Skip to main content
Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Intraventricular infusion of quinolinic acid impairs spatial learning and memory in young rats: a novel mechanism of lead-induced neurotoxicity

Fig. 8

Schematic representation of probable role of quinolinic acid in lead-neurotoxicity. Pb accumulation in the brain results in decreased NMDAR activity, which results in decreased LTP leading to impaired learning and memory (reviewed by Rahman, 2013 [1]). In addition, Pb induces astroglyosis and microglyosis [38]. Activated astrocytes and microglia produce inflammatory cytokines, which activates the KP, converting tryptophan into QA [11]. High levels of QA are toxic to astrocytes, microglia, and neurons [12, 14]. QA is an NMDAR agonist and causes excitotoxicity in neurons [10]. In addition, it increases synaptic glutamate levels, further increasing excitotoxicity [35]. This increased excitotoxicity in neurons, together with tau hyperphosphorylation [22, 98], eventually results in neurodegeneration. Up arrows indicated upregulation/increase; down arrows indicate downregulation/decrease

Back to article page