Acetylcholine Becomes the Major Excitatory Neurotransmitter in the Hypothalamus In Vitro in the Absence of Glutamate Excitation
Open accessAbstract
Glutamate and GABA are two major fast neurotransmitters (excitatory and inhibitory, respectively) in the CNS, including the hypothalamus. They play a key role in the control of excitation/inhibition balance and determine the activity and excitability of neurons in many neuronal circuits. Using neuronal cultures, whole-cell recording, Ca(2+) imaging, and Northern blots, we studied the compensatory regulation of neuronal activity during a prolonged decrease in glutamate excitation. We report here that after a chronic (6-17 d) blockade of ionotropic glutamate receptors, neurons in hypothalamic cultures revealed excitatory electrical and Ca(2+) synaptic activity, which was not elicited in the control cultures that were not subjected to glutamate blockade. This activity was suppressed with acetylcholine (ACh) receptor antagonists and was potentiated by eserine, an inhibitor of acetylcholinesterase, suggesting its cholinergic nature. The upregulation of ACh receptors and the contribution of ACh to the control of the excitation/inhibition balance in cultures after a prolonged decrease in glutamate activity were also demonstrated. Enhanced ACh transmission was also found in chronically blocked cerebellar but not cortical cultures, suggesting the region-specific character of glutamate-ACh interactions in the brain. We believe that in the absence of glutamate excitation in the hypothalamus in vitro, ACh, a neurotransmitter normally exhibiting only weak activity in the hypothalamus, becomes the major excitatory neurotransmitter and supports the excitation/inhibition balance. The increase in excitatory ACh transmission during a decrease in glutamate excitation may represent a novel form of neuronal plasticity that regulates activity and excitability of neurons during the glutamate/GABA imbalance.
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ACh signaling can be upregulated to compensate for prolonged blockade of glutamatergic signaling in hypothalamic neurons in culture.
“There is also some indication from studies of hypothalamic neurons in culture that ACh signaling can be upregulated to compensate for prolonged blockade of glutamatergic signaling (Belousov et al., 2001).”
From Acetylcholine as a Neuromodulator: Cholinergic Signaling Shapes Nervous System Function and Behavior (2012) · cites this paper as Belousov et al., 2001
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- Authors
- Belousov, A. B., O'Hara, B. F., & Denisova, J. V.
- Affiliations
- Tulane University (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2001-03-15
- Volume
- 21
- Issue
- 6
- Pages
- 2015-2027
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6762624
- OpenAlex
- W1851272093
- Cited by
- 44
- References
- 60
- Citations by year
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- FWCI
- 1.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Tulane University
- National Institutes of Health (5k21da000187-05)
- National Institute on Drug Abuse (DA00187)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Keywords
- acetylcholine, glutamate, hypothalamus, excitation-inhibition balance, cholinergic neurotransmission, neuroplasticity, calcium imaging, cerebellar neurons, physostigmine
- MeSH terms
- Acetylcholine, Animals, Calcium, Cells, Cultured, Cerebellum, Cerebral Cortex, Fluorescent Dyes, Hypothalamus, Membrane Potentials, Synaptic Transmission, Up-Regulation, Rats, Sprague-Dawley, Receptors, Glutamate, Neurotransmitter Agents, Patch-Clamp Techniques, Excitatory Amino Acid Antagonists, Glutamic Acid, GABA Antagonists, Excitatory Postsynaptic Potentials, Calcium Signaling, Rats
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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