Increased locomotor response to amphetamine, but not other psychostimulants, in adult mice submitted to a low-protein diet

Abstract

Protein malnutrition results in a variety of brain dysfunctions, ultimately affecting cognitive functions. The effects of protein malnutrition in brain response to psychostimulants have been less studied in adult animals. We therefore aimed to study the response to psychoactive drugs on the locomotor activity (a behavior paradigm) of adult protein malnourished mice. Two-month-old mice were divided in two groups: (a) low-protein group (LP), which received 6% of protein diet, and (b) a control group that received a 25% of protein diet. After 3 months, they were tested for locomotor activity after an i.p. injection of one of psychoactive drugs: D-amphetamine (5.0 mg/kg), apomorphine (2.0 mg/kg), dizocilpine (0.25 mg/kg), or caffeine (30 mg/kg). Mice submitted to the LP diet presented prolonged induction of hyperlocomotion caused by amphetamine (about 350% between 90 and 180 min post drug injection as compared with well-nourished mice, p<0.01) but presented unaltered response to apomorphine, caffeine, and dizocilpine. These data point to altered catecholamine metabolism induced by protein restriction in adult mice. The results are discussed based on previous works, presenting theoretical hypotheses about the possible mechanisms involved in the present findings.

Protein deficiency decreases stereotypic behavior frequency and prevalence and activity in the striped mouse Rhabdomys dilectus chakae

“…Thirdly, long-term changes in the composition of dietary macronutrients are known to affect brain chemistry, neurotransmitter systems (Morgane, Mokler, & Galler, 2002) and cause neurophysiological, morphological, and neurochemical changes in the developing brain (reviewed in: Alamy & Bengelloun, 2012). Low dietary protein results in reduced dopamine receptor density in the brain (Hamdi, Onaivi, & Prasad, 1992) and altered catecholamine metabolism (Dietrich et al, 2004). Moreover, prenatal protein-restriction can cause abnormal synaptogenesis in the basal ganglia (Alamy & Bengelloun, 2012), and damage or dysfunction in the basal ganglia system have been linked to stereotypies in several vertebrate species (Garner, 2005;Graybiel, 2008;Lewis et al, 2006).…”