Hebbian plasticity, a mechanism believed to be the substrate of learning and memory, detects and further enhances correlated neural activity. Because this constitutes an unstable positive feedback loop, it requires additional homeostatic control. Computational work suggests that in recurrent networks, the homeostatic mechanisms observed in experiments are too slow to compensate instabilities arising from Hebbian plasticity and need to be complemented by rapid compensatory processes. We suggest presynaptic inhibition as a candidate that rapidly provides stability by compensating recurrent excitation induced by Hebbian changes. Presynaptic inhibition is mediated by presynaptic GABA receptors that effectively and reversibly attenuate transmitter release. Activation of these receptors can be triggered by excess network activity, hence providing a stabilising negative feedback loop that weakens recurrent interactions on sub-second timescales. We study the stabilising effect of presynaptic inhibition in recurrent networks, in which presynaptic inhibition is implemented as a multiplicative reduction of recurrent synaptic weights in response to increasing inhibitory activity. We show that networks with presynaptic inhibition display a gradual increase of firing rates with growing excitatory weights, in contrast to traditional excitatory-inhibitory networks. This alleviates the positive feedback loop between Hebbian plasticity and network activity and thereby allows homeostasis to act on timescales similar to those observed in experiments. Our results generalise to spiking networks with a biophysically more detailed implementation of the presynaptic inhibition mechanism. TGF-beta tumor In conclusion, presynaptic inhibition provides a powerful compensatory mechanism that rapidly reduces effective recurrent interactions and thereby stabilises Hebbian learning.We aimed to evaluate the relationship between serum testosterone (T) levels and penile curvature in a cohort of men presenting for chronic phase Peyronie’s disease (PD). Clinical data from 149 patients assessed for chronic phase PD between 2016 and 2019 at a single academic center were analyzed. Deformity assessment was conducted during an intracavernosal injection-induced rigid erection. Both total T (tT) and calculated free T (cFT) were assessed in every patient and considered as continuous variables or according to quartiles of the normal range. Hypogonadism was defined for tT  less then  10.4 nmol/L. Descriptive statistics and linear regression models tested the association between T values and the severity of penile curvature. Overall, median tT value was 15.9 (11.4-20.8) nmol/L in the whole cohort; median curvature magnitude and plaque size were 45 (30-60) degrees and 1.5 (0.8-2.0) cm, respectively. Penile curvature (40.0 vs. 45.0 degree; p = 0.7) and plaque size (1.5 vs. 1.3 cm; p = 0.4) were similar between eugonadal and hypogonadal patients. The magnitude of penile curvature did not differ across tT quartiles (p = 0.31). Both at univariable (β 1.32; p  less then  0.01) and multivariable (β 1.34; p  less then  0.01) linear regression model, only duration of PD was associated with the severity of penile curvature magnitude. The results of this cross-sectional study confirmed that there is no association between serum T values and the severity of penile curvature in patients with chronic phase PD. Only PD duration is associated with penile deformity severity.The liver is the only solid organ that uses regenerative mechanisms to ensure that the liver-to-bodyweight ratio is always at 100% of what is required for body homeostasis. Other solid organs (such as the lungs, kidneys and pancreas) adjust to tissue loss but do not return to 100% of normal. The current state of knowledge of the regenerative pathways that underlie this ‘hepatostat’ will be presented in this Review. Liver regeneration from acute injury is always beneficial and has been extensively studied. Experimental models that involve partial hepatectomy or chemical injury have revealed extracellular and intracellular signalling pathways that are used to return the liver to equivalent size and weight to those prior to injury. On the other hand, chronic loss of hepatocytes, which can occur in chronic liver disease of any aetiology, often has adverse consequences, including fibrosis, cirrhosis and liver neoplasia. The regenerative activities of hepatocytes and cholangiocytes are typically characterized by phenotypic fidelity. However, when regeneration of one of the two cell types fails, hepatocytes and cholangiocytes function as facultative stem cells and transdifferentiate into each other to restore normal liver structure. Liver recolonization models have demonstrated that hepatocytes have an unlimited regenerative capacity. However, in normal liver, cell turnover is very slow. All zones of the resting liver lobules have been equally implicated in the maintenance of hepatocyte and cholangiocyte populations in normal liver.Animal-associated microbiota is expected to impose crucial effects on the host’s fitness-related performance, including reproduction. Most research to date has focused on interactions between the host with its gut microbiota; however, there remain considerable gaps in knowledge regarding microbial consortia in other organs, including interspecific divergence, temporal stability, variation drivers, and their effects on the host. To fill these gaps, we examined oral and vaginal microbiota composition in four free-living mouse species of the genus Apodemus, each varying in the degree of female promiscuity. To assess temporal stability and microbiota resistance to environmental change, we exposed one of the species, Apodemus uralensis, to standardized captive conditions and analyzed longitudinal changes in its microbiota structure. Our results revealed the existence of a “core” oral microbiota that was not only shared among all four species but also persisted almost unchanged in captivity. On the other hand, vaginal microbiota appears to be more plastic in captive conditions and less species-specific in comparison with oral microbiota. This study is amongst the first to describe oral microbiota dynamics. Furthermore, the vaginal microbiota results are especially surprising in light of the well-known role of stable vaginal microbiota as a defense against pathogens. The results indicate the existence of diverse mechanisms that shape each microbiota. On the other hand, our data provides somewhat ambiguous support for the systematic effect of phylogeny and social system on both oral and vaginal microbiota structures.