Housing and road transport modify the brain neurotransmitter systems of pigs: Do pigs raised in different conditions cope differently with unknown environments?

AbstractObesity and the brain are linked since the brain can control the weight of the body through its neurotransmitters. The aim of the present study was to investigate the effect of high-fat diet (HFD)-induced obesity on brain functioning through the measurement of brain glutamate, dopamine, and serotonin metabolic pools. In the present study, two groups of rats served as subjects. Group 1 was fed a normal diet and named as the lean group. Group 2 was fed an HFD for 4 weeks and named as the obese group. Markers of oxidative stress (malondialdehyde, glutathione, glutathione-s-transferase, and vitamin C), inflammatory cytokines (interleukin [IL]-6 and IL-12), and leptin along with a lipid profile (cholesterol, triglycerides, high-density lipoprotein, and low-density lipoprotein levels) were measured in the serum. Neurotransmitters dopamine, serotonin, and glutamate were measured in brain tissue. Fecal samples were collected for observing changes in gut flora. In brain tissue, significantly high levels of dopamine and glutamate as well as significantly low levels of serotonin were found in the obese group compared to those in the lean group (P > 0.001) and were discussed in relation to the biochemical profile in the serum. It was also noted that the HFD affected bacterial gut composition in comparison to the control group with gram-positive cocci dominance in the control group compared to obese. The results of the present study confirm that obesity is linked to inflammation, oxidative stress, dyslipidemic processes, and altered brain neurotransmitter levels that can cause obesity-related neuropsychiatric complications.

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Specific features of learning with nociceptive electrical reinforcement in rats of different genetic strains: Role of brain neurotransmitter systems

Bulletin of Experimental Biology and Medicine ◽

10.1007/s10517-005-0198-1 ◽

2005 ◽

Vol 139 (1) ◽

pp. 11-14

Author(s):

A. L. Kalyuzhnyi ◽

S. V. Litvinova ◽

V. V. Shul’govskii ◽

L. F. Panchenko

Keyword(s):

Neurotransmitter Systems ◽

Genetic Strains ◽

Brain Neurotransmitter

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Amplification and Suppression of Distinct Brain-wide Activity Patterns by Catecholamines

10.1101/270645 ◽

2018 ◽

Author(s):

RL van den Brink ◽

S Nieuwenhuis ◽

TH Donner

Keyword(s):

Spatial Distribution ◽

Human Brain ◽

Spatial Patterns ◽

Large Scale ◽

Network Dynamics ◽

Brain Network ◽

Heterogeneous Distribution ◽

Neurotransmitter Systems ◽

The Brain ◽

Catecholamine Levels

ABSTRACTThe widely projecting catecholaminergic (norepinephrine and dopamine) neurotransmitter systems profoundly shape the state of neuronal networks in the forebrain. Current models posit that the effects of catecholaminergic modulation on network dynamics are homogenous across the brain. However, the brain is equipped with a variety of catecholamine receptors with distinct functional effects and heterogeneous density across brain regions. Consequently, catecholaminergic effects on brain-wide network dynamics might be more spatially specific than assumed. We tested this idea through the analysis of functional magnetic resonance imaging (fMRI) measurements performed in humans (19 females, 5 males) at ‘rest’ under pharmacological (atomoxetine-induced) elevation of catecholamine levels. We used a linear decomposition technique to identify spatial patterns of correlated fMRI signal fluctuations that were either increased or decreased by atomoxetine. This yielded two distinct spatial patterns, each expressing reliable and specific drug effects. The spatial structure of both fluctuation patterns resembled the spatial distribution of the expression of catecholamine receptor genes: α1 norepinephrine receptors (for the fluctuation pattern: placebo > atomoxetine), ‘D2-like’ dopamine receptors (pattern: atomoxetine > placebo), and β norepinephrine receptors (for both patterns, with correlations of opposite sign). We conclude that catecholaminergic effects on the forebrain are spatially more structured than traditionally assumed and at least in part explained by the heterogeneous distribution of various catecholamine receptors. Our findings link catecholaminergic effects on large-scale brain networks to low-level characteristics of the underlying neurotransmitter systems. They also provide key constraints for the development of realistic models of neuromodulatory effects on large-scale brain network dynamics.SIGNIFICANCE STATEMENTThe catecholamines norepinephrine and dopamine are an important class of modulatory neurotransmitters. Because of the widespread and diffuse release of these neuromodulators, it has commonly been assumed that their effects on neural interactions are homogenous across the brain. Here, we present results from the human brain that challenge this view. We pharmacologically increased catecholamine levels and imaged the effects on the spontaneous covariations between brain-wide fMRI signals at ‘rest’. We identified two distinct spatial patterns of covariations: one that was amplified and another that was suppressed by catecholamines. Each pattern was associated with the heterogeneous spatial distribution of the expression of distinct catecholamine receptor genes. Our results provide novel insights into the catecholaminergic modulation of large-scale human brain dynamics.

