Connecting the dots of the cerebro‐cerebellar role in cognitive function: Neuronal pathways for cerebellar modulation of dopamine release in the prefrontal cortex
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Cerebellar involvement in autism, schizophrenia, and other cognitive disorders is typically associated with prefrontal cortical pathology. However, the underlying neuronal mechanisms are largely unknown. It has previously been shown in mice that stimulation of the dentate nucleus (DN) of the cerebellum evokes dopamine (DA) release in the medial prefrontal cortex (mPFC). Here, we investigated the neuronal circuitry by which the cerebellum modulates mPFC DA release. Fixed potential amperometry was used to determine the contribution of two candidate pathways by which the cerebellum may modulate mPFC DA release. In urethane anesthetized mice, DA release evoked by DN stimulation (50 Hz) was recorded in mPFC following local anesthetic lidocaine (0.02 μg) or ionotropic glutamate receptor antagonist kynurenate (0.5 μg) infusions into the mediodorsal or ventrolateral thalamic nucleus (ThN md; ThN vl), or the ventral tegmental area (VTA). Following intra-VTA lidocaine or kynurenate infusions, DA release was decreased by ∼50%. Following intra-ThN md and ThN vl infusions of either drug, DA release was decreased by ∼35% and 15%, respectively. Reductions in DA release following lidocaine or kynurenate infusions were not significantly different indicating that neuronal cells in the VTA and ThN were activated primarily if not entirely by glutamatergic inputs. The present study suggests that neuropathological changes in the cerebellum commonly observed in autism, schizophrenia, and other cognitive disorders could result in a loss of functionality of cerebellar-mPFC circuitry that is manifested as aberrant dopaminergic activity in the mPFC. Additionally, these results specifically implicate glutamate as a modulator of mPFC dopaminergic activity.
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Repeated stimulation of the cerebellum increases dopamine in the mouse medial prefrontal cortex.
“The existence of such a pathway would explain how repeated stimulation of the cerebellum increases dopamine in the mouse medial prefrontal cortex (Rogers et al., 2011).”
From The Forward Model: A Unifying Theory for the Role of the Cerebellum in Motor Control and Sense of Agency (2021) · cites this paper as Rogers et al., 2011
Dentato-thalamo-cortical neurons are thought to be glutamatergic, implicating glutamate as a modulator of mPFC dopaminergic activity.
“The dentato-thalamo-cortical neurons are thought to be glutamatergic and thus implicate glutamate as a modulator of mPFC dopaminergic activity [179].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [179]
Cerebellar pathology in autism and other cognitive disorders could result from functional loss of cerebellar-mPFC circuitry due to abnormal dopaminergic activity in mPFC.
“It has been recently reported that cerebellar pathology in autism and other cognitive disorders could result from the functional loss of cerebellar-mPFC circuitry due to abnormal dopaminergic activity in the mPFC [179].”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [179]
Recent studies report cerebellar control of dopamine release in prefrontal cortex, a mechanism that might be triggered by spatiotemporal cortical activity patterns.
“Important new clues, however, come from recent studies reporting cerebellar control of dopamine release in the prefrontal cortex [179, 180], a mechanism that might be triggered by spatiotemporal cortical activity patterns, as proposed here.”
From Consensus Paper: Pathological Role of the Cerebellum in Autism (2012) · cites this paper as [179]
Changes in cerebellar-mPFC functional connectivity have been identified in mouse models of cerebellar PC loss and in genetic mouse models of ASD.
“in mouse models of cerebellar PC loss, and in genetic mouse models of ASD17,18.”
From Regulation of autism-relevant behaviors by cerebellar-prefrontal cortical circuits (2020) · cites this paper as [17]
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- Authors
- Rogers, T. D., Dickson, P. E., Heck, D. H., Goldowitz, D., Mittleman, G., & Blaha, C. D.
- Affiliations
- University of Memphis (US)
- University of Tennessee Health Science Center (US)
- University of British Columbia (CA)
- Corresponding author
- Blaha, Charles D.
- Venue
- Synapse
- Publisher
- Wiley
- Published
- 2011-06-17
- Volume
- 65
- Issue
- 11
- Pages
- 1204-1212
- ISSN
- 0887-4476 (ISSN-L)
- 1098-2396
- PMC
- PMC3854794
- OpenAlex
- W2132327443
- Cited by
- 120
- References
- 64
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 6 · 2023: 6 · 2022: 6 · 2021: 7 · 2020: 10 · 2019: 15 · 2018: 8 · 2017: 3 · 2016: 9 · 2015: 11 · 2014: 10 · 2013: 10 · 2012: 9
- FWCI
- 3.98
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Synapse (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Autism Speaks (AS1780)
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (R01NS063009)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- cerebellum, medial prefrontal cortex, dopamine release, dentate nucleus, ventral tegmental area, thalamic nuclei, glutamate modulation, kynurenic acid, lidocaine, autism spectrum disorder, schizophrenia, cognitive disorders, neural pathways
- MeSH terms
- Animals, Cerebellum, Cognition, Dopamine, Humans, Mice, Inbred CBA, Mice, Neurologic Mutants, Nerve Net, Neural Pathways, Prefrontal Cortex, Mice
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