scholarly journals Hypoxia-Induced Electrical Changes in Striatal Neurons

1995 ◽  
Vol 15 (6) ◽  
pp. 1141-1145 ◽  
Author(s):  
Paolo Calabresi ◽  
Antonio Pisani ◽  
Nicola B. Mercuri ◽  
Giorgio Bernardi
Keyword(s):  
Excitatory Amino Acid ◽  
Acute Hypoxia ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
Striatal Neurons ◽  
Slice Preparation ◽  
Inward Current ◽  
Low Sodium ◽  
Inward Currents

We have studied the effects of hypoxia on the membrane properties of striatal neurons intracellularly recorded from a corticostriatal slice preparation. Brief (2–10 min) periods of hypoxia produced reversible membrane depolarizations. Longer periods of hypoxia (12–20 min) produced irreversible membrane depolarizations. In voltage-clamp experiments, hypoxia caused an inward current coupled with an increased membrane conductance. Tetrodotoxin or low calcium (Ca2+)-high magnesium-containing solutions blocked synaptic transmission, but they did not reduce the hypoxia-induced electrical changes. Antagonists of excitatory amino acid (EAA) receptors failed to affect the electrical effects caused by oxygen (O2) deprivation. In low sodium (Na+)-containing solutions the hypoxia-induced inward current was largely reduced. Blockade of ATP-dependent Na+-potassium (K+) pump by ouabain enhanced hypoxia-induced membrane depolarizations and/or inward currents. Our findings indicate that, at least for in vitro experiments, the release of EAAs is not required for the acute hypoxia-induced electrical changes in striatal neurons.

Segment-specific effects of FMRFamide on membrane properties of heart interneurons in the leech

1995 ◽  
Vol 74 (4) ◽  
pp. 1485-1497 ◽  
Author(s):  
J. Schmidt ◽  
S. Gramoll ◽  
R. L. Calabrese
Keyword(s):  
Outward Current ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
Inward Current ◽  
Specific Effects ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
Conductance Increase

1. The effects of Phe-Met-Arg-Phe (FMRF)amide (10(-6) M) on membrane properties of heart interneurons in the third, fourth, and fifth segmental ganglia [HN(3), HN(4), and HN(5) cells, respectively] of the leech were studied using discontinuous current-clamp and single-electrode voltage-clamp techniques. FMRFamide was focally applied onto the soma of the cell under investigation. 2. Application of FMRFamide depolarized HN(3) and HN(4) cells by evoking an inward current. These responses were subject to pronounced desensitization. The inward currents evoked by application of FMRFamide were associated with an increase in membrane conductance and appeared to be voltage dependent. Currents were enhanced at more depolarized potentials. 3. The responsiveness of the HN(3) and HN(4) cells was not affected when the Ca2+ concentration in the bath saline was reduced from normal (1.8 mM) to 0.1 mM. The depolarizing response on application of FMRFamide was blocked when Co2+ was substituted for Ca2+. 4. HN(3) and HN(4) cells did not respond to FMRFamide application in Na(+)-free solution. Inward currents were largely reduced when bath saline with 30% of the normal Na+ concentration was used. When Li+ was substituted for Na+ in the saline, application of FMRFamide still evoked depolarizing responses in HN(3) and HN(4) cells. 5. We conclude that focal application of FMRFamide onto the somata of HN(3) and HN(4) cells evokes a voltage-dependent inward current, carried largely by Na+. 6. Focal application of FMRFamide onto somata of HN(5) cells hyperpolarized these cells by activating a voltage-dependent outward current. 7. HN(5) cells were loaded with Cl- until inhibitory postsynaptic potentials carried by Cl- reversed. Cl(-)-loaded cells still responded with a hyperpolarization when FMRFamide was applied onto their somata. Therefore the outward current evoked by FMRFamide appears to be mediated by a K+ conductance increase. 8. Application of FMRFamide onto the somata of HN(5) cells enhanced outward currents that were evoked by depolarizing voltage steps from a holding potential of -45 mV. 9. We conclude that the hyperpolarizing response of HN(5) cells to focal application of FMRFamide onto their somata is the result of an up-regulation of a voltage-dependent K+ current.