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Exploring the Multi-Target Performance of Mitochondriotropic Antioxidants against the Pivotal Alzheimer’s Disease Pathophysiological Hallmarks

Molecules ◽

10.3390/molecules25020276 ◽

2020 ◽

Vol 25 (2) ◽

pp. 276 ◽

Cited By ~ 1

Author(s):

Sofia Benfeito ◽

Carlos Fernandes ◽

Santiago Vilar ◽

Fernando Remião ◽

Eugenio Uriarte ◽

...

Keyword(s):

Protein Misfolding ◽

Neuronal Damage ◽

Memory Loss ◽

Carbon Chain ◽

New Chemical Entities ◽

Brain Neurotransmitter ◽

Β Amyloid ◽

Target Performance ◽

Protein Misfolding And Aggregation ◽

The Brain

Alzheimer disease (AD) is the most common neurodegenerative disease featuring progressive and degenerative neurological impairments resulting in memory loss and cognitive decline. The specific mechanisms underlying AD are still poorly understood, but it is suggested that a deficiency in the brain neurotransmitter acetylcholine, the deposition of insoluble aggregates of fibrillar β-amyloid 1–42 (Aβ42), and iron and glutamate accumulation play an important role in the disease progress. Despite the existence of approved cholinergic drugs, none of them demonstrated effectiveness in modifying disease progression. Accordingly, the development of new chemical entities acting on more than one target is attracting progressively more attention as they can tackle intricate network targets and modulate their effects. Within this endeavor, a series of mitochondriotropic antioxidants inspired on hydroxycinnamic (HCA’s) scaffold were synthesized, screened toward cholinesterases and evaluated as neuroprotectors in a differentiated human SH-SY5Y cell line. From the series, compounds 7 and 11 with a 10-carbon chain can be viewed as multi-target leads for the treatment of AD, as they act as dual and bifunctional cholinesterase inhibitors and prevent the neuronal damage caused by diverse aggressors related to protein misfolding and aggregation, iron accumulation and excitotoxicity.

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Myriocin, a serine palmitoyltransferase inhibitor, alters regional brain neurotransmitter levels without concurrent inhibition of the brain sphingolipid biosynthesis in mice

Toxicology Letters ◽

10.1016/j.toxlet.2003.10.016 ◽

2004 ◽

Vol 147 (1) ◽

pp. 87-94 ◽

Cited By ~ 14

Author(s):

Marcin F. Osuchowski ◽

Victor J. Johnson ◽

Quanren He ◽

Raghubir P. Sharma

Keyword(s):

Serine Palmitoyltransferase ◽

Regional Brain ◽

Brain Neurotransmitter ◽

Sphingolipid Biosynthesis ◽

The Brain

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Fluorescent signalling of the brain neurotransmitter γ-aminobutyric acid and related amino acid zwitterions

Chemical Communications ◽

10.1039/cc9960002191 ◽

1996 ◽

pp. 2191-2192 ◽

Cited By ~ 76

Author(s):

A. Prasanna de Silva ◽

H. Q. Nimal Gunaratne ◽

Catherine McVeigh ◽

Glenn E. M. Maguire ◽

Pamela R. S. Maxwell ◽

...

Keyword(s):

Amino Acid ◽

Aminobutyric Acid ◽

Brain Neurotransmitter ◽

The Brain ◽

Related Amino Acid

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Pharmacodynamics of addictive substances

10.1093/med/9780198797746.003.0006 ◽

2018 ◽

Author(s):

David J. Nutt ◽

Liam J. Nestor

Keyword(s):

The Body ◽

Psychological Effects ◽

Neurotransmitter Systems ◽

The Brain

Pharmacodynamics refers to the effects addictive substances have on the body. Acutely, substances of addiction target various neurotransmitter systems in the brain. The pharmacological actions of these substances at receptors results in their physiological and psychological effects. The chronic abuse of these substances, however, leads to pharmacodynamic tolerance at receptors within neurotransmitter systems and leads to addiction. This tolerance means that a greater amount of the substance is required to achieve the desired effect and it has significant implications for relapse during early abstinence in addiction. Treatments target these neurotransmitter disturbances in addiction to prevent relapse.

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