Traumatic brain injury, alone or with striatal hemorrhage-like extension, transiently decreases GABA and glutamate levels along motor deficits in the rat striatum: an in vivo study.

The cerebral cortex is connected to the striatum via the axons of the pyramidal glutamatergic neurons, and this pathway is intimately involved in motor function. In the striatum, glutamatergic afferents initiate the activity of GABAergic medium spiny neurons. This study addressed whether traumatic brain injury (TBI) affects GABA and glutamate extracellular levels in the dorsal striatum as an indicator of effects on the cortico-striatal pathway, in rats with motor deficits and recovered animals.

Changes in Noradrenergic Synthesis and Dopamine Beta-Hydroxylase Activity in Response to Oxidative Stress after Iron-induced Brain Injury.

Noradrenaline (NA) levels are altered during the first hours and several days after cortical injury. NA modulates motor functional recovery. The present study investigated whether iron-induced cortical injury modulated noradrenergic synthesis and dopamine beta-hydroxylase (DBH) activity in response to oxidative stress in the brain cortex, pons and cerebellum of the rat.

Traumatic brain injury extending to the striatum alters autonomic thermoregulation and hypothalamic monoamines in recovering rats.

The brain cortex is the structure that is typically injured in traumatic brain injury (TBI) and is anatomically connected with other brain regions, including the striatum and hypothalamus, which are associated in part with motor function and the regulation of body temperature, respectively. We investigated whether a TBI extending to the striatum could affect peripheral and core temperatures as an indicator of autonomic thermoregulatory function. Moreover, it is unknown whether thermal modulation is accompanied by hypothalamic and cortical monoamine changes in rats with motor function recovery.

Role of the MicroRNAs in the Pathogenic Mechanism of Painful Symptoms in Long COVID: Systematic Review.

The ongoing pandemic of COVID-19 has caused more than 6.7 million tragic deaths, plus, a large percentage of people who survived it present a myriad of chronic symptoms that last for at least 6 months; this has been named as long COVID. Some of the most prevalent are painful symptoms like headache, joint pain, migraine, neuropathic-like pain, fatigue and myalgia.

Alpha-adrenergic receptor activation reinstates motor deficits in rats recovering from cortical injury.

Norepinephrine plays an important role in motor functional recovery after a brain injury caused by ferrous chloride. Inhibition of norepinephrine release by clonidine is correlated with motor deficits after motor cortex injury. The aim of this study was to analyze the role of α-adrenergic receptors in the restoration of motor deficits in recovering rats after brain damage.

Experimental Applications and Factors Involved in Validating Thermal Windows Using Infrared Thermography to Assess the Health and Thermostability of Laboratory Animals.

Evaluating laboratory animals' health and thermostability are fundamental components of all experimental designs. Alterations in either one of these parameters have been shown to trigger physiological changes that can compromise the welfare of the species and the replicability and robustness of the results obtained. Due to the nature and complexity of evaluating and managing the species involved in research protocols, non-invasive tools such as infrared thermography (IRT) have been adopted to quantify these parameters without altering them or inducing stress responses in the animals.

Glutamate, Glutamine, GABA and Oxidative Products in the Pons Following Cortical Injury and Their Role in Motor Functional Recovery.

Brain injury leads to an excitatory phase followed by an inhibitory phase in the brain. The clinical sequelae caused by cerebral injury seem to be a response to remote functional inhibition of cerebral nuclei located far from the motor cortex but anatomically related to the injury site. It appears that such functional inhibition is mediated by an increase in lipid peroxidation (LP).

Role of the Dopaminergic System in the Striatum and Its Association With Functional Recovery or Rehabilitation After Brain Injury.

Disabilities are estimated to occur in approximately 2% of survivors of traumatic brain injury (TBI) worldwide, and disability may persist even decades after brain injury. Facilitation or modulation of functional recovery is an important goal of rehabilitation in all patients who survive severe TBI. However, this recovery tends to vary among patients because it is affected by the biological and physical characteristics of the patients; the types, doses, and application regimens of the drugs used; and clinical indications.

Histamine H receptor activation reduces the impairment in prepulse inhibition (PPI) of the acoustic startle response and Akt phosphorylation induced by MK-801 (dizocilpine), antagonist at N-Methyl-d-Aspartate (NMDA) receptors.

