Cited by 40Neurotransmitter Receptor Influence on BehaviorSchizophrenia research and treatmentStress Responses and Cortisol

Effects of neonatal ventral hippocampal lesion in rats on stress-induced acetylcholine release in the prefrontal cortex

Laplante, François, Stevenson, Carl W., Gratton, Alain, Srivastava, Lalit K., Quirion, Rémi·2004·Journal of Neurochemistry

Abstract

Excitotoxic neonatal ventral hippocampus (NVH) lesions in rats result in characteristic post-pubertal hyper-responsiveness to stress and cognitive abnormalities analogous to those described in schizophrenia and suggestive of alterations in dopamine (DA) neurotransmission. Converging lines of evidence also point to dysfunctions in the cortical cholinergic system in neuropsychiatric disorders. In previous studies, we observed alterations in dopaminergic modulation of acetylcholine (Ach) release in the prefrontal cortex (PFC) in post-pubertal NVH-lesioned rats. These two neurotransmitter systems are involved in the stress response as PFC release of DA and Ach is enhanced in response to some stressful stimuli. As adult NVH-lesioned rats are behaviorally more reactive to stress, we investigated the effects of NVH lesions on tail-pinch stress-induced Ach and DA release in the PFC. Using in vivo microdialysis, we observed that tail-pinch stress resulted in significantly greater increases in prefrontal cortical Ach release in post-pubertal NVH-lesioned rats (220% baseline) compared with sham-operated controls (135% baseline). Systemic administration of the D1-like receptor antagonist SCH 23390 (0.5 mg/kg i.p.) or the D2-like receptor antagonist haloperidol (0.2 mg/kg i.p.), as well as intra-PFC administration of the D2-like antagonist sulpiride (100 microm), reduced stress-induced Ach release in PFC of adult NVH-lesioned rats. By contrast, intra-PFC administration of SCH 23390 (100 microm) failed to affect stress-induced Ach release in PFC of NVH-lesioned rats. Interestingly, using in vivo voltammetry, stress-induced stimulation of PFC DA release was found to be attenuated in adult NVH-lesioned rats. Taken together, these data suggest developmentally specific reorganization of prefrontal cortical cholinergic innervation notably regarding its regulation by DA neurotransmission.

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Crossref · 10.1111/j.1471-4159.2004.02831.x

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  • There is evidence that extracellular levels of acetylcholine fluctuate in a manner that is not consistent with localized clearance of a synaptic transmitter.

    “There is also evidence that extracellular levels of ACh fluctuate in a manner that is not consistent with localized clearance of a synaptic transmitter (Hajnal et al., 1998; Laplante et al., 2004; Mark et al., 1996; Parikh et al., 2004; Reid et al., 1998).”

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Authors
Laplante, F., Stevenson, C. W., Gratton, A., Srivastava, L. K., & Quirion, R.
Affiliations
Douglas Mental Health University Institute (CA)
Corresponding author
Quirion, Rémi
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2004-12
Volume
91
Issue
6
Pages
1473-1482
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W1597954511
Cited by
40
References
74
Citations by year
2021: 1 · 2020: 1 · 2015: 2 · 2014: 3 · 2012: 5
FWCI
1.41
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • McGill University
  • Canadian Institutes of Health Research
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
  • Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Keywords
excitotoxic lesions, prefrontal cortex, dopamine release, cholinergic-dopaminergic interaction, D1-like receptors, D2-like receptors, dopamine antagonists, schizophrenia model
MeSH terms
Acetylcholine, Animals, Animals, Newborn, Benzazepines, Brain Diseases, Dopamine, Haloperidol, Hippocampus, Stress, Physiological, Sulpiride, Rats, Sprague-Dawley, Prefrontal Cortex, Microdialysis, Dopamine Antagonists, Rats

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