Characterization of pharmacologically identified voltage-gated calcium channel currents in acutely isolated rat neocortical neurons. I. Adult neurons

Lorenzon, Nancy M.; Foehring, Robert C.

doi:10.1152/jn.1995.73.4.1430

Cited by 69 publications

(89 citation statements)

References 33 publications

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“…For example, the ␣1A (corresponding to P/Qtype currents), and ␣1B (N-type) calcium channel subunits (Bourinet et al, 1994(Bourinet et al, , 1996Herlitze et al, 1996) expressed in cell lines or in oocytes, as well as N-and P-type currents in situ (Mintz et al, 1992;Mintz and Bean, 1993;Toselli and Taglietti, 1995), display agonist-or GTP␥S-induced inhibition and facilitation. However, in a similar manner to what is observed in BF cholinergic neurons, facilitation in cortical neurons also occurs principally through disinhibition of the N current (Swartz, 1993), although other types of calcium currents (T, L, P, and R) are known to be present (Lorenzon and Foehring, 1995;Markram et al, 1995).…”

Section: Disinhibition Of N-type Currentsupporting

confidence: 52%

Facilitation of N-Type Calcium Current Is Dependent on the Frequency of Action Potential-Like Depolarizations in Dissociated Cholinergic Basal Forebrain Neurons of the Guinea Pig

Williams¹,

Serafin²,

Mühlethaler³

et al. 1997

J. Neurosci.

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Voltage-dependent inhibition of high voltage-activated (HVA) calcium currents by G-proteins can be transiently relieved (facilitated) by strong depolarizing prepulses. However, with respect to the physiological significance of facilitation, it remains to be established if it can be induced by action potentials (AP) in central neurons. With the use of whole-cell recordings of dissociated cholinergic basal forebrain neurons of the guinea pig, it is shown that the GTP␥S-inhibited HVA currents that occur through N-ethylmaleimide (NEM)-sensitive G i -G o subtypes of G-proteins can be facilitated. Furthermore, although different types of HVA channels are present in these neurons, facilitation occurred mostly through disinhibition of the N-type current. On the basis of data indicating that the recovery from facilitation was relatively slow, we tested if more physiological stimuli that crudely mimicked APs (2 msec long depolarizations to 40 mV from a holding of Ϫ50 mV) potentially could induce facilitation of HVA currents inhibited by GTP␥S and cholinergic agonists. Indeed, evidence is provided that the extent of facilitation is dependent on both the number and frequency of AP-like depolarizations. These results suggest that firing rates and patterns of discharge of neurons could influence their responsiveness to transmitters acting on N-type HVA calcium channels.

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Section: Disinhibition Of N-type Currentsupporting

confidence: 52%

Facilitation of N-Type Calcium Current Is Dependent on the Frequency of Action Potential-Like Depolarizations in Dissociated Cholinergic Basal Forebrain Neurons of the Guinea Pig

Williams¹,

Serafin²,

Mühlethaler³

et al. 1997

J. Neurosci.

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“…Although it is currently unknown whether Na ϩ channel function is changed after repeated cocaine administration, a possible increase in I Ca in cocaine-withdrawn mPFC neurons has been suggested . It is well established that cortical neurons express various subtypes of Ca 2ϩ channels (Brown et al, 1993;Ye and Akaike, 1993;Lorenzon and Foehring, 1995), which are modulated by DA receptors (Young and Yang, 2004). Based on those findings, we hypothesize that chronic cocaineinduced alterations in DA neurotransmission may change the activity of whole-cell I Ca , thereby increasing the membrane excitability in rat pyramidal mPFC neurons, particularly in response to certain stimuli.…”

Section: Introductionmentioning

confidence: 71%

“…Voltagesensitive I Ca was isolated by using an internal solution consisting of (in mM) 180 N-methylglutamine, 40 HEPES, 4 MgCl 2 , 0.1 BAPTA, 12 phosphocreatine, 2 Na 2 ATP, 0.2 Na 2 GTP, and 0.1 leupeptin, pH 7.3 (270 -275 mOsm/l) and an external solution consisting of (in mM) 135 NaCl, 20 CsCl, 1 MgCl 2 , 10 glucose, 10 HEPES, 0.001 TTX, and 5 BaCl 2 , pH 7.4 (300 -305 mOsm/l). Ba 2ϩ was used as a charge carrier and K ϩ channel blocker (Lorenzon and Foehring, 1995). Recordings were performed using an amplifier and controlled/monitored with a personal computer.…”

Section: Methodsmentioning

confidence: 99%

Repeated Cocaine Administration Increases Voltage-Sensitive Calcium Currents in Response to Membrane Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

