Dopamine abnormalities in the neocortex of patients with temporal lobe epilepsy

Rocha, Luisa; Alonso-Vanegas, Mario; Villeda‐Hernández, Juana; Mújica, Mario; Cisneros-Franco, J. Miguel; López-Gómez, Mario; Zavala-Tecuapetla, Cecilia; Frías‐Soria, Christian Lizette; Segovia-Vila, José; Borsodi, Anna

doi:10.1016/j.nbd.2011.09.006

Cited by 58 publications

(32 citation statements)

References 48 publications

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“…In addition to the brain areas discussed here, the circadian rhythms of other brain areas also may be influenced by DA’s activity. For example, the hippocampus receives a large dopaminergic input from the VTA via the mesolimbic pathway, and this input may regulate clock genes and proteins (McCarthy and Welsh, 2012), which could be involved in hippocampus-dependent learning (Ito and Schuman, 2007) and could protect against hippocampal cell death (Bozzi et al, 2000; Rocha et al, 2012; Bozzi and Borrelli, 2013). …”

Section: Discussionmentioning

confidence: 99%

Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Korshunov

Blakemore

Trombley

2017

Front. Cell. Neurosci.

111

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Circadian rhythms are daily rhythms that regulate many biological processes – from gene transcription to behavior – and a disruption of these rhythms can lead to a myriad of health risks. Circadian rhythms are entrained by light, and their 24-h oscillation is maintained by a core molecular feedback loop composed of canonical circadian (“clock”) genes and proteins. Different modulators help to maintain the proper rhythmicity of these genes and proteins, and one emerging modulator is dopamine. Dopamine has been shown to have circadian-like activities in the retina, olfactory bulb, striatum, midbrain, and hypothalamus, where it regulates, and is regulated by, clock genes in some of these areas. Thus, it is likely that dopamine is essential to mechanisms that maintain proper rhythmicity of these five brain areas. This review discusses studies that showcase different dopaminergic mechanisms that may be involved with the regulation of these brain areas’ circadian rhythms. Mechanisms include how dopamine and dopamine receptor activity directly and indirectly influence clock genes and proteins, how dopamine’s interactions with gap junctions influence daily neuronal excitability, and how dopamine’s release and effects are gated by low- and high-pass filters. Because the dopamine neurons described in this review also release the inhibitory neurotransmitter GABA which influences clock protein expression in the retina, we discuss articles that explore how GABA may contribute to the actions of dopamine neurons on circadian rhythms. Finally, to understand how the loss of function of dopamine neurons could influence circadian rhythms, we review studies linking the neurodegenerative disease Parkinson’s Disease to disruptions of circadian rhythms in these five brain areas. The purpose of this review is to summarize growing evidence that dopamine is involved in regulating circadian rhythms, either directly or indirectly, in the brain areas discussed here. An appreciation of the growing evidence of dopamine’s influence on circadian rhythms may lead to new treatments including pharmacological agents directed at alleviating the various symptoms of circadian rhythm disruption.

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Section: Discussionmentioning

confidence: 99%

Dopamine: A Modulator of Circadian Rhythms in the Central Nervous System

Korshunov

Blakemore

Trombley

2017

Front. Cell. Neurosci.

111

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“…In PWE suffering from TLE, alterations in the neocortical DA content, D1-like and D2-like receptor expression, and DA transporter (DAT) binding have been reported (Rocha et al, 2012). Reduced D 2 R/D 3 R binding, sustained impairment of the DAergic system, was demonstrated in extrastriatal and/or striatal brain regions of PWE, specifically with TLE (Bernedo Paredes et al, 2015).…”

Section: Monoamines In Epilepsy: Preclinical and Clinical Evidencementioning

confidence: 99%

Monoaminergic Mechanisms in Epilepsy May Offer Innovative Therapeutic Opportunity for Monoaminergic Multi-Target Drugs

et al. 2016

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A large body of experimental and clinical evidence has strongly suggested that monoamines play an important role in regulating epileptogenesis, seizure susceptibility, convulsions, and comorbid psychiatric disorders commonly seen in people with epilepsy (PWE). However, neither the relative significance of individual monoamines nor their interaction has yet been fully clarified due to the complexity of these neurotransmitter systems. In addition, epilepsy is diverse, with many different seizure types and epilepsy syndromes, and the role played by monoamines may vary from one condition to another. In this review, we will focus on the role of serotonin, dopamine, noradrenaline, histamine, and melatonin in epilepsy. Recent experimental, clinical, and genetic evidence will be reviewed in consideration of the mutual relationship of monoamines with the other putative neurotransmitters. The complexity of epileptic pathogenesis may explain why the currently available drugs, developed according to the classic drug discovery paradigm of “one-molecule-one-target,” have turned out to be effective only in a percentage of PWE. Although, no antiepileptic drugs currently target specifically monoaminergic systems, multi-target directed ligands acting on different monoaminergic proteins, present on both neurons and glia cells, may represent a new approach in the management of seizures, and their generation as well as comorbid neuropsychiatric disorders.

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“…Similarly, patients with longer duration of the epilepsy and those with long-term history of antiepileptic drug administration exhibited reduced 5-HT4 and 5-HT7 binding. Different neurotransmitters and receptors might also be associated with epilepsy-related clinical variables (Kandratavicius et al, 2013a;Li et al, 2014;PalomeroGallagher et al, 2012;Rocha et al, 2012). This analysis is part of an ongoing study.…”

Section: Discussionmentioning

confidence: 98%

“…A possible explanation for this finding is that serotonin depletion in the hippocampus might be involved in the genesis of GTC seizures from limbic epilepsies, but the susceptibility to seizures might involve serotonin depletion in other regions, such as the superior colliculus (Merrill et al, 2007), and other serotonergic mechanisms. Rocha et al (2012) evaluated the temporal neocortical tissues of patients with TLE-HS by autoradiography, finding that the patients in whom epileptic seizures began at young ages presented with reduced 5-HT7 binding. Similarly, patients with longer duration of the epilepsy and those with long-term history of antiepileptic drug administration exhibited reduced 5-HT4 and 5-HT7 binding.…”

Section: Discussionmentioning

confidence: 99%