Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex

Research output: Contribution to journalArticle

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Abstract

The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (P<0.01) decrease (-28%) in ACh release in the frontal association cortex, a significant (P<0.01) decrease (-23%) in respiratory rate, and a significant (P<0.01) increase (223%) in time to righting after anesthesia. Additional in vitro studies used the [35S]guanylyl-5′-O-(γ-thio) -triphosphate ([35S]GTPγS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain. In vitro treatment with carbachol (1 mM) caused a significant (P<0.01) increase in [35S]GTPγS binding in the frontal association cortex (62%) and basal forebrain nuclei including medial septum (227%), vertical (210%) and horizontal (165%) limbs of the diagonal band of Broca, and substantia innominata (127%). G protein activation by carbachol was concentration- dependent and blocked by atropine, indicating that the carbachol-stimulated [35S]GTPγS binding was mediated by muscarinic cholinergic receptors. Together, the in vitro and in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.

Original languageEnglish (US)
Pages (from-to)17-29
Number of pages13
JournalNeuroscience
Volume123
Issue number1
DOIs
StatePublished - Jan 1 2004

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Carbachol
Frontal Lobe
Prefrontal Cortex
Inbred C57BL Mouse
Acetylcholine
Microdialysis
Cholinergic Receptors
Muscarinic Receptors
Respiratory Rate
Arousal
GTP-Binding Proteins
Brain Stem
Anesthesia
Substantia Innominata
Diagonal Band of Broca
Guanine Nucleotides
Basal Ganglia
Atropine
Synaptic Transmission
Cholinergic Agents

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Carbachol in the pontine reticular formation of C57BL/6J mouse decreases acetylcholine release in prefrontal cortex. / Demarco, G. J.; Baghdoyan, Helen; Lydic, Ralph.

In: Neuroscience, Vol. 123, No. 1, 01.01.2004, p. 17-29.

Research output: Contribution to journalArticle

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abstract = "The prefrontal cortex and brainstem modulate autonomic and arousal state control but the neurotransmitter mechanisms underlying communication between prefrontal cortex and brainstem remain poorly understood. This study examined the hypothesis that microdialysis delivery of carbachol to the pontine reticular formation (PRF) of anesthetized C57BL/6J (B6) mouse modulates acetylcholine (ACh) release in the frontal association cortex. Microdialysis delivery of carbachol (8.8 mM) to the PRF caused a significant (P<0.01) decrease (-28{\%}) in ACh release in the frontal association cortex, a significant (P<0.01) decrease (-23{\%}) in respiratory rate, and a significant (P<0.01) increase (223{\%}) in time to righting after anesthesia. Additional in vitro studies used the [35S]guanylyl-5′-O-(γ-thio) -triphosphate ([35S]GTPγS) assay to test the hypothesis that muscarinic cholinergic receptors activate guanine nucleotide binding proteins (G proteins) in the frontal association cortex and basal forebrain. In vitro treatment with carbachol (1 mM) caused a significant (P<0.01) increase in [35S]GTPγS binding in the frontal association cortex (62{\%}) and basal forebrain nuclei including medial septum (227{\%}), vertical (210{\%}) and horizontal (165{\%}) limbs of the diagonal band of Broca, and substantia innominata (127{\%}). G protein activation by carbachol was concentration- dependent and blocked by atropine, indicating that the carbachol-stimulated [35S]GTPγS binding was mediated by muscarinic cholinergic receptors. Together, the in vitro and in vivo data show for the first time in B6 mouse that cholinergic neurotransmission in the PRF can significantly alter ACh release in frontal association cortex, arousal from anesthesia, and respiratory rate.",
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