Dopamine D4 receptor stimulation in GABAergic projections of the globus pallidus to the reticular thalamic nucleus and the substantia nigra reticulata of the rat decreases locomotor activity

Erlij, David; Acosta-García, Jacqueline; Rojas-Márquez, Martín; González-Hernández, Brenda; Escartín-Perez, Erick; Aceves, Jorge; Florán, Benjamí­n

doi:10.1016/j.neuropharm.2011.11.001

Cited by 32 publications

(21 citation statements)

References 35 publications

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“…It has also been described that MPH increased dopamine levels in the TRN, reducing hyperlocomotion through activation of D4 receptors (Erlij et al . ), thus suggesting a limiting process that might explain why MPH repetitive administration did not increase hyperlocomotion levels above acute‐mediated levels.…”

Section: Discussionmentioning

confidence: 90%

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Differential effects of methylphenidate and cocaine on GABA transmission in sensory thalamic nuclei

Goitia

Raineri

González

et al. 2013

Journal of Neurochemistry

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Methylphenidate (MPH) is widely used to treat children and adolescents diagnosed with attention deficit/hyperactivity disorder. Although MPH shares mechanistic similarities to cocaine, its effects on GABAergic transmission in sensory thalamic nuclei are unknown. Our aim was to compare cocaine and MPH effects on GABAergic projections between thalamic reticular and ventrobasal (VB) nuclei. Mice (P18-30) were subjected to binge-like cocaine and MPH acute and sub-chronic administrations. Cocaine and MPH enhanced hyperlocomotion, though sub-chronic cocaine-mediated effects were stronger than MPH effects. Cocaine and MPH sub-chronic administration altered paired-pulse and spontaneous GABAergic input differently. The effects of cocaine on evoked paired-pulse GABA-A mediated currents changed from depression to facilitation with the duration of the protocols used, while MPH induced a constant increase throughout administration protocols. Thalamic reticular nucleus GAD67 and VB CaV3.1 protein levels were measured using Western blot in order to better understand their link to increased GABA release. Both proteins were increased by sub-chronic administration of cocaine. These results suggest that cocaine and MPH produced distinct presynaptic alterations on GABAergic transmission. MPH showed effects on GABAergic transmission that seems less disruptive than cocaine. Unique effects of cocaine on postsynaptic VB calcium currents might explain deleterious cocaine effects on sensory thalamic nuclei. These results might help to understand the impact of MPH repetitive administration on sensory thalamic nuclei.

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Section: Discussionmentioning

confidence: 90%

“…) and in vivo (Erlij et al . ). Nevertheless, the effects of repetitive MPH administration on GABAergic transmission between sensory thalamic nuclei remain unknown.…”

mentioning

confidence: 97%

Differential effects of methylphenidate and cocaine on GABA transmission in sensory thalamic nuclei

Goitia

Raineri

González

et al. 2013

Journal of Neurochemistry

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“…One of the things that make psychiatric disorders so distressing is that the overabundance of neurological activity bombards the mind with unintended thoughts and feelings like spam on a computer. For many persons with neuronal hyperexcitability, this can overwhelm the modulatory function of the thalamic reticular nucleus (TRN) [112,[114][115][116], prompting the individual to respond to various thoughts and feelings before the brain can fully process them. This may be expressed clinically as inattention, hyperactivity, and impulsivity, thus explaining why attention deficit hyperactivity disorder (ADHD) is such a common comorbidity in psychiatric disorders.…”

Section: Psychophysiological Evidencementioning

confidence: 99%

“…This may be expressed clinically as inattention, hyperactivity, and impulsivity, thus explaining why attention deficit hyperactivity disorder (ADHD) is such a common comorbidity in psychiatric disorders. What allows psychostimulants to help alleviate ADHD symptoms is that both dopamine and norepinephrine increase the output of TRN collaterals [114,115], which, being primarily inhibitory, act as circuit-breakers that help reduce the volume of extraneous electrical activity in the brain. With less information popping up on the thalamic computer screen, the mind is better able to focus on one thing at a time.…”