ANG II AT1 receptors induce depolarization and inward current in rat median preoptic neurons in vitro

1998 ◽  
Vol 275 (2) ◽  
pp. R632-R639 ◽  
Author(s):  
Donglin Bai ◽  
Leo P. Renaud
Keyword(s):  
Brain Slice ◽  
Lucifer Yellow ◽  
Membrane Conductance ◽  
Inward Rectification ◽  
Ang Ii ◽  
Slice Preparation ◽  
Inward Currents ◽  
Whole Cell Recordings ◽  
Brain Slice Preparation

To examine ANG II receptors in rat median preoptic (MnPO) neurons, we used patch-clamp whole cell recordings in a parasagittal brain slice preparation. Lucifer yellow-filled neurons displayed a simple morphology with two to three aspiny dendrites. Bath-applied ANG II (1–2,000 nM for 30 s) induced a response in 37 of 70 cells. In current-clamp recordings, cells displayed a prolonged (10- to 30-min) depolarizing plateau with action potential discharges and an associated reduction in postburst afterhyperpolarization and spike frequency adaptation. In voltage-clamp recordings (holding potential −65 mV), cells displayed tetrodotoxin-resistant inward currents of 7.6 ± 1.9 ( n = 5), 9.9 ± 1.9 ( n = 9), and 9.2 ± 2.2 pA ( n = 6) at 10, 200, and 2,000 nM, respectively. Responses were blockable by pretreatment with losartan (2 μM; n = 6) but not by PD-123177 (20 μM; n = 3). Net ANG II-induced current revealed a 7.8 ± 0.9% reduction in membrane conductance, decreasing but not reversing at hyperpolarized levels. Neurons expressing a strong hyperpolarization-activated, time-independent inward rectification were more likely to respond to ANG II. There was no correlation between the response of a neuron to ANG II and its response to norepinephrine.

A calcium-dependent slow afterdepolarization recorded in rat dorsolateral septal nucleus neurons in vitro

1990 ◽  
Vol 64 (6) ◽  
pp. 1838-1846 ◽  
Author(s):  
H. Hasuo ◽  
K. D. Phelan ◽  
M. J. Twery ◽  
J. P. Gallagher
Keyword(s):  
Channel Blocker ◽  
Excitatory Amino Acid ◽  
Brain Slices ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Slow Inward Current ◽  
Septal Nucleus ◽  
Inward Current ◽  
Bursting Activity

1. Conventional intracellular and single-electrode voltage-clamp recordings were obtained from rat brain slices containing dorsolateral septal nucleus (DLSN) neurons in vitro. 2. We observed a slow afterdepolarizing potential (slow-ADP) that lasted up to several seconds (half-decay time was in the range of 0.7-1.4 s) in almost 15% of DLSN neurons; these same neurons could exhibit burst firing activity. The amplitude of this slow-ADP was not affected by hyperpolarization of the membrane potential. 3. The slow-ADP was associated with an increased membrane conductance. Hybrid voltage clamping of the slow-ADP revealed a transient slow inward current (slow-ADC). The current-voltage relationship of the slow-ADC was linear between -40 and -100 mV and generated an extrapolated reversal potential of -30 mV. 4. We investigated the ionic mechanism of the slow-ADP in the rat DLSN. Slow-ADPs were not blocked by 1 microM tetrodotoxin (TTX) but were markedly depressed by 200 microM Cd2+, Ca2(+)-free, low-Na+ solutions, and the intracellular injection of ethylene glycol-bis(B-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). Neither diltiazam (10 microM), an L-type Ca2+ channel blocker nor omega-conatoxin (0.2–2.5 microM), an N-type Ca2+ channel blocker affected the slow-ADP. Similarly, the slow-ADP was not affected in a low-Cl- solution. On the other hand, the slow-ADP was enhanced in a K(+)-free solution. In addition, the slow-ADP was not affected by 1 mM kynurenic acid, a broad-spectrum excitatory amino acid antagonist. 5. We conclude that the slow-ADP in the rat DLSN is mediated by a novel Ca2(+)-dependent, Na(+)-dependent, and nonsynaptic inward current that may be similar to the Ca2(+)-activated nonspecific cation channel currents (i.e., CAN-currents) described in various tissues. This current appears to underlie some forms of spontaneous bursting activity recorded from rat DLSN neurons. It may also be responsible for some types of bursting activity recorded in other CNS neurons

