A vitamin A-free diet results in impairment of the rat hippocampal somatostatinergic system

Abstract

Abstract-Previous studies have revealed the presence of retinoid specific receptors in the hippocampus and have demonstrated that vitamin A deficiency produces a severe deficit in spatial learning and memory which are linked to a proper hippocampal functioning. It is also well known that the tetradecapeptide somatostatin binds to specific receptors in the hippocampus and, when injected into this brain area, facilitates the acquisition of spatial tasks. In addition, depletion of somatostatin by cysteamine impairs acquisition of these tasks. Taken together, these studies support the idea that the hippocampal somatostatinergic system might be regulated by vitamin A. Hence, we evaluated the effects of vitamin A deprivation and subsequent administration of vitamin A on the rat hippocampal somatostatinergic system. Rats fed a vitamin A-free diet exhibited a significant reduction of somatostatin-like immunoreactivity content in the hippocampus whereas the somatostatin mRNA levels were unaltered. Vitamin A deficiency increased the somatostatin receptor density and its dissociation constant. Functional Gi activity as well as the capacity of somatostatin to inhibit basal and forskolin-stimulated adenylyl cyclase activity was decreased in vitamin A deficiency rats as compared with the control animals. All these parameters were fully restored when vitamin A was replaced in the diet. Furthermore, we found that the Gi␣ 1 , Gi␣ 2 and Gi␣ 3 protein levels were unaltered in hippocampal membranes from rats fed a vitamin A-free diet whereas subsequent vitamin A administration to these rats caused a significant increase in the levels of Gi␣1 and Gi␣2. Altogether, the present findings suggest that dietary vitamin A levels modulate the somatostatinergic system in the rat hippocampus.

Buriti oil (Mauritia flexuosa L.) negatively impacts somatic growth and reflex maturation and increases retinol deposition in young rats

“…The monitoring of serum and liver retinol concentrations in this study is important, considering that vitamin A is closely related to the function of the central nervous system, in the neurogenesis induction and neuronal patterning control (Shearer et al, 2012) and that the deficiency of this vitamin produces severe deficits in spatial learning and memory, which is associated with the correct functioning of the hippocampus (Hernández-Pinto et al, 2006) and consequently with the development of the reflex ontogeny in animals. In addition, vitamin A has defined function in the proper development of vertebrates (Gutierrez-Mazariegos et al, 2011), since its deficiency causes growth retardation in neonates (Samarut and Rochette-Egly, 2012), which reinforces its importance when it comes to irsomatic maturation.…”

Systematic review of the literature on vitamin A and memory

“…Ten reviews were identified among the publications, 12 , 29 , 30 , 32 , 34 , 37 , 45 - 47 , 51 while 34 papers presented original data. 15 - 28 , 31 , 33 - 36 , 38 - 44 , 48 - 50 , 52 - 57 …”

Therapeutic insights elaborating the potential of retinoids in Alzheimer’s disease

“…VAD-mediated learning and spatial cognition deficits in rats may be facilitated by RA and RARs, according to some investigations ( Etchamendy et al, 2003b ). RA activates the RAR, a nuclear receptor that controls genes regulating the neuronal proliferation and differentiation, neurite outgrowth, synaptic plasticity, and other activities ( Hernández-Pinto et al, 2006 ; McCaffery et al, 2006 ). The downstream pathways in RA activation, however, are unknown.…”