Section: Psychophysiological Evidencementioning

confidence: 99%

The Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders

Binder¹

2019

AJCEM

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After nearly a century of intensive research and clinical investigation, the pathophysiology of psychiatric disorders remains an enigma. Short of a clear understanding of how psychiatric symptoms are produced, the various cognitive, emotional, and behavior patterns that characterize psychiatric disorders continue to be grouped into syndromes and treated accordingly. The weakness of this approach is that the treatment is administered without a clear understanding of what pathological process is being treated. Moreover, the symptoms of most psychiatric disorders are frequently changing and melding into one another. This leads to diagnostic confusion, medication stacking, and poor treatment outcomes, all of which erode patient trust and perpetuate the stigma of mental illness. In this seminal report, a new hypothesis on the pathophysiology of psychiatric disorders will be presented based on multidisciplinary evidence that nearly all psychiatric disorders and their functional comorbidities are rooted in a single, shared, neurophysiological abnormality. The report will then trace that abnormality to its molecular roots and introduce a new paradigm through which the many faces of mental illness can be understood and uniformly treated. The Multi-Circuit Neuronal Hyperexcitability hypothesis of psychiatric disorders posits that an inherent hyperexcitability of the neurological system is at the root of mental illness and provides a precise, functionallyspecific framework that eliminates diagnostic confusion, informs a unified treatment approach, and helps remove the long-held stigma of mental illness. + Itemized comparison showing that the same conditions and chemicals that increase the potential for seizures (upper section) also increase the potential for psychiatric symptoms, and the same conditions and chemicals that decrease the potential for seizures (lower section) also decrease the potential for psychiatric symptoms.

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“…Monoamines like dopamine (DA), norepinephrine (NE), and serotonin (5-HT); released by ascending afferents from brainstem nuclei onto thalamocortical neurons, play an important role in the transitions from low frequency oscillations to high-frequency, gamma band resonance during conscious states [23]. In the somatosensory VB thalamus, cocaine is known to rapidly increase synaptic NE and 5-HT [24], while MPH was able to increase DA levels in the thalamic reticular nucleus (i.e., origin of GABAergic afferents to VB neurons, [25]). A recent work using transgenic mouse has described a specific 5-HT modulatory role on GABA release onto VB neurons, modulated by a cocaine binge [26].…”

Section: Introductionmentioning

confidence: 99%

Differential alterations of intracellular [Ca2+] dynamics induced by cocaine and methylphenidate in thalamocortical ventrobasal neurons

Rozas

Goitia

Bisagno

et al. 2017

Transl Brain Rhythmicity

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The ventrobasal (VB) thalamus relay nucleus processes information from rodents’ whiskers, projecting to somatosensory cortex. Cocaine and methylphenidate (MPH) have been described to differentially alter intrinsic properties of, and spontaneous GABAergic input to, VB neurons. Here we studied using bis-fura 2 ratiometric fluorescence the effects of cocaine and MPH on intracellular [Ca2+] dynamics at the soma and dendrites of VB neurons. Cocaine increased baseline fluorescence in VB somatic and dendritic compartments. Peak and areas of fluorescence amplitudes were reduced by cocaine binge treatment in somas and dendrites at different holding potentials. MPH binge treatment did not alter ratiometric fluorescence at either somatic or dendritic levels. These novel cocaine-mediated blunting effects on intracellular [Ca2+] might account for alterations in the capacity of thalamocortical neurons to maintain gamma band oscillations, as well as their ability to integrate synaptic afferents.

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Dopamine D4 receptor stimulation in GABAergic projections of the globus pallidus to the reticular thalamic nucleus and the substantia nigra reticulata of the rat decreases locomotor activity

Cited by 32 publications

References 35 publications

Differential effects of methylphenidate and cocaine on GABA transmission in sensory thalamic nuclei

Differential effects of methylphenidate and cocaine on GABA transmission in sensory thalamic nuclei

The Multi-Circuit Neuronal Hyperexcitability Hypothesis of Psychiatric Disorders

Differential alterations of intracellular [Ca2+] dynamics induced by cocaine and methylphenidate in thalamocortical ventrobasal neurons

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