Species-specific Effects of Nitromethylene Heterocycle Insecticides on Nicotinic Receptors in Locust Neurons and Mouse N1E-115 and BC3H1 Cells

1994 ◽  
Vol 22 (6) ◽  
pp. 454-461
Author(s):  
Marga Oortgiesen ◽  
Ruud Zwart ◽  
Henk P.M. Vijverberg
Keyword(s):  
Mammalian Cells ◽  
Neuroblastoma Cells ◽  
Receptor Subtypes ◽  
Inward Current ◽  
Specific Effects ◽  
Blocking Effects ◽  
Inward Currents ◽  
Species Specific ◽  
Ganglion Neurons

The effects of nitromethylene heterocycle (NMH) insecticides on subtypes of nicotinic acetylcholine (nACh) receptors were investigated in locust thoracic ganglion neurons, mouse N1E-115 neuroblastoma cells, and mouse BC3H1 muscle cells by using electrophysiological techniques. In locust neurons, all of the six NMH insecticides tested induced transient inward currents resembling nicotinic ACh-induced inward currents, while, in the continued presence of the NMH compounds, the ACh-induced inward current was blocked. The amplitude of the inward current and the blocking effects of the NMH insecticides were enhanced by concentrations between 0.1 and 10μM. Cross-desensitisation with the ACh-induced inward current confirmed that the NMH-induced inward current was governed by the activation of nACh receptors. Mammalian endplate type nACh receptors in BC3H1 cells and mammalian neuronal type nACh receptors in N1E-115 cells were much less sensitive to the NMH insecticides than the locust neuronal nACh receptors. At a concentration of 10μM, which blocked 80–100% of the ACh-induced inward current in locust neurons, NMH insecticides only partially blocked the ACh-induced inward currents mediated by the two subtypes of mammalian nACh receptors. NMH insecticides also failed to induce significant agonist effects in the mammalian cells at this concentration. The results provide a possible explanation for the selectively greater toxicity of NMH insecticides to insects than to vertebrates, at the level of nACh receptor subtypes and, hence, demonstrate that this in vitro approach is valuable for the investigation of species-specific interactions of compounds at their target site.

Ligand-gated currents of alpha and beta ganglion cells in the cat retinal slice

1994 ◽  
Vol 72 (3) ◽  
pp. 1260-1269 ◽  
Author(s):  
E. D. Cohen ◽  
Z. J. Zhou ◽  
G. L. Fain
Keyword(s):  
Synaptic Transmission ◽  
Beta Cells ◽  
Ganglion Cells ◽  
Excitatory Amino Acid ◽  
Ringer Solution ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Inward Current ◽  
Inward Currents

