Glucocorticoid Receptor Activation Lowers the Threshold for NMDA-Receptor-Dependent Homosynaptic Long-Term Depression in the Hippocampus Through Activation of Voltage-Dependent Calcium Channels

1997 ◽  
Vol 78 (1) ◽  
pp. 1-9 ◽  
Author(s):  
Christine M. Coussens ◽  
D. Steven Kerr ◽  
Wickliffe C. Abraham
Keyword(s):  
Nmda Receptor ◽  
Calcium Channels ◽  
Glucocorticoid Receptor ◽  
Receptor Agonist ◽  
Receptor Activation ◽  
Bay K 8644 ◽  
Long Term Depression ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Coussens, Christine M., D. Steven Kerr, and Wickliffe C. Abraham. Glucocorticoid receptor activation lowers the threshold for NMDA-receptor-dependent homosynaptic long-term depression in the hippocampus through activation of voltage-dependent calcium channels. J. Neurophysiol. 78: 1–9, 1997. The effects of the glucocorticoid receptor agonist RU-28362 on homosynaptic long-term depression (LTD) were examined in hippocampal slices obtained from adrenal-intact adult male rats. Field excitatory postsynaptic potentials were evoked by stimulation of the Schaffer collateral/commissural pathway and recorded in stratum radiatum of area CA1. Low-frequency stimulation (LFS) was delivered at LTD threshold (2 bouts of 600 pulses, 1 Hz, at baseline stimulation intensity). LFS of the Schaffer collaterals did not produce significant homosynaptic LTD in control slices. However, identical conditioning in the presence of the glucocorticoid receptor agonist RU-28362 (10 μM) produced a robust LTD, which was blocked by the selective glucocorticoid antagonist RU-38486. The LTD induced by glucocorticoid receptor activation was dependent on N-methyl-d-aspartate (NMDA) receptor activity, because the specific NMDA receptor antagonist d(−)-2-amino-5-phosphonopentanoic acid (d-AP5) blocked the facilitation. However, the facilitation of LTD was not due to a potentiation of the isolated NMDA receptor potential by RU-28362. The facilitation of LTD byRU-28362 was also blocked by coincubation of the L-type voltage-dependent calcium channel (VDCC) antagonist nimodipine. Selective activation of the L-type VDCCs by the agonist Bay K 8644 also facilitated LTD induction. Both nimodipine and d-AP5 were effective in blocking the facilitation of LTD by Bay K 8644. These results indicate that L-type VDCCs can contribute to NMDAreceptor-dependent LTD induction.

NMDA-Receptor-Dependent Synaptic Activation of Voltage-Dependent Calcium Channels in Basolateral Amygdala

2000 ◽  
Vol 83 (2) ◽  
pp. 685-692 ◽  
Author(s):  
Jeffrey L. Calton ◽  
Maeng-Hee Kang ◽  
Wilkie A. Wilson ◽  
Scott D. Moore
Keyword(s):  
Nmda Receptor ◽  
Calcium Channels ◽  
Basolateral Amygdala ◽  
Pyramidal Cells ◽  
Activation Threshold ◽  
Afferent Stimulus ◽  
Voltage Dependent ◽  
Nmda Glutamate Receptors ◽  
Voltage Dependent Calcium Channels ◽  
Cell Current

Afferent stimulation of pyramidal cells in the basolateral amygdala produced mixed excitatory postsynaptic potentials (EPSPs) mediated by N-methyl-d-aspartate (NMDA) and non-NMDA glutamate receptors during whole cell current-clamp recordings. In the presence of GABAA receptor blockade, the mixed EPSPs recruited a large “all-or-none” depolarizing event. This recruited event was voltage dependent and had a distinct activation threshold. An analogous phenomenon elicited by exogenous glutamate in the presence of tetrodotoxin (TTX) was blocked by Cd2+, suggesting that the event was a Ca2+ spike. Selective glutamatergic blockade revealed that these Ca2+ spikes were recruited readily by single afferent stimulus pulses that elicited NMDA EPSPs. In contrast, non-NMDA EPSPs induced by single stimuli failed to elicit the Ca2+ spike even at maximal stimulus intensities although these non-NMDA EPSPs depolarized the soma more effectively than mixed EPSPs. Elongation of non-NMDA EPSPs by cyclothiazide or brief trains of stimulation were also unable to elicit the Ca2+ spike. Blockade of K+ channels with intracellular Cs+enabled single non-NMDA EPSPs to activate the Ca2+ spike. The finding that voltage-dependent calcium channels are activated preferentially by NMDA-receptor-mediated EPSPs provides a mechanism for NMDA-receptor-dependent plasticity independent of Ca2+influx through the NMDA receptor.

scholarly journals Up-regulation of L-type Voltage-dependent Calcium Channels after Long Term Exposure to Nicotine in Cerebral Cortical Neurons

2001 ◽  
Vol 277 (10) ◽  
pp. 7979-7988 ◽  
Author(s):  
Masashi Katsura ◽  
Yutaka Mohri ◽  
Keijiro Shuto ◽  
Yan Hai-Du ◽  
Taku Amano ◽  
...  
Keyword(s):  
Calcium Channels ◽  
Cortical Neurons ◽  
Cerebral Cortical Neurons ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Voltage-dependent calcium channels in rat midbrain dopamine neurons: modulation by dopamine and GABAB receptors

1995 ◽  
Vol 74 (3) ◽  
pp. 1137-1148 ◽  
Author(s):  
D. L. Cardozo ◽  
B. P. Bean
Keyword(s):  
Calcium Channels ◽  
Calcium Current ◽  
Receptor Agonist ◽  
Gabab Receptor ◽  
Calcium Currents ◽  
Dopamine Neurons ◽  
Gabab Receptors ◽  
High Threshold ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

1. Voltage-dependent calcium channels were studied with whole cell voltage-clamp recordings from neurons enzymatically dispersed from the ventral mesencephalon of rat brains (postnatal days 3-10) and identified as dopamine neurons by 5,7-dihydroxytryptamine autofluorescence. 2. Dopamine neurons had large high-threshold calcium currents activated by depolarizations positive to -50 mV. Different components of calcium channel current were not readily distinguishable by voltage dependence or kinetics, but pharmacological experiments showed the existence of different channel types. The overall current had significant components blocked by nimodipine (28%), by omega-conotoxin GVIA (22%), and by omega-agatoxin-IVA (omega-Aga-IVA) (37%), and there was a significant amount of current (16%) remaining in saturating concentrations of all three blockers. 3. High-threshold calcium current was reversibly reduced by the gamma-aminobutyric acid-B (GABAB) receptor agonist baclofen and by dopamine and the D2 receptor agonist quinpirole. Inhibition by GABAB or dopamine agonists developed and reversed within seconds. 4. Quinpirole reduced both omega-conotoxin-sensitive and omega-Aga-IVA-sensitive components of calcium current. 5. With physiological ionic conditions, inward calcium currents were outweighed by outward currents, in part through calcium-activated potassium channels activated by omega-conotoxin-sensitive and omega-Aga-IVA-sensitive calcium entry.

scholarly journals Dopamine D1/D5 Receptor Activation Reverses NMDA Receptor-Dependent Long-Term Depression in Rat Hippocampus

2007 ◽  
Vol 27 (11) ◽  
pp. 2918-2926 ◽  
Author(s):  
B. G. Mockett ◽  
D. Guevremont ◽  
J. M. Williams ◽  
W. C. Abraham
Keyword(s):  
Nmda Receptor ◽  
Receptor Activation ◽  
Rat Hippocampus ◽  
Long Term Depression
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