Nasif¹,

Hu²,

White³

2005

J. Neurosci.

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The medial prefrontal cortex (mPFC) plays a critical role in cocaine addiction. However, evidence to elucidate how the mPFC is functionally involved in cocaine addiction remains incomplete. Recent studies have revealed that repeated cocaine administration induces various neuroadaptations in pyramidal mPFC neurons, including a reduction in voltage-gated K ϩ currents (VGKCs) and a possible increase in voltage-sensitive Ca 2ϩ currents (I Ca ). Here, we performed both current-clamp recordings in brain slices and voltage-clamp recordings in freshly dissociated cells to determine whether I Ca is altered in mPFC pyramidal neurons after chronic cocaine treatment with a short-term or long-term withdrawal. In addition, a critical role of VGKCs in regulating the generation of Ca 2ϩ plateau potential was also studied in mPFC neurons. Repeated cocaine administration significantly prolonged the duration of evoked Ca 2ϩ plateau potentials and increased the whole-cell I Ca in mPFC neurons after a 3 d withdrawal. Selective blockade of L-type Ca 2ϩ channels by nifedipine not only significantly increased the threshold but also reduced the duration and amplitude of Ca 2ϩ plateau potentials in both saline-and cocaine-withdrawn mPFC neurons. However, there was no significant difference in the increased threshold, reduced duration, and decreased amplitude of Ca 2ϩ potentials between saline-and cocaine-withdrawn neurons after blockade of L-type Ca 2ϩ channels. Moreover, an increase in amplitude was also observed, whereas the prolonged duration persisted, in Ca 2ϩ potentials after 2-3 weeks of withdrawal. These findings indicate that chronic exposure to cocaine facilitates the responsiveness of I Ca , particularly via the activated L-type Ca 2ϩ channels, to excitatory stimuli in rat mPFC pyramidal neurons.

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“…We also constructed steady-state activation curves based on tail currents [31]. Cells were repolarized to -40 mV, after a depolarization from -60 mV to a series of test potentials (from -60 to +30 mV).…”

Section: Effects Of Gdnf On the Kinetics Of Hva Channelsmentioning

confidence: 99%

GDNF Acutely Potentiates Ca<sup>2+</sup> Channels and Excitatory Synaptic Transmission in Midbrain Dopaminergic Neurons

Wang

Chen

et al. 2003

Neurosignals

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Glial cell line-derived neurotrophic factor (GDNF) is best known for its long-term survival effect on dopaminergic neurons in the ventral midbrain. A recent study showed that acute application of GDNF to these neurons suppresses A-type potassium channels and potentiates neuronal excitability. Here we have characterized the acute effects of GDNF on Ca²⁺ channels and synaptic transmission. GDNF rapidly and reversibly potentiated the high voltage-activated (HVA) Ca²⁺ channel currents in cultured dopaminergic neurons. Analyses of channel kinetics indicate that GDNF decreased the activation time constant, increased the inactivation and deactivation time constants of HVA Ca²⁺ channel currents. Ca²⁺ imaging experiments demonstrate that GDNF facilitated Ca²⁺ influx induced by membrane depolarization. To investigate the physiological consequences of the Ca²⁺ channel modulation, we examined the acute effects of GDNF on excitatory synaptic transmission at synapses made by these dopaminergic neurons, which co-release the transmitter glutamate. Within 3 min of application, GDNF increased the amplitude of spontaneous and evoked excitatory autaptic- or multiple-postsynaptic currents. The frequency as well as the amplitude of miniature excitatory postsynaptic currents was also increased. These results reveal, for the first time, an acute effect of GDNF on synaptic transmission and its potential mechanisms, and suggest that an important function of GDNF for midbrain dopaminergic neurons is the acute modulation of transmission and ion channels.

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Characterization of pharmacologically identified voltage-gated calcium channel currents in acutely isolated rat neocortical neurons. I. Adult neurons

Cited by 69 publications

References 33 publications

Facilitation of N-Type Calcium Current Is Dependent on the Frequency of Action Potential-Like Depolarizations in Dissociated Cholinergic Basal Forebrain Neurons of the Guinea Pig

Facilitation of N-Type Calcium Current Is Dependent on the Frequency of Action Potential-Like Depolarizations in Dissociated Cholinergic Basal Forebrain Neurons of the Guinea Pig

Repeated Cocaine Administration Increases Voltage-Sensitive Calcium Currents in Response to Membrane Depolarization in Medial Prefrontal Cortex Pyramidal Neurons

GDNF Acutely Potentiates Ca<sup>2+</sup> Channels and Excitatory Synaptic Transmission in Midbrain Dopaminergic Neurons

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