We have investigated the effect of the local activation of histamine H receptors (HRs) in the rat prefrontal cortex (PFCx) on the impairment of pre-pulse inhibition (PPI) of the startle response induced by the systemic administration of MK-801, antagonist at glutamate N-Methyl-d-Aspartate (NMDA) receptors, and the possible functional interaction between HRs and MK-801 on PFCx dopaminergic transmission. Infusion of the HR agonist RAMH (19.8 ng/1 μl) into the PFCx reduced or prevented the inhibition by MK-801 (0.

The Systemic Administration of the Histamine H Receptor Antagonist/Inverse Agonist Chlorpheniramine to Pregnant Rats Impairs the Development of Nigro-Striatal Dopaminergic Neurons.

The dopaminergic and histaminergic systems are the first to appear during the development of the nervous system. Through the activation of H receptors (HRs), histamine increases neurogenesis of the cortical deep layers, while reducing the dopaminergic phenotype (cells immunoreactive to tyrosine hydroxylase, TH) in embryo ventral mesencephalon. Although the function of histamine in neuronal differentiation has been studied, the role of HRs in neurogenesis has not been addressed.

GABAergic imbalance is normalized by dopamine D receptor activation in the striatum contralateral to the cortical injury in motor deficit-recovered rats.

Rationale: The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function, which may be modulated by dopamine.

Objectives: We studied whether the activation of dopamine D receptors (DRs) modulates the γ-aminobutyric acid (GABA) and glutamate levels in the striatum of recovered rats at 192 h after cortical injury.

Methods: The DR agonist SKF-38393 (0, 2, 3, or 4 mg/kg) was administered at 24, 48, 96, and 192 h post-injury, and then rats were decapitated to determine GABA and glutamate levels and the levels of DR mRNA on both sides of the striatum.

Chronic administration of the histamine H receptor agonist immepip decreases L-Dopa-induced dyskinesias in 6-hydroxydopamine-lesioned rats.

Rationale: Histamine H receptors (HRs) are co-expressed with dopamine D receptors (DRs) by striato-nigral medium spiny GABAergic neurons, where they functionally antagonize DR-mediated responses.

Objectives And Methods: We examined whether the chronic administration of the HR agonist immepip modifies dyskinesias induced by L-3,4-dihydroxyphenylalanine, L-Dopa (LIDs), in rats lesioned with 6-hydroxydopamine in the substantia nigra pars compacta, and the effect of DR and HR co-activation on glutamate and GABA content in dialysates from the dorsal striatum of naïve rats.

Results: The systemic administration (i.

Dopamine D receptor activation maintains motor coordination and balance in rats.

Dopamine (DA) modulates motor coordination, and its depletion, as in Parkinson's disease, produces motor impairment. The basal ganglia, cerebellum and cerebral cortex are interconnected, have functional roles in motor coordination, and possess dopamine D receptors (DRs), which are expressed at a particularly high density in the basal ganglia. In this study, we examined whether the activation of DRs modulates motor coordination and balance in the rat using a beam-walking test that has previously been used to detect motor coordination deficits.

Dopamine D receptor activation maintains motor coordination in injured rats but does not accelerate the recovery of the motor coordination deficit.

The sensorimotor cortex and the striatum are interconnected by the corticostriatal pathway, suggesting that cortical injury alters the striatal function that is associated with skilled movements and motor learning, which are functions that may be modulated by dopamine (DA). In this study, we explored motor coordination and balance in order to investigate whether the activation of D receptors (DRs) modulates functional recovery after cortical injury. The results of the beam-walking test showed motor deficit in the injured group at 24, 48 and 96h post-injury, and the recovery time was observed at 192h after cortical injury.

Sensorimotor Intervention Recovers Noradrenaline Content in the Dentate Gyrus of Cortical Injured Rats.

Nowadays, a consensus has been reached that designates the functional and structural reorganization of synapses as the primary mechanisms underlying the process of recovery from brain injury. We have reported that pontine noradrenaline (NA) is increased in animals after cortical ablation (CA). The aim of the present study was to explore the noradrenergic and morphological response after sensorimotor intervention (SMI) in rats injured in the motor cortex.

