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors, whereas the IPSPs appear to be due to gamma-aminobutyric acid and glycine. EPSPs and IPSPs were also recorded in SupV premotor interneurons after stimulation of IntV and MotV, respectively, thus suggesting that reciprocal connections exist between premotor areas and also between premotor interneurons of SupV and inhibitory interneurons located within MotV. It is concluded that the preparation used here will doubtless prove useful for further investigation of the circuitry involved in the bilateral coordination of the jaw.

Animals↗
PubMed1997

Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons.

Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons. J. Neurophysiol. 78: 2287-2295, 1997. Using neocortical layer I neurons as a model for GABAergic interneurons, we have studied gamma-aminobutyric acid-A (GABAA) receptor-mediated spontaneous inhibitory postsynaptic currents (IPSCs) and modulation by metabotropic glutamate receptors (mGluRs). In the presence of 0.5 mu M tetrodotoxin (TTX) and ionotropic glutamate receptor antagonists and under symmetrical Cl- conditions, the mean amplitude of miniature IPSCs (mIPSCs) was approximately 50 pA at a holding potential of -70 mV with individual events ranging from 10 to 400 pA. Averaged mIPSCs had a 10-90% rise time of approximately 0.6 ms. The decay was double exponential. The fast component had a time constant of approximately 4 ms and comprised approximately 40% of the total amplitude. The slow component had a time constant of approximately 22 ms. The frequency of spontaneous IPSCs (sIPSCs), recorded in the absence of TTX, was increased by bath application of the mGluR agonist 1S,3R-1-aminocyclopentane-1, 3-dicarboxylic acid (ACPD; 10-100 mu M) or the group I mGluR selective agonist quisqualic acid (Quis; 0.5-1 mu M). Under identical conditions, mIPSCs were not affected. The kinetics of sIPSCs and mIPSCs were not altered by ACPD or Quis. Quis (1 mu M) induced an inward current of approximately 70 pA at a holding potential of -70 mV, whereas ACPD (40-200 mu M) induced a smaller inward current. This current was linear over the voltage range -70 to +30 mV and reversed polarity near 0 mV. In current-clamp recordings, both Quis and ACPD induced a depolarization and action potential firing in layer I and deeper layer interneurons. We conclude that neocortical layer I neurons receive GABAA receptor-mediated inhibitory synaptic inputs. Activation of mGluRs, possibly mGluR1 and/or mGluR5, causes an enhancement of inhibitory synaptic transmission by directly depolarizing corticalGABAergic interneurons through the opening of nonselective cation channels.

Action Potentials↗
PubMed1997

Recurrent inhibitory interneurons of the Rabbit's lateral posterior-pulvinar complex.

We recorded from 118 neurons in the visual sector of the thalamic reticular nucleus (TRN) in anesthetized rabbits. Cells were identified by their location and characteristic burst responses to stimulation of the primary visual cortex (Cx) and optic chiasm (OX) and were classified into two groups. Type I cells had relatively short latencies from both OX and Cx stimulation, and the latency from OX was always longer than from Cx. In contrast, type II cells had much longer latencies after OX and Cx stimulation, and the latency from OX was always shorter than from Cx. Type I cells were located in the dorsal part of TRN, whereas type II cells were located in the ventral part of TRN. The physiological properties and location of type I TRN cells indicate that they are recurrent inhibitory interneurons of the dorsal lateral geniculate nucleus (LGN). Type II TRN cells most likely function as recurrent inhibitory interneurons for the lateral posterior nucleus-pulvinar complex (LP) because they could be activated antidromically by LP stimulation and orthodromically activated via axonal collaterals of LP cells. Type II TRN cells exhibited a prolonged depression after Cx or OX stimulation. Intracellular recordings showed that a prolonged inhibitory postsynaptic potential was evoked by Cx or OX stimulation. Therefore, these recurrent interneurons of LP, type II cells form mutual inhibitory connections just like those recurrent interneurons of LGN, type I cells. Our data suggest that the geniculocortical and extrageniculate visual pathways have similar recurrent inhibitory circuits.

Animals↗
PubMed1998

Intrinsic circuitry of the superior colliculus: pharmacophysiological identification of horizontally oriented inhibitory interneurons.

