Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport.

Title Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport.
Authors Y. Sun; J. Yang; X. Hu; X. Gao; Y. Li; M. Yu; S. Liu; X. Lu; C. Jin; S. Wu; Y. Cai
Journal Arch Toxicol
DOI 10.1007/s00204-017-2148-x
Abstract

Lanthanum (La) can impair learning memory and induce behavioral abnormalities in animals. However, the mechanism underlying these adverse effects of La is still elusive. It has been demonstrated that lactate derived from astrocytes is the major energy source for neurons during long-term memory (LTM) formation and the deficiency of lactate supply can result in LTM damage. However, little work has been done with respect to the impact of La on the lactate production in astrocytes and astrocyte-neuron lactate transport (ANLT). Herein, experiments were undertaken to explore if there was such an adverse effect of La. Primary culture rat cortical astrocytes and primary co-culture rat cortical astrocyte-neuron were treated with (0.125, 0.25 and 0.5 mM) lanthanum chloride (LaCl3) for 24 h. The results showed that LaCl3 treatment significantly downregulated the mRNA and protein expression of glucose transporter 1 (GLUT1), glycogen synthase (GS), glycogen phosphorylase (GP), lactate dehydrogenase A (LDHA), and monocarboxylate transporter 1, 2 and 4 (MCT 1 2 and 4); upregulated the mRNA and protein expression of lactate dehydrogenase B (LDHB); and decreased the glycogen level, total LDH and GP activity, GS/p-GS ratio and lactate contents. Moreover, rolipram (20, 40 ?M) or forskolin (20, 40 ?M) could increase the lactate content by upregulating GP expression and the GS/p-GS ratio, as well as antagonize the effects of La. These results suggested that La-induced learning-memory damage was probably related to its suppression of lactate production in astrocytes and ANLT. This study provides some novel clues for clarifying the mechanism underlying the neurotoxicity of La.

Citation Y. Sun; J. Yang; X. Hu; X. Gao; Y. Li; M. Yu; S. Liu; X. Lu; C. Jin; S. Wu; Y. Cai.Lanthanum chloride reduces lactate production in primary culture rat cortical astrocytes and suppresses primary co-culture rat cortical astrocyte-neuron lactate transport.. Arch Toxicol. 2017. doi:10.1007/s00204-017-2148-x

Related Elements

Lanthanum

See more Lanthanum products. Lanthanum (atomic symbol: La, atomic number: 57) is a Block F, Group 3, Period 6 element with an atomic weight of 138.90547. Lanthanum Bohr ModelThe number of electrons in each of lanthanum's shells is [2, 8, 18, 18, 9, 2] and its electron configuration is [Xe] 5d1 6s2. The lanthanum atom has a radius of 187 pm and a Van der Waals radius of 240 pm. Lanthanum was first discovered by Carl Mosander in 1838. In its elemental form, lanthanum has a silvery white appearance.Elemental Lanthanum It is a soft, malleable, and ductile metal that oxidizes easily in air. Lanthanum is the first element in the rare earth or lanthanide series. It is the model for all the other trivalent rare earths and it is the second most abundant of the rare earths after cerium. Lanthanum is found in minerals such as monazite and bastnasite. The name lanthanum originates from the Greek word Lanthaneia, which means 'to lie hidden'.

Chlorine

Chlorine is a Block P, Group 17, Period 3 element. Its electron configuration is [Ne]3s23p5. The chlorine atom has a covalent radius of 102±4 pm and its Van der Waals radius is 175 pm. Chlorine ModelIn its elemental form, chlorine is a yellow-green gas. Chlorine is the second lightest halogen after fluorine. It has the third highest electronegativity and the highest electron affinity of all elements, making it a strong oxidizing agent. It is rarely found by itself in nature. Chlorine was discovered and first isolated by Carl Wilhelm Scheele in 1774. It was first recognized as an element by Humphry Davy in 1808.

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