Cav1.2 calcium channels modulate the spiking pattern of hippocampal pyramidal cells

Lacinová, Ľubica; Moosmang, Sven; Langwieser, Nicolas; Hofmann, Franz; Kleppisch, Thomas

doi:10.1016/j.lfs.2007.10.009

Cited by 29 publications

(26 citation statements)

References 44 publications

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“…Whole-cell patch-clamp recording Acute slices (200-300 lm) were prepared from 2-weekold mice using a vibration microtome (Leica) as outlined elsewhere [28]. For recording, brain slices were placed in a recording chamber perfused continuously with aCSF bubbled with carbogen at room temperature.…”

Section: Field Epsp Recordings In Hippocampal Slicesmentioning

confidence: 99%

HCN2 channels in local inhibitory interneurons constrain LTP in the hippocampal direct perforant path

Matt¹,

Michalakis

Hofmann

et al. 2010

Cell. Mol. Life Sci.

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Neuronal hyperpolarization-activated cyclic nucleotide-gated (HCN) channels are known to modulate spontaneous activity, resting membrane potential, input resistance, afterpotential, rebound activity, and dendritic integration. To evaluate the role of HCN2 for hippocampal synaptic plasticity, we recorded long-term potentiation (LTP) in the direct perforant path (PP) to CA1 pyramidal cells. LTP was enhanced in mice carrying a global deletion of the channel (HCN2(-/-)) but not in a pyramidal neuron-restricted knockout. This precludes an influence of HCN2 located in postsynaptic pyramidal neurons. Additionally, the selective HCN blocker zatebradine reduced the activity of oriens-lacunosum moleculare interneurons in wild-type but not HCN2(-/-) mice and decreased the frequency of spontaneous inhibitory currents in postsynaptic CA1 pyramidal cells. Finally, we found amplified LTP in the PP of mice carrying an interneuron-specific deletion of HCN2. We conclude that HCN2 channels in inhibitory interneurons modulate synaptic plasticity in the PP by facilitating the GABAergic output onto pyramidal neurons.

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Section: Field Epsp Recordings In Hippocampal Slicesmentioning

confidence: 99%

HCN2 channels in local inhibitory interneurons constrain LTP in the hippocampal direct perforant path

Matt¹,

Michalakis

Hofmann

et al. 2010

Cell. Mol. Life Sci.

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“…Both VGCCs and NMDA receptors are known to be important sources of Ca 2+ influx for the induction of LTP in certain conditions [30], [31], [32]. Various L-type calcium channels have been demonstrated to be important in different forms of memories [33], [34], [35], [36], [37], [38]. However, the involvement of particular T- channel subtypes remains controversial.…”

Section: Introductionmentioning

confidence: 99%

Retrieval of Context-Associated Memory is Dependent on the Cav3.2 T-Type Calcium Channel

et al. 2012

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Among all voltage-gated calcium channels, the T-type Ca2+ channels encoded by the Cav3.2 genes are highly expressed in the hippocampus, which is associated with contextual, temporal and spatial learning and memory. However, the specific involvement of the Cav3.2 T-type Ca2+ channel in these hippocampus-dependent types of learning and memory remains unclear. To investigate the functional role of this channel in learning and memory, we subjected Cav3.2 homozygous and heterozygous knockout mice and their wild-type littermates to hippocampus-dependent behavioral tasks, including trace fear conditioning, the Morris water-maze and passive avoidance. The Cav3.2 −/− mice performed normally in the Morris water-maze and auditory trace fear conditioning tasks but were impaired in the context-cued trace fear conditioning, step-down and step-through passive avoidance tasks. Furthermore, long-term potentiation (LTP) could be induced for 180 minutes in hippocampal slices of WTs and Cav3.2 +/− mice, whereas LTP persisted for only 120 minutes in Cav3.2 −/− mice. To determine whether the hippocampal formation is responsible for the impaired behavioral phenotypes, we next performed experiments to knock down local function of the Cav3.2 T-type Ca2+ channel in the hippocampus. Wild-type mice infused with mibefradil, a T-type channel blocker, exhibited similar behaviors as homozygous knockouts. Taken together, our results demonstrate that retrieval of context-associated memory is dependent on the Cav3.2 T-type Ca2+ channel.

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“…Even if L-type calcium current may contribute to the membrane depolarization necessary for an action potential upstroke (Lacinova et al 2008), its full abolishment suggest involvement of sodium current inhi-bition. Indeed, micromolar concentrations of haloperidol inhibited sodium current activated in guinea-pig ventricular myocytes (Ogata and Narahashi 1989), in retinal ganglia (Ito et al 1996), in human atrial myocytes (Crumb et al 2006), or in rat ventricular myocytes (present work).…”

Section: Discussionmentioning

confidence: 99%

Haloperidol moderately inhibits cardiovascular L-type calcium current

Tarabová

Novàkovâ²,

Lacinová³

2009

gpb

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Abstract. Effects of haloperidol on L-type Ca V 1.2 channel were studied. Calcium current was measured in whole cell patch-clamp using calcium as a charge carrier. Inhibition by haloperidol was investigated in Ca V 1.2 channel natively expressed in rat cardiac myocytes and recombinant cardiac (Ca V 1.2 a ) and vascular (Ca V 1.2 b ) splice variants of the channel expressed in HEK 293 cells. Haloperidol inhibited L-type calcium current in a concentration-dependent manner with a threshold of 1 nmol/l. 1 μmol/l haloperidol inhibited 20.6 ± 3.6% of calcium current amplitude in cardiomyocytes, 25.4 ± 2.6% of current amplitude through the Ca V 1.2 b channel and 28.0 ± 2.7% of current through the Ca V 1.2 a channel. Inhibition was not accompanied by alteration of current waveform or by shift of current-voltage relation. In a current clamp haloperidol suppressed action potential generation. 1 μmol/l of the drug shortened the action potential duration in part of the cells and suppressed fully action potential in other cells. Moderate inhibition of the L-type calcium channels by haloperidol might cause shortening of action potential. Complete abolishment of action potential must have been mediated by inhibition of another, likely sodium channel.

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Cav1.2 calcium channels modulate the spiking pattern of hippocampal pyramidal cells

Cited by 29 publications

References 44 publications

HCN2 channels in local inhibitory interneurons constrain LTP in the hippocampal direct perforant path

HCN2 channels in local inhibitory interneurons constrain LTP in the hippocampal direct perforant path

Retrieval of Context-Associated Memory is Dependent on the Cav3.2 T-Type Calcium Channel

Haloperidol moderately inhibits cardiovascular L-type calcium current

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