Role of nerve terminal L-type Ca2+ channel in the brain

Watanabe, Yasuo; Lawlor, George F.; Fujiwara, Michihiro

doi:10.1016/s0024-3205(98)00126-x

Cited by 23 publications

(11 citation statements)

References 14 publications

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“…Results of the current studies contradict those of two prior studies, which demonstrated 1 100-fold increase in rat striatal dopamine microdialysates after 8 BayK 8644 [Watanabe et al, 1998;Okita et al, 2000]. The discrepancy could refl ect the different species used, the location of the microdialysis probe within the striatum, or the mode of drug delivery.…”

Section: Discussioncontrasting

confidence: 97%

“…Two prior studies have suggested that activation of L-type calcium channels with 8 BayK 8644 stimulates a massive release of presynaptic dopamine stores [Watanabe et al, 1998;Okita et al, 2000]. Other studies have shown 8 BayK 8644 to stimulate dopamine release from striatal synpatosomes, slices of striatum in vitro, and cultured midbrain dopamine neurons [Nordstrom et al, 1986;Woodward and Leslie, 1986;Woodward et al, 1988;Chaudieu et al, 1992].…”

Section: Introductionmentioning

confidence: 99%

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The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

et al. 2006

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In rodents, activation of L-type calcium channels with ±BayK 8644 causes an unusual behavioral syndrome that includes dystonia and self-biting. Prior studies have linked both of these behaviors to dysfunction of dopaminergic transmission in the striatum. The current studies were designed to further elucidate the relationship between ±BayK 8644 and dopaminergic transmission in the expression of the behavioral syndrome. The drug does not appear to release presynaptic dopamine stores, since microdialysis of the striatum revealed dopamine release was unaltered by ±BayK 8644. In addition, the behaviors were preserved or even exaggerated in mice or rats with virtually complete dopamine depletion. On the other hand, pretreatment of mice with D₃ or D_1/5 dopamine receptor antagonists attenuated the behavioral effects of ±BayK 8644, while pretreatment with D₂ or D₄ antagonists had no effect. In D₃ receptor knockout mice, ±BayK 8644 elicited both dystonia and self-biting, but these behaviors were less severe than in matched controls. In D₁ receptor knockout mice, behavioral responses to ±BayK 8644 appeared exaggerated. These results argue that the behavioral effects of ±BayK 8644 are not mediated by a presynaptic influence. Instead, the behaviors appear to result from a postsynaptic activation of the drug, which does not require but can be modified by D₃ or D_1/5 receptors.

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Section: Discussioncontrasting

confidence: 97%

Section: Introductionmentioning

confidence: 99%

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

et al. 2006

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“…BBay K 8644 is known to stimulate dopamine release from rat striatal synaptosomes [34,35], rat striatal slices [36], and rat midbrain dopamine neurons in culture [37]. BBay K 8644 also increases the synthesis and turnover of dopamine in the intact mouse brain [6,38,39], and recent microdialysis studies have shown it to dramatically increase dopamine efflux in the rat striatum [40,41]. According to this hypothesis, reserpine and tetrabenazine may attenuate SB and SIB by blunting the release of dopamine in response to BBay K 8644.…”

Section: Discussionmentioning

confidence: 99%

Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences

Kasim¹,

Jinnah²

2003

Dev Neurosci

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The L-type calcium channel activator ±Bay K 8644 induces repetitive self-biting and self-injurious behavior in young mice. Since dopaminergic systems have been implicated in prior studies of these behaviors in both humans and animals, the present experiments were designed to test whether drugs influencing the dopaminergic systems could modify the behavioral responses to ±Bay K 8644. The ability of ±Bay K 8644 to provoke self-biting and self-injurious behavior was increased by amphetamine and GBR 12909, drugs that augment synaptic dopaminergic concentrations by blocking the reuptake and/or stimulating the release of dopamine. Conversely, self-biting and self-injurious behavior were decreased by tetrabenazine or reserpine, two drugs that deplete vesicular stores of dopamine. These results suggest that dopaminergic systems may play a role in the ability of ±Bay K 8644 to provoke self-biting and self-injurious behavior.

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“…LTCCs have been suggested to play a role in the augmented dopamine release observed during the expression of sensitized behaviors (Pierce and Kalivas, 1997). Although the neuronal distribution and physiology of Cav1.2 do not support a role in neurotransmitter release, LTCCs have been found to be involved in neurotransmitter release (Watanabe et al, 1998;Evans and Pocock, 1999;Okita et al, 2000), and Cav1.2 recently has been suggested to play this role in fearmediated behavior (Shinnick-Gallagher et al, 2003). Additional experiments are required to explore further the relevance of this mechanism in contributing to longterm changes in neurotransmitter release in forebrain targets innervated by VTA neurons, which may contribute to recurrent psychostimulant-induced behaviors.…”

Section: The Role Of Ltccs In Mediating Long-term Potentiationmentioning

confidence: 99%

L-Type Ca²⁺Channels Mediate Adaptation of Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in the Ventral Tegmental Area after Chronic Amphetamine Treatment

Rajadhyaksha¹,

Husson²,

Satpute³

et al. 2004

J. Neurosci.

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Role of nerve terminal L-type Ca2+ channel in the brain

Cited by 23 publications

References 14 publications

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences

L-Type Ca²⁺Channels Mediate Adaptation of Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in the Ventral Tegmental Area after Chronic Amphetamine Treatment

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Role of nerve terminal L-type Ca2+ channel in the brain

Cited by 23 publications

References 14 publications

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

The Role of Dopamine Receptors in the Neurobehavioral Syndrome Provoked by Activation of L-Type Calcium Channels in Rodents

Self-Biting Induced by Activation of L-Type Calcium Channels in Mice: Dopaminergic Influences

L-Type Ca2+Channels Mediate Adaptation of Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in the Ventral Tegmental Area after Chronic Amphetamine Treatment

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L-Type Ca²⁺Channels Mediate Adaptation of Extracellular Signal-Regulated Kinase 1/2 Phosphorylation in the Ventral Tegmental Area after Chronic Amphetamine Treatment