Table 1.

Studies of the role of CCR5 in HAND or neuronal plasticity and excitability with animal models.

Methods	Main Findings	Author & Date
Mice: Transgenic mice expressing HIV gp120 in the brain (with or without Ccr5 KO plus Lcn2 KO)	Knockout of LCN2 in HIVgp120tg mice abrogates memory impairment and ameliorates neuronal damage. Genetic ablation of Ccr5 in LCN2-deficient HIVgp120tg mice restores neuropathology	Ojeda-Juárez et al., 2020
Mice: V3 peptide injection to the dorsal hippocampus or barrel cortex of mice with Ccr5 knockout or Ccr5 knockdown	Ccr5 knockout rescued LTP deficits caused by gp120 V3 peptide both in hippocampus and cortex. Both Ccr5 knockout and knockdown ameliorated V3 peptide induced memory deficits	Zhou et al., 2016
Mice: Transgenic mice expressing gp120, and double transgenic mice expressing gp120 and Ccr5 knockout	Ccr5 knockout prevented microglial activation and neuronal damage in HIVgp120tg mice. LCN2 neurotoxicity is CCR5 dependent, and Ccr5 knockout rescued learning and memory deficits in HIVgp120tg mice	Maung et al., 2014
Rats: Cultured hippocampal neurons from rat embryos with acute gp120 treatment	Modifications in Kv2.1 and neuronal excitability after gp120 treatment were dependent on the activation of CCR5 and CXCR4. Blockade of Kv2.1 led to significant enhancement of neuronal death upon gp120 treatment	Shepherd et al., 2013

∗LCN2: Protein lipocalin-2, LTP: long-term potentiation.