The astrocytes（AS） and hippocampal neurons were primarily cultured.The AS were divided into control group and Aβ_1-42+different doses （0.25，0.50 and 1.00 mmol?L^－1）of lithium chloride groups. After treated with lithium for 2 weeks， the AS were stimulated with 250 nmol?L^－1 Aβ_1-42.The Ca²⁺ level in AS was detected by fluorescence probe technique， the release amount of glutamate of AS was measured by HPLC method， and Western blotting method was performed to detect the expression levels of transient receptor potential channel 1（TRPC1），Na⁺/Ca²⁺ exchanger 1（NCX1） and CACNA1C （Cav1.2） proteins in AS. The cultured hippocampal neurons were divided into control group， Aβ_1-42 group and Aβ_1-42+different doses of lithium chloride groups. The conditioned medium containing AS or not treated with Aβ_1-42 were added，respectively.The total dendrite branch length （TDBL）， number of primary-order dendrite（PDN）， maximum branch order（MBO） of hippocampal neurons were observed by inverted phase-contrast microscope.The amount of NO release in culture solution was measured by Griess method.

Compared with control group， the levels of Ca²⁺ in AS in Aβ_1-42 +different doses of lithium chloride groups were significantly decreased （P<0.05）， the Ca²⁺ influx was reduced（P<0.05），the release amounts of glutamate were decreased significantly （P<0.05）， and the expression levels of TRPC1 protein were decreased significantly （P<0.05）， but the expression levels of NCX1 and Cav1.2 proteins had no significant differences （P>0.05）. Compared with control group， the release amount of NO in hippocampal neurons in Aβ_1-42 group was significantly increased（P<0.05）， and TDBL， PDN and MBO were significantly decreased（P<0.01）. Compared with Aβ_1-42 group， the release amounts of NO in hippocampal neurons in Aβ_1-42 +different doses of lithium chloride groups were decreased （P<0.01）， and TDBL， PDN and MBO were significantly increased（P<0.01）. The release amounts of NO in hippocampal newrons in various groups had significant difference after cultured with Aβ_1-42-treated culture medium without AS（P>0.05）.

Lithium chloride has inhibitory effect on Aβ_1-42-induced Ca²⁺-dependent glutamate release in AS，and its mechanism may be related to down-regulation of TRPC1 receptor expression；lithium chloride can alleviate the injury of hippocampal neurons by inhibiting the release of NO in the neurons.