Emergence of behavioral phenomena and adaptation effects in human numerosity decoder using recurrent neural networks.

Humans possess an innate ability to visually perceive numerosities, which refers to the cardinality of a set. Numerous studies indicate that the lateral intraparietal cortex (LIP) and other intraparietal sulcus (IPS) regions (region) of the brain contain the neurological substrates responsible for number processing. Existing computational models of number perception often focus on a limited range of numbers and fail to account for important behavioral characteristics like adaptation effects, despite simulating fundamental aspects such as size and distance effects. To address these limitations, our study develops (introduces) a novel computational model of number perception utilizing a network of neurons with self-excitatory and mutual inhibitory properties. Our approach assumes that the mean activation of the network at steady state can encode numerosity by exhibiting a monotonically increasing relationship with the input variable set size. By optimizing the total number of inhibition strengths required, we achieve coverage of the full range of numbers through three distinct intervals: 1 to 4, 5 to 17, and 21 to 50. Remarkably, this division aligns closely with the breakpoints in numerosity perception identified in behavioral studies. Furthermore, our study develops a method for decoding the mean activation into a continuous scale of numbers spanning from 1 to 50. Additionally, we propose a mechanism for dynamically selecting the inhibition strength based on current inputs, enabling the network to operate effectively across an extended (entire) range of numerosities. Our model not only sheds new light on the generation of diverse behavioral phenomena in the brain but also elucidates how continuous visual attributes and adaptation effects influence perceived numerosity.

Cerebrolysin reduces excitotoxicity by modulation of cell-death proteins in delayed hours of ischemic reperfusion injury.

Recent preclinical and clinical reports suggest that cerebrolysin shows neuroprotective properties similar to endogenous neurotrophic factors in neurodegenerative disorders including ischemic stroke. However, little is known about its underlying antiexcitotoxic action. Adult male Wistar rats were intraperitoneally treated with cerebrolysin (0.15 or 0.30 mg/kg) or vehicle at 3, 6 and 12 h after ischemic reperfusion and were assessed 24 h after reperfusion in ischemic rats. We added cerebrolysin (2.5 or 5 mg/ml) or vehicle in primary cortical culture cells at 3, 6 and 12 h of post-glutamate exposure and performed cell viability assays at 24 h. Our in-vivo and in-vitro findings showed that cerebrolysin substantially reduced neuronal cell death in delayed hours of post ischemic- and glutamate-insult conditions respectively. Further, we have assessed the influence of NR-2 A/-2B receptor antagonism on neuroprotective action of cerebrolysin at 6 h in in-vivo as well as in-vitro conditions. Neuroprotective effect of cerebrolysin at 6 h of reperfusion was enhanced by pretreatment of NR2B antagonist RO25-6981.We found that cerebrolysin restrained upregulation of extrasynaptic NR2B responsible for triggering apoptotic pathways. Cerebrolysin reduced expression of important cell death proteins such as, JNK, PTEN, Calpain and Caspase-3 components. Importantly, we also found that cerebrolysin reduced SREBP1 expression, which gets activated only after 6 h of ischemia. These results demonstrate that cerebrolysin reduces excitotoxicity and protect neuronal cells in delayed hours of ischemic reperfusion injuries by decreasing cell death proteins.