Altered CSF constituents and retrograde amnesia in rats: A biochemical approach

Manthei, R.C.; Wright, Dennis C.; Kenny, Alexander D.

doi:10.1016/0031-9384(73)90214-x

Cited by 13 publications

(10 citation statements)

References 12 publications

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“…We also investigated whether potassium currents act to inhibit bursting. We increased the concentration of potassium from 2.5 to 3.5 mM, which is closer to the value measured in the CSF of rats (Manthie at al., 1973). Membrane potential was maintained at Ϫ67 mV, with DC injection as needed.…”

Section: Resultssupporting

confidence: 80%

“…This difference may be attributable to extracellular calcium concentration. We limited our manipulations to a narrow range reflecting physiologically relevant conditions (Manthie et al, 1973). Sodium current plays a more predominant role in creating the ADP under conditions of lower-to-absent calcium, which causes upregulation of persistent sodium current and changes in channel gating Cota, 1991, 1999;Azouz et al, 1996;Su et al, 2001).…”

Section: Calcium and Sodium Currents Partner To Create Burstingmentioning

confidence: 99%

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R-Type Calcium Channels Contribute to Afterdepolarization and Bursting in Hippocampal CA1 Pyramidal Neurons

Metz

Jarsky²,

Martina³

et al. 2005

Journal of Neuroscience

160

150

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Action potentials in pyramidal neurons are typically followed by an afterdepolarization (ADP), which in many cells contributes to intrinsic burst firing. Despite the ubiquity of this common excitable property, the responsible ion channels have not been identified. Using current-clamp recordings in hippocampal slices, we find that the ADP in CA1 pyramidal neurons is mediated by an Ni 2ϩ -sensitive calcium tail current. Voltage-clamp experiments indicate that the Ni 2ϩ -sensitive current has a pharmacological and biophysical profile consistent with R-type calcium channels. These channels are available at the resting potential, are activated by the action potential, and remain open long enough to drive the ADP. Because the ADP correlates directly with burst firing in CA1 neurons, R-type calcium channels are crucial to this important cellular behavior, which is known to encode hippocampal place fields and enhance synaptic plasticity.

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Section: Resultssupporting

confidence: 80%

Section: Calcium and Sodium Currents Partner To Create Burstingmentioning

confidence: 99%

R-Type Calcium Channels Contribute to Afterdepolarization and Bursting in Hippocampal CA1 Pyramidal Neurons

Metz

Jarsky²,

Martina³

et al. 2005

Journal of Neuroscience

160

150

View full text Add to dashboard Cite

show abstract

“…Stimulation consisted of regular and irregular trains. Experiments were conducted at 34°C and divalent ion concentrations in the external saline (1 mM Mg 2ϩ , 1.5 mM Ca 2ϩ in control conditions) were near reported values for rat CSF (Manthei et al, 1973).…”

Section: Resultsmentioning

confidence: 99%

“…Slices were superf used with an external saline solution containing (in mM): 125 NaC l, 2.5 KC l, 1.5 C aC l 2 , 1 MgC l 2 , 26 NaHC O 3 , 1.25 NaH 2 PO 4 , and 25 glucose, bubbled with 95% O 2 /5% C O 2 . Divalent ion concentrations were matched near reported values for rat C SF (Manthei et al, 1973), and experiments were conducted at 34 Ϯ 1°C to better simulate physiological conditions. Bicuculline (20 M) was added to the external solution to suppress synaptic currents mediated by GABA A receptors.…”

