Ginkgo biloba treatments reverse the impairment of conditioned suppression acquisition induced by GluN2B-NMDA and 5-HT1A receptor blockade: Modulatory effects of the circuitry of the dorsal hippocampal formation

BDNF as a Putative Target for Standardized Extract of Ginkgo biloba-Induced Persistence of Object Recognition Memory

“…Taken together, these results corroborate previous data from our group showing that that treatment with EGb improves long-term memory in a dose-dependent manner, as assessed by conditioned suppression of licking behavior as well as modulation of the spontaneous recovery of conditioned fear [11][12][13]52]. Here, we reveal a relationship between acute EGb treatment and the persistence of non-aversive memory for the first time.…”

“…Moreover, another study revealed that a sample session of 10 min each for three days supports the encoding of strong object memory [ 60 , 71 ], and promotes persistence of object memory. Consistent with these data and previous data from our lab showing the effects of EGb as a cognitive enhancer [ 13 , 14 , 56 , 57 ] we hypothesized that associated effects, such as a longer sample phase and EGb treatment, would improve recognition memory formation and support the persistence of long-term recognition memory in rats in the object recognition test (ORT), since both the familiarity and recollection components become less persistent over time [ 22 , 23 ].…”

“…Interactions of these different pathways, which converge on CREB and BDNF expression, are thought to be crucial for the effects of flavonoids on memory enhancement [ 1 , 66 ]. In previous studies from our group, we analysed the neural circuits and neurochemical changes following EGb treatment and fear memory formation [ 13 , 15 , 57 , 60 ] as well as the effects of crude extract of erythrina (CE), flavonoidic fraction or isolated compounds from CE on conditioned suppression [ 14 , 67 ]. EGb treatment prior to conditioning was subsequently evaluated after 72 or 96 h during the extinction retention test, and EGb was demonstrated to have effects on the spontaneous recovery of extinction.…”

“…Conversely, our group reported an impairment in conditioned fear memory following diazepam treatment, which was associated with reduced CREB-1 expression (both mRNA and protein) in the dorsal hippocampus [ 11 ]. In addition, we showed that the mRNA and protein expression of the serotonin type-1A (5-HT 1A ) receptor and the GluN2B and GluN2A subunits of the N-methyl-D-aspartate (NMDA)-type glutamate receptor in the dHF are modulated after EGb treatment and fear memory acquisition [ 13 ]. We also showed that flavones modulate fear memory formation and persistence through gamma-aminobutyric acid type A receptor (GABA A R) modulation [ 14 , 15 ].…”

Proteome analysis indicates participation of the dorsal hippocampal formation in fear-motivated memory in a time-dependent manner.

“…Conditioned suppression of the licking response was assessed as previously described (de Oliveira et al, 2014; Gaiardo et al, 2019; Zamberlam et al, 2019) and was conducted for either 8 or 46 days. On Days 1–5, the rats were subjected to the acquisition of a licking response for 20 min per day to establish a stable baseline of licking behavior.…”