1. We studied the receptor pharmacology of the ligand-gated currents of ON- and OFF- alpha and beta ganglion cells in a cat retinal slice preparation using the whole cell recording variation of the patch-clamp technique. Cat retinal slices were cut in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES) buffer and incubated in a bicarbonate-buffered solution. Ganglion cells were voltage clamped at -70 mV in HEPES-buffered Ringer solution. The pipette solution contained a low concentration of Cl- to distinguish mixed cationic from Cl(-)-mediated conductances, and Lucifer yellow (0.5%) was included for identification of the cell type. 2. In Ringer solution containing 1.2 mM Mg2+, current-voltage (I-V) curves of responses to the excitatory amino acid agonist (EAA) N-methyl-D-aspartate (NMDA) (200 microM) revealed a J-shaped function. In Mg(2+)-free Ringer solution containing 200 microM Cd2+ to block synaptic transmission, NMDA (200 microM) elicited an inward current 5-8 times larger at -70 mV. In both conditions I-V curves of the NMDA-induced currents reversed near 0 mV. These results suggest that there are NMDA EAA receptors present directly on the dendrites of alpha and beta ganglion cells. Responses to NMDA were blocked by +/- 2-amino-7-phosphonoheptanoic acid (AP7) (200 microM). 3. In Ringer solution containing 200-1,000 microM Cd2+ to block synaptic transmission, both ON- and OFF- alpha and beta cells responded to kainic acid (10-50 microM), alpha-amino-3-hydroxy-5-methylisoxazole-4-proprionic acid (AMPA) (20-70 microM), and quisqualic acid (0.1-30 microM) with inward currents that reversed near 0 mV. These responses were blocked by the quinoxaline EAA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (10 microM). The metabotropic agonists 1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) (25 microM) and L-2-amino-4-phosphonobutyric acid (L-APB) (50 microM) and L-2-amino-4-phosphonobutyric acid (L-APB) (50 microM) in the presence of Cd2+ evoked little or no response for all cells tested. 4. In the presence of Cd2+, alpha and beta cells responded to gamma-amino-butyric acid (GABA) (200 microM) and glycine (200 microM) with inward currents that reversed near -35 mV, the calculated chloride equilibrium potential Ecl. Responses to GABA and glycine were both strongly desensitizing. (+)Bicuculline methyl chloride (20 microM) blocked an average of 90% of the inward current evoked by 200 microM GABA on all ganglion cell types.(ABSTRACT TRUNCATED AT 400 WORDS)

Excitatory amino acid receptors of guinea pig medial nucleus tractus solitarius neurons

1990 ◽  
Vol 259 (5) ◽  
pp. H1389-H1395 ◽  
Author(s):  
J. A. Drewe ◽  
R. Miles ◽  
D. L. Kunze
Keyword(s):  
Amino Acid ◽  
Glutamate Receptor ◽  
Nucleus Tractus Solitarius ◽  
Excitatory Amino Acid ◽  
Membrane Conductance ◽  
Diethyl Ester ◽  
Receptor Subtypes ◽  
Amino Acid Receptors ◽  
Medial Nucleus ◽  
Inward Currents

Neurons isolated from the medial subnuclei of nucleus tractus solitarius in adult guinea pigs were studied for responses to the excitatory amino acid glutamate and its analogues using the whole cell tight-seal voltage clamp technique. In 80% of the cells studied (n = 60) 100 microM glutamate produced inward currents at negative voltages. To further characterize the glutamate response, the agonists for three glutamate receptor subtypes, N-methyl-D-aspartate (NMDA), kainate, and quisqualate, were examined for their effects on membrane conductance. NMDA (25-250 microM) activated currents in 85% of the neurons tested (n = 30). NMDA currents were generally very small in amplitude. Of the neurons tested, 84% responded to kainate (10-30 microM, n = 19) and only 50% to quisqualate (25-50 microM, n = 26). The conductance activated by NMDA was outwardly rectifying. The conductance activated by kainate was voltage independent, while that activated by quisqualate showed varying degrees of outward rectification. Responses to NMDA were specifically antagonized by DL-2-amino-5-phosphonovaleric acid (AP-5, 50-100 microM). Kainate responses were blocked by kynurenate at concentrations (0.5-1.5 mM) ineffective on quisqualate-induced current. Glutamic acid diethyl ester (GDEE, 2-15 mM) was effective in reducing quisqualate responses at concentrations that had no effect on kainate responses. This characterization of the glutamate receptor subtypes and effective antagonists provides a basis for future determination of the specific receptor of glutamate responsible for mediation of the excitatory postsynaptic potentials produced by activation of the baroreceptor input.

