Inhibition of nicotine-induced hippocampal norepinephrine release in rats by alpha-conotoxins MII and AulB microinjected into the locus coeruleus

Yitong Fu, Shannon G. Matta, J. Michael McIntosh, Burt Sharp

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27 Citations (Scopus)

Abstract

Hippocampal norepinephrine (NE) is secreted by neurons projecting from the locus coeruleus (LC) to the hippocampus; LC nicotinic receptors (NAchRs) are involved in the effects of systemic nicotine on this pathway. To clarify the NAchR subtypes, NAchR antagonists, termed α-conotoxins, were microinjected into the LC before nicotine; MII and AulB were used to assess the potential involvement of α3β2 and α3β4 subunit-containing NAchRs, respectively. Nicotine dose-dependently stimulated hippocampal NE release (P < 0.01). MII (>0.25 pmol) reduced the NE response to nicotine (67% decrease; P < 0.05), as did AulB (44% reduction by 25 pmol; P < 0.05). Administered together, however, MII and AulB were no more effective than MII. Thus, MII and AulB are capable of interacting with NAchR subtypes other than those previously defined as α3β2 and α3β4, respectively. NAchRs containing both β2 and β4subunits may be involved.

Original languageEnglish (US)
Pages (from-to)113-116
Number of pages4
JournalNeuroscience Letters
Volume266
Issue number2
DOIs
StatePublished - May 7 1999

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Locus Coeruleus
Nicotine
Norepinephrine
Conotoxins
Nicotinic Receptors
Hippocampus
Neurons
alpha-conotoxin MII

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Inhibition of nicotine-induced hippocampal norepinephrine release in rats by alpha-conotoxins MII and AulB microinjected into the locus coeruleus. / Fu, Yitong; Matta, Shannon G.; McIntosh, J. Michael; Sharp, Burt.

In: Neuroscience Letters, Vol. 266, No. 2, 07.05.1999, p. 113-116.

Research output: Contribution to journalArticle

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abstract = "Hippocampal norepinephrine (NE) is secreted by neurons projecting from the locus coeruleus (LC) to the hippocampus; LC nicotinic receptors (NAchRs) are involved in the effects of systemic nicotine on this pathway. To clarify the NAchR subtypes, NAchR antagonists, termed α-conotoxins, were microinjected into the LC before nicotine; MII and AulB were used to assess the potential involvement of α3β2 and α3β4 subunit-containing NAchRs, respectively. Nicotine dose-dependently stimulated hippocampal NE release (P < 0.01). MII (>0.25 pmol) reduced the NE response to nicotine (67{\%} decrease; P < 0.05), as did AulB (44{\%} reduction by 25 pmol; P < 0.05). Administered together, however, MII and AulB were no more effective than MII. Thus, MII and AulB are capable of interacting with NAchR subtypes other than those previously defined as α3β2 and α3β4, respectively. NAchRs containing both β2 and β4subunits may be involved.",
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