Effects of dopamine D1 receptor activation and blockade on dopamine and noradrenaline levels in the rat brain.

The noradrenergic and dopaminergic systems are associated with the motor system and have anatomical and functional connections that have not yet been studied. The present study aimed to examine the specific role of D1 receptors (D1Rs) on noradrenergic and dopaminergic responses in the rat brain. Male Wistar rats were assigned to eight groups to receive systemic injection of a D1R agonist (SKF-38393) at 0, 1, 5 or 10mg/kg or injection of a D1R antagonist (SCH-23390) at 0, 0.

Histamine H3 receptor activation inhibits dopamine synthesis but not release or uptake in rat nucleus accumbens.

We studied the effect of activating histamine H3 receptors (H3Rs) on rat nucleus accumbens (rNAcc) dopaminergic transmission by analyzing [(3)H]-dopamine uptake by synaptosomes, and dopamine synthesis and depolarization-evoked [(3)H]-dopamine release in slices. The uptake of [(3)H]-dopamine by rNAcc synaptosomes was not affected by the H3R agonist RAMH (10(-10)-10(-6) M). In rNAcc slices perfusion with RAMH (1 μM) had no significant effect on [(3)H]-dopamine release evoked by depolarization with 30 mM K(+) (91.

D1 Antagonists and D2 Agonists Have Opposite Effects on the Metabolism of Dopamine in the Rat Striatum.

The striatum is known to possess high levels of D1-like and D2-like receptors (D1Rs and D2Rs, respectively). We have previously shown that selective inhibition of D1Rs increases the dopaminergic metabolic response and proposed that this effect is associated with the concomitant activation of postsynaptic D2Rs by endogenous dopamine (DA). Here, we examined whether activation of D2Rs modulates the metabolism and synthesis of DA in the striatum.

Histamine H3 receptor activation prevents dopamine D1 receptor-mediated inhibition of dopamine release in the rat striatum: a microdialysis study.

Histamine H3 receptors (H3Rs) co-localize with dopamine (DA) D1 receptors (D1Rs) on striatal medium spiny neurons and functionally antagonize D1R-mediated responses. The intra-striatal administration of D1R agonists reduces DA release whereas D1R antagonists have the opposite effect. In this work, a microdialysis method was used to study the effect of co-activating D1 and H3 receptors on the release of DA from the rat dorsal striatum.

[Intraventricular yohimbine infusion induces noradrenergic changes in motor cerebral injured rats and enhances motor recovery].

Introduction: It has been proposed that noradrenaline is one of the neurotransmitters involved in the functional recovery. In this sense, it has been proposed that the alpha-2 noradrenergic receptors play an important role in the functional reinstatement.

Objective: the aim of this work was to study the role of the alpha-2 noradrenergic receptors on the noradrenaline contents in cerebellum and pons of rats iron-injured in the motor cortex.

[Measurement of acetylcholine and sleep patterns].

Introduction: Acetylcholine is an essential neurotransmitter in the central nervous system as it has an effect on sleep, memory and learning. Intracerebral microdialysis is an in vivo surgical technique that is used to measure the concentration of substances in the extracellular space.

Methods: The rats were stereotaxically implanted with microdialysis cannulae guided to the hypothalamic medial preoptic area and bipolar stainless steel electrodes to obtain sleep records simultaneously with microdialysis samplings during 24 hours exposed to clean air followed by 24 hours of exposure to ozone.

Effects of oxcarbazepine on monoamines content in hippocampus and head and body shakes and sleep patterns in kainic acid-treated rats.

The aim of this work was to analyze the effect of oxcarbazepine (OXC) on sleep patterns, "head and body shakes" and monoamine neurotransmitters level in a model of kainic-induced seizures. Adult Wistar rats were administered kainic acid (KA), OXC or OXC + KA. A polysomnographic study showed that KA induced animals to stay awake for the whole initial 10 h.

Chronic exposure to toluene changes the sleep-wake pattern and brain monoamine content in rats.

Toluene, found in glues and cleaners, is among the inhalants most commonly abused by workers and young drug addicts. In this study, we examined the changes in sleep patterns and monoamine content induced by chronic toluene exposure. Rats were chronically exposed to toluene vapors beginning at 30 days of age for a duration of 30 days.