Developmental changes in membrane properties and postsynaptic currents of granule cells in rat dentate gyrus

1996 ◽  
Vol 76 (2) ◽  
pp. 1074-1088 ◽  
Author(s):  
Y. B. Liu ◽  
P. A. Lio ◽  
J. F. Pasternak ◽  
B. L. Trommer
Keyword(s):  
Action Potentials ◽  
Granule Cells ◽  
Molecular Layer ◽  
Membrane Potentials ◽  
Perforant Path ◽  
Membrane Properties ◽  
Inward Current ◽  
Postsynaptic Currents ◽  
Immature Neurons ◽  
Inward Currents

1. Whole cell patch-clamp recordings were used to study dentate gyrus granule cells in hippocampal slices from juvenile rats (postnatal days 8-32). Membrane properties were measured with the use of current-clamp recordings and were correlated with the morphology of a subgroup of neurons filled with biocytin. The components of the postsynaptic currents (PSCs) induced by medial perforant path stimulation were characterized with the use of specific receptor antagonists in voltage-clamp recordings. 2. Granule cells located in the middle third of the superior blade of stratum granulosum from the rostral third of hippocampus were divided into three groups according to their input resistance (IR). Neurons with low IR (206 +/- 182 M omega, mean +/- SD) had hyperpolarized resting membrane potentials (-82 +/- 7 mV) and high-amplitude action potentials (108 +/- 23 mV). Neurons were high IR (1,259 +/- 204 M omega) had more depolarized resting membrane potentials (-54 +/- 6 mV) and lower-amplitude action potentials (71 +/- 10 mV). Neurons with intermediate IR (619 +/- 166 M omega) also had intermediate resting membrane potentials (-63 +/- 7 mV) and action potential amplitudes (86 +/- 14 mV). Low-IR neurons became increasingly prevalent with advancing postnatal age, but neurons from each group could be found throughout the entire period under study. 3. Morphological studies of low-IR neurons revealed an extensive dendritic arborization that traversed the entire molecular layer and was characteristic of mature granule cells. High-IR cells had smaller somata and short, simple dendritic arborization that incompletely penetrated the molecular layer and were classified as immature. Intermediate-IR cells had morphological features of intermediate maturity. 4. The initial phase of the PSC evoked at -80 mV was a fast inward current that was comparable with respect to latency to peak, latency to onset, and 10-90% rise time in neurons of all maturities held at -80 mV. This current was 6-cyano-7-nitroquinoxaline-2,3-dione sensitive. 5. The decay phases of PSCs at -80 mV varied with neuronal maturity. Mature neurons had monoexponential decays (tau = 8.9 +/- 3.6). Intermediate and immature neurons had prominent later inward currents that resulted in slower decays. In the case of the immature neurons, the inward current during the decay phase could be separated from the initial fast inward peak. The later inward currents in intermediate and immature neurons were bicuculline sensitive. 6. With the use of uniform ionic conditions of the extracellular and patch solutions, current-voltage relations and reversal potentials for pharmacologically isolated alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), N-methyl-D-aspartate (NMDA), and gamma-aminobutyric acid-A (GABAA) currents were comparable across all cell maturities. Calculated ratios for peak GABAA/NMDA/AMPA currents decreased significantly with maturation as follows: 9.4 +/- 2.9/1.4 +/- 0.5/1.0 for immature cells, 7.2 +/- 2.5/1.5 +/- 0.7O/1.0 for intermediate cells, and 2.0 +/- 1.2/0.9 +/- 0.4/1.0 for mature cells. 7. GABA current was mediated both by polysynaptic activation of interneurons and by direct activation of interneurons with monosynaptic input onto granule cells. The proportional contributions of mono- and polysynaptic GABA to total GABA were comparable across all cell maturities; latency to peak GABA current decreased with increasing cell maturity for both mono- and polysynaptic components. 8. We conclude that PSCs evoked in granule cells by medial perforant path activation in neurons of all maturities consist of both glutamatergic and GABAergic components. PSCS are dominated by GABAergic neurotransmission in immature granule cells, and the contribution of glutamatergic neurotransmission increases with neuronal maturation. The greater ratio of peak GABAA to glutamate currents and the longer time interval between their respective peaks combine to produce a distinctive PSC shape

scholarly journals Electrophysiological characterization of Grueneberg ganglion olfactory neurons: spontaneous firing, sodium conductance, and hyperpolarization-activated currents

