Anxiety may be attenuated via actions of y-aminobutyric acid (GABA), the major inhibitory neurotransmitter. Several flavonoids, including quercetin from red wine, bind to the benzodiazepine GABAA receptor . Since EGCG is structurally related to these compounds, it may also exert effects via this receptor. At low concentrations, it enhances benzodiazepine's activity on GABAA-receptor-mediated currents in Xenopus oocytes and partially reverses the effects of P-carboline, a negative benzodiazepine modulator, in rat hippocampal neurons without enhancing glutamate-mediated spontaneous excitatory synaptic transmission [29,30]. Both chlorodiazepoxide and EGCG induced the anxiolytic activity of mice in an elevated plus maze test . EGCG reduced anxiety and was sedative for chicks experiencing social separation stress, partially by decreasing plasma corticosterone levels, perhaps via the GABAA receptor .
Memory loss during aging and brain senescence may be at least partially due to oxidative DNA damage. Impaired learning and memory appear to be causally linked to atrophy in the hippocampus and forebrain. In a murine model of aging, cerebral weight decreased with age. The rate of decrease slowed in mice ingesting green tea catechins, and oxidative DNA damage in the cerebrum was reduced . Memory loss was also inhibited, but no effect was seen with regard to learning time or lifespan. Thus, tea catechins appear to primarily improve quality of life rather than its length.
Green tea polyphenols were beneficial to cognitive memory in aged mice and rats [33, 34]. Epidemiological studies in humans also found negative correlations between green tea consumption and cognitive impairment .
9.2.9 HIV-Associated Dementia (HAD)
Retroviral invasion of the CNS and establishment in microglia are common occurrences in HIV-infected individuals and may result in severe neuropyschiatric disease, such as HAD, which is resistant to highly active antiretroviral therapy. Survival time after this diagnosis averages 6 months. Production of interferon-y (IFN-y) increases during HIV infection; this cytokine enhances neuronal damage induced by viral gp120 and Tat via the JAK/STAT pathway . EGCG reduced this IFN-y-augmented damage both in vitro and in vivo by inhibiting JAK/STAT signaling.
Viral proteins bind NMDA glutamate receptors and can pathologically dysreg-ulate calcium concentrations and mitochondrial functions . As described below, ECGC also affects these processes. Another factor enhancing gp120 neurotoxicity is the cytokine TNF-a, whose production is altered by EGCG (see below).
The addition of EGCG to primary cultures of rat medial vestibular nuclear neurons lowered their spontaneous firing rate and hyperpolarized their membrane potential. This is believed to result from alteration of the potassium currents. No effects were noted on the amplitude of the afterhyperpolarization or the action potential's spike width . EGCG also depolarized membranes of myenteric neurons in small intestines of guinea pigs .
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