Cocaine- and amphetamine-regulated transcript peptide modulation of voltage-gated Ca2+ signaling in hippocampal neurons

Elena Petroff, Jianguo Chen, Pastor R. Couceyro, Toshinori Hoshi

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95 Citations (Scopus)

Abstract

Administration of cocaine and amphetamine increases cocaine- and amphetamine-regulated transcript (CART) expression in the rat striatum (Douglass et al., 1995). CART mRNA is highly expressed in different parts of the human and rat brain, including hippocampus (Douglass et al., 1995; Couceyro et al., 1997; Kuhar and Yoho, 1999; Hurd and Fagergren, 2000). The presence of CART peptide 55-102 immunoreactivity in dense core vesicles of axon terminals suggests that the peptide may be released and may act as a neuromodulator (Smith et al., 1997) to induce neurophysiological and behavioral effects. Little is known, however, about CART peptide-responsive cells, receptor(s), or intracellular signaling mechanisms that mediate CART peptide action. Here we show that CART peptide 55-102 inhibits voltage-dependent intracellular Ca2+ signaling and attenuates cocaine enhancement of depolarization-induced Ca2+ influx in rat hippocampal neurons. The inhibitory effect of CART peptide 55-102 on Ca2+ signaling is likely mediated by an inhibition of L-type voltage-gated Ca2+ channel activity via a G-protein-dependent pathway. These results indicate that voltage-gated Ca2+ channels in hippocampal neurons are targets for CART peptide 55-102 and suggest that CART peptides may be important in physiology and behavior mediated by the hippocampus, such as certain forms of learning and memory.

Original languageEnglish
Pages (from-to)7474-7480
Number of pages7
JournalJournal of Neuroscience
Volume21
Issue number19
StatePublished - 1 Oct 2001

Fingerprint

Amphetamine
Cocaine
Neurons
Peptides
Hippocampus
Presynaptic Terminals
Secretory Vesicles
GTP-Binding Proteins
Neurotransmitter Agents
Learning
Messenger RNA
cocaine- and amphetamine-regulated transcript protein (55-102)
Brain

Keywords

  • Calcium
  • CART
  • Cocaine
  • Hippocampus
  • Neuropeptide
  • Voltage-gated calcium channels

Cite this

Petroff, Elena ; Chen, Jianguo ; Couceyro, Pastor R. ; Hoshi, Toshinori. / Cocaine- and amphetamine-regulated transcript peptide modulation of voltage-gated Ca2+ signaling in hippocampal neurons. In: Journal of Neuroscience. 2001 ; Vol. 21, No. 19. pp. 7474-7480.
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abstract = "Administration of cocaine and amphetamine increases cocaine- and amphetamine-regulated transcript (CART) expression in the rat striatum (Douglass et al., 1995). CART mRNA is highly expressed in different parts of the human and rat brain, including hippocampus (Douglass et al., 1995; Couceyro et al., 1997; Kuhar and Yoho, 1999; Hurd and Fagergren, 2000). The presence of CART peptide 55-102 immunoreactivity in dense core vesicles of axon terminals suggests that the peptide may be released and may act as a neuromodulator (Smith et al., 1997) to induce neurophysiological and behavioral effects. Little is known, however, about CART peptide-responsive cells, receptor(s), or intracellular signaling mechanisms that mediate CART peptide action. Here we show that CART peptide 55-102 inhibits voltage-dependent intracellular Ca2+ signaling and attenuates cocaine enhancement of depolarization-induced Ca2+ influx in rat hippocampal neurons. The inhibitory effect of CART peptide 55-102 on Ca2+ signaling is likely mediated by an inhibition of L-type voltage-gated Ca2+ channel activity via a G-protein-dependent pathway. These results indicate that voltage-gated Ca2+ channels in hippocampal neurons are targets for CART peptide 55-102 and suggest that CART peptides may be important in physiology and behavior mediated by the hippocampus, such as certain forms of learning and memory.",
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Cocaine- and amphetamine-regulated transcript peptide modulation of voltage-gated Ca2+ signaling in hippocampal neurons. / Petroff, Elena; Chen, Jianguo; Couceyro, Pastor R.; Hoshi, Toshinori.

In: Journal of Neuroscience, Vol. 21, No. 19, 01.10.2001, p. 7474-7480.

Research output: Contribution to journalArticleResearchpeer-review

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