2012 ◽  
Vol 108 (5) ◽  
pp. 1318-1334 ◽  
Author(s):  
Cambrian Y. Liu ◽  
Cheng Xiao ◽  
Scott E. Fraser ◽  
Henry A. Lester ◽  
David S. Koos
Keyword(s):  
Electrophysiological Study ◽  
Ionic Currents ◽  
Membrane Properties ◽  
Spontaneous Firing ◽  
Firing Patterns ◽  
Grueneberg Ganglion ◽  
Single Spike ◽  
Inward Currents ◽  
Electrophysiological Characterization

Mammals rely on their acute olfactory sense for their survival. The most anterior olfactory subsystem in the nose, the Grueneberg ganglion (GG), plays a role in detecting alarm pheromone, cold, and urinary compounds. GG neurons respond homogeneously to these stimuli with increases in intracellular [Ca2+] or transcription of immediate-early genes. In this electrophysiological study, we used patch-clamp techniques to characterize the membrane properties of GG neurons. Our results offer evidence of functional heterogeneity in the GG. GG neurons fire spontaneously and independently in several stable patterns, including phasic and repetitive single-spike modes of discharge. Whole cell recordings demonstrated two distinct voltage-gated fast-inactivating Na+ currents with different steady-state voltage dependencies and different sensitivities to tetrodotoxin. Hodgkin-Huxley simulations showed that these Na+ currents confer dual mechanisms of action potential generation and contribute to different firing patterns. Additionally, GG neurons exhibited hyperpolarization-activated inward currents that modulated spontaneous firing in vitro. Thus, in GG neurons, the heterogeneity of firing patterns is linked to the unusual repertoire of ionic currents. The membrane properties described here will aid the interpretation of chemosensory function in the GG.

scholarly journals A Possible Mechanism for the Aglycemia-Induced Depression of Glutamatergic Excitation in the Striatum

1997 ◽  
Vol 17 (10) ◽  
pp. 1121-1126 ◽  
Author(s):  
Paolo Calabresi ◽  
Diego Centonze ◽  
Antonio Pisani ◽  
Giorgio Bernardi
Keyword(s):  
Field Potential ◽  
Membrane Conductance ◽  
Glucose Deprivation ◽  
Channel Blockers ◽  
Partial Recovery ◽  
Striatal Neurons ◽  
Inward Current ◽  
Potential Amplitude ◽  
Excitatory Transmission ◽  
Electrophysiological Recordings

We have studied the possible mechanisms underlying the decrease of excitatory transmission induced by glucose deprivation by using electrophysiological recordings in corticostriatal slices. Extracellular field potentials were recorded in the striatum after cortical stimulation; these potentials were progressively reduced by glucose deprivation. The reduction started 5 minutes after the onset of aglycemia. The field potential was fully suppressed after 40 minutes of glucose deprivation. After the washout of the aglycemic solution only a partial recovery was observed. Aglycemia also induced a delayed inward current during single-microelectrode voltage-clamp recordings from spiny neurons. This inward current was coupled with an increased membrane conductance. The A1 adenosine receptor antagonists, 8-cyclopentyl-1,3-dimethylxanthine (CPT, 1 μmol/L) and 1,3-dipropyl-8-cyclopentylxanthine (CPX, 300 nmol/L), significantly reduced the aglycemia-induced decrease of field potential amplitude. Moreover, in the presence of CPT and CPX, a full recovery of the field potential amplitude after the interruption of the aglycemic solution was observed. Conversely, these antagonists affected neither the inward current nor the underlying conductance increase produced by glucose deprivation. The ATP-sensitive potassium channel blockers glibenclamide (10 μmol/L) and glipizide (100 nmol/L) had no effect on the aglycemia-induced decrease of the field potential amplitude. We suggest that endogenous adenosine, but not ATP-dependent potassium channels, plays a significant role in the aglycemia-induced depression of excitatory transmission at corticostriatal synapses probably through a presynaptic mechanism. Moreover, adenosine is not involved in the postsynaptic changes induced by glucose deprivation in spiny striatal neurons.

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