Much of what is known about the organization of the superior colliculus is based on the arrangement of its external connections. Consequently, there is little information regarding pathways that remain intrinsic to it, even though recent data suggest that a horizontally oriented local circuit may mediate the functional reciprocity among fixation and saccade-related neurons. Therefore, the present experiments sought physiological evidence for neurons intrinsic to the superior colliculus that might participate in a horizontally oriented local circuit. Parasagittal slices of the ferret superior colliculus were prepared for in vitro recording, and 125 intermediate/deep layer neurons were examined in response to electrical stimulation rostral or caudal to the recording site. A substantial proportion (37%) of neurons responded with a prolonged period (means = 59.3 +/- 30 ms) of poststimulus suppression of spontaneous action potential activity. Of the suppressed neurons, most (53%) were disinhibited when the excitatory amino acid receptor antagonists D-2-amino-5-phosphonovaleric acid (D-APV) and 6-nitro-7 sulphamoylbeno[f]-quinoxaline-2,3-dione (NBQX) were administered, indicating that excitatory input to inhibitory interneurons was blocked. Of the neurons that received inputs from inhibitory interneurons, all had their suppressive responses decreased or eliminated by the gamma-aminobutyric acid antagonist, bicuculline. Finally, severing the superficial layers from the slice had no effect on intermediate layer responses to intrinsic stimulation. These data provide physiological evidence for the presence of horizontally oriented inhibitory interneurons in the superior colliculus. Furthermore, these findings are consistent with the hypothesis that an intrinsic circuit, routed through interneurons, might account for the reciprocal inhibition observed among fixation and saccade-related neurons.

2-Amino-5-phosphonovalerate↗
PubMed1999

Electrophysiological recordings and calcium measurements in striatal large aspiny interneurons in response to combined O2/glucose deprivation.

Electrophysiological recordings and calcium measurements in striatal large aspiny interneurons in response to combined O2/glucose deprivation. The effects of combined O2/glucose deprivation were investigated on large aspiny (LA) interneurons recorded from a striatal slice preparation by means of simultaneous electrophysiological and optical recordings. LA interneurons were visually identified and impaled with sharp microelectrodes loaded with the calcium (Ca2+)-sensitive dye bis-fura-2. These cells showed the morphological, electrophysiological, and pharmacological features of large striatal cholinergic interneurons. O2/glucose deprivation induced a membrane hyperpolarization coupled to a concomitant increase in intracellular Ca2+ concentration ([Ca2+]i). Interestingly, this [Ca2+]i elevation was more pronounced in dendritic branches rather than in the somatic region. The O2/glucose-deprivation-induced membrane hyperpolarization reversed its polarity at the potassium (K+) equilibrium potential. Both membrane hyperpolarization and [Ca2+]i rise were unaffected by TTX or by a combination of ionotropic glutamate receptors antagonists, D-2-amino-5-phosphonovaleric acid and 6cyano-7-nitroquinoxaline-2, 3-dione. Sulfonylurea glibenclamide, a blocker of ATP-sensitive K+ channels, markedly reduced the O2/glucose-deprivation-induced membrane hyperpolarization but failed to prevent the rise in [Ca2+]i. Likewise, charybdotoxin, a large K+-channel (BK) inhibitor, abolished the membrane hyperpolarization but did not produce detectable changes of [Ca2+]i elevation. A combination of high-voltage-activated Ca2+ channel blockers significantly reduced both the membrane hyperpolarization and the rise in [Ca2+]i. In a set of experiments performed without dye in the recording electrode, either intracellular bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid or external barium abolished the membrane hyperpolarization induced by O2/glucose deprivation. The hyperpolarizing effect on membrane potential was mimicked by oxotremorine, an M2-like muscarinic receptor agonist, and by baclofen, a GABAB receptor agonist. However, this membrane hyperpolarization was not coupled to an increase but rather to a decrease of the basal [Ca2+]i. Furthermore glibenclamide did not reduce the oxotremorine- and baclofen-induced membrane hyperpolarization. In conclusion, the present results suggest that in striatal LA cells, O2/glucose deprivation activates a membrane hyperpolarization that does not involve ligand-gated K+ conductances but is sensitive to barium, glibenclamide, and charybdotoxin. The increase in [Ca2+]i is partially due to influx through voltage-gated high-voltage-activated Ca2+ channels.

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