The energy balance theory is an inconsistent paradigm.

Metabolic physiology asserts that body weight stability is achieved when over time the average absorbed energy intake equals the average expended energy. This principle, known as energy balance, justifies the design of numerous investigations that aim to elucidate the biology of obesity. The present work provides a mathematical analysis that demonstrates, nonetheless, that weight stability must coexist with a constant energy imbalance, i.

Computational and theoretical insights into the homeostatic response to the decreased cell size of midbrain dopamine neurons.

Midbrain dopamine neurons communicate signals of reward anticipation and attribution of salience. This capacity is distorted in heroin or cocaine abuse or in conditions such as human mania. A shared characteristic among rodent models of these behavioral disorders is that dopamine neurons in these animals acquired a small size and manifest an augmented spontaneous and burst activity.

Erratum to "Serious analytical inconsistencies challenge the validity of the energy balance theory" [Heliyon 6 7 (July 2020) e04204].

[This corrects the article DOI: 10.1016/j.heliyon.

Serious analytical inconsistencies challenge the validity of the energy balance theory.

Energy metabolism theory affirms that body weight stability is achieved as over time the average energy intake equals the average energy expenditure, a state known as energy balance. Here it is demonstrated, however, that weight stability coexists with a persistent energy imbalance. Such unexpected result emerges as a consequence of the answers to three fundamental problems: 1.

Cocaine sensitization increases subthreshold activity in dopamine neurons from the ventral tegmental area.

Unlabelled: The progressive escalation of psychomotor responses that results from repeated cocaine administration is termed sensitization. This phenomenon alters the intrinsic properties of dopamine (DA) neurons from the ventral tegmental area (VTA), leading to enhanced dopaminergic transmission in the mesocorticolimbic network. The mechanisms underlying this augmented excitation are nonetheless poorly understood.

New method to visualize neurons with DAT in slices of rat VTA using fluorescent substrate for DAT, ASP+.

The ventral tegmental area (VTA), and in particular dopamine (DA) neurons in this region of midbrain, has been shown to play an important role in motivation (goal-directed behavior), reward, and drug addiction. Most evidence that implicates VTA DA neurons in these functions are based on widely accepted but indirect electrophysiological characterization, including the hyperpolarization activated non-specific cation current (Ih), spike frequency, and inhibition by D2 receptor agonists. In this study, we used a known neuronal dopamine transporter (DAT) fluorescent substrate [4-(4- (dimethylamino) styryl)-N-methylpyridinium iodide] (ASP+) to visualize DAT-containing cell bodies of DA neurons in VTA region in rat brain slices.

Cocaine sensitization increases I h current channel subunit 2 (HCN₂) protein expression in structures of the mesocorticolimbic system.

Alteration of the biological activity among neuronal components of the mesocorticolimbic (MCL) system has been implicated in the pathophysiology of drug abuse. Changes in the electrophysiological properties of neurons involved in the reward circuit seem to be of utmost importance in addiction. The hyperpolarization-activated cyclic nucleotide current, I h, is a prominent mixed cation current present in neurons.

Presynaptic inhibition of glutamate transmission by α2 receptors in the VTA.

The ventral tegmental area (VTA) forms part of the mesocorticolimbic system and plays a pivotal role in reward and reinforcing actions of drugs of abuse. Glutamate transmission within the VTA controls important aspects of goal-directed behavior and motivation. Noradrenergic receptors also present in the VTA have important functions in the modulation of neuronal activity.

Cocaine sensitization inhibits the hyperpolarization-activated cation current Ih and reduces cell size in dopamine neurons of the ventral tegmental area.

The progressive augmentation of motor activity that results from repeated cocaine administration is termed behavioral sensitization. This phenomenon is thought to be a critical component in compulsive drug taking and relapse. Still, the cellular mechanisms that underlie sensitization remain elusive.