Section: Methodsmentioning

confidence: 99%

Modulation of Transmission during Trains at a Cerebellar Synapse

Kreitzer

Regehr

2000

J. Neurosci.

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Activity-dependent processes dynamically regulate synapses on the time scale of milliseconds to seconds. Here, we examine the factors governing synaptic strength during repetitive stimulation, both in control conditions and during presynaptic inhibition. Field recordings of presynaptic volleys, optical measurements of presynaptic calcium, and voltage-clamp recordings of postsynaptic currents were used to examine parallel fiber to Purkinje cell synapses in cerebellar brain slices at 34°C. In control conditions, regular stimulus trains (1-50 Hz) evoked up to a 250% peak synaptic enhancement, whereas during irregular stimulation, a threefold variability in EPSC amplitude was observed. When initial EPSC amplitudes were reduced by 50%, either by lowering external calcium or by activating adenosine A 1 or GABA B receptors, the peak enhancement during regular trains was 500%, and synaptic variability during irregular trains was nearly sixfold. By contrast, changes in fiber excitability and calcium influx per pulse were small during trains. Presynaptic calcium measurements indicated that by pulse 10, stimulusevoked calcium influx had increased by ϳ15%, which on the basis of the measured relationship between calcium influx and release corresponds to an EPSC enhancement of 50%. This enhancement was the same in all experimental conditions, even in the presence of N 6 -cyclopentyladenosine or baclofen, suggesting that repetitive stimulation does not relieve the G-protein inhibition of calcium channels by these modulators. Therefore, for our experimental conditions, changes in synaptic strength during trains are primarily attributable to residual calcium (Ca res )-dependent short-term plasticities, and the actions of neuromodulators during repetitive stimulation result from their inhibition of initial calcium influx and the resulting effects on Ca res and calcium-driven processes.

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“…The standard external solution, which will be referred to as "1.2 Ca Tyrode's solution," consisted of (in mM) 150 NaCl, 3.5 KCl, 1.2 CaCl 2 , 1 MgCl 2 , 10 HEPES, and 10 glucose, pH 7.4 with ϳ5 NaOH). The concentrations of CaCl 2 and KCl were chosen to mimic rat CSF more closely than the higher CaCl 2 and lower KCl commonly used for electrophysiological recordings (Manthei et al, 1973;Jones and Keep, 1988;Brumberg et al, 2000). For "0 Ca Tyrode's," the CaCl 2 was replaced by an equimolar amount of MgCl 2 or CoCl 2 .…”

Section: Scn Cell Preparationmentioning

confidence: 99%

Mechanism of Spontaneous Firing in Dorsomedial Suprachiasmatic Nucleus Neurons

Jackson¹,

Yao²,

Bean³

2004

J. Neurosci.

160

218

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We studied acutely dissociated neurons from the dorsomedial (shell) region of the rat suprachiasmatic nucleus (SCN) with the aim of determining the ionic conductances that underlie spontaneous firing. Most isolated neurons were spontaneously active, firing rhythmically at an average frequency of 8 Ϯ 4 Hz. After application of TTX, oscillatory activity generally continued, but more slowly and at more depolarized voltages; these oscillations were usually blocked by 2 M nimodipine. To quantify the ionic currents underlying normal spontaneous activity, we voltage clamped cells using a segment of the spontaneous activity of each cell as voltage command and then used ionic substitution and selective blockers to isolate individual currents. TTX-sensitive sodium current flowed throughout the interspike interval, averaging Ϫ3 pA at Ϫ60 mV and Ϫ11 pA at Ϫ55 mV. Calcium current during the interspike interval was, on average, fourfold smaller. Except immediately before spikes, calcium current was outweighed by calcium-activated potassium current, and in current clamp, nimodipine usually depolarized cells and slowed firing only slightly (average, ϳ8%). Thus, calcium current plays only a minor role in pacemaking of dissociated SCN neurons, although it can drive oscillatory activity with TTX present. During normal pacemaking, the early phase of spontaneous depolarization (Ϫ85 to Ϫ60 mV) is attributable mainly to background conductance; cells have relatively depolarized resting potentials (with firing stopped by TTX and nimodipine) of Ϫ55 to Ϫ50 mV, although input resistance is high (9.5 Ϯ 4.1 G⍀). During the later phase of pacemaking (positive to Ϫ60 mV), TTX-sensitive sodium current is dominant.

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Altered CSF constituents and retrograde amnesia in rats: A biochemical approach

Cited by 13 publications

References 12 publications

R-Type Calcium Channels Contribute to Afterdepolarization and Bursting in Hippocampal CA1 Pyramidal Neurons

R-Type Calcium Channels Contribute to Afterdepolarization and Bursting in Hippocampal CA1 Pyramidal Neurons

Modulation of Transmission during Trains at a Cerebellar Synapse

Mechanism of Spontaneous Firing in Dorsomedial Suprachiasmatic Nucleus Neurons

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