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Mendes, A. P.

Publications and source records attributed to Mendes, A. P..

2 recordsLinked to original sources

A galanin-positive population of lumbar spinal cord neurons modulates sexual behavior and arousal

During sex, male arousal increases to the ejaculatory threshold, allowing genital sensory input to trigger ejaculation. While copulation and sexual arousal are thought to be centrally regulated by the brain, ejaculation is considered a reflex controlled by a spinal circuit. In this framework, the spinal cord is assumed to be strongly inhibited by descending input from the brain until the ejaculatory threshold, playing no role in the regulation of copulatory behavior. However, this remains untested. Here, we mapped the spinal circuit controlling the bulbospongiosus muscle, which is involved in sperm expulsion in mice. Our findings reveal that bulbospongiosus muscle-motor neurons receive input from galanin-expressing interneurons. This galanin-positive population receives genital input and, while its stimulation leads to bulbospongiosus muscle activity, the evoked muscle-potentials are dependent on spinalization, the males internal state and decrease with repeated stimulation. Moreover, ablation of galanin neurons affected the latency to ejaculate and altered the copulatory pattern. These results suggest an unexpected role of spinal circuits in the control of copulation and arousal, in addition to its established role in ejaculation.

neuroscience↗

Monozygotic twins discordant for schizophrenia differ in maturation and synaptic transmission

Schizophrenia affects approximately 1% of the world population. Genetics, epigenetics, and environmental factors are known to play a role in this psychiatric disorder. While there is a high concordance in monozygotic twins, about half of twin pairs are discordant for schizophrenia. We characterized human-induced pluripotent stem cell (iPSC)-derived hippocampal neurons from two pairs of monozygotic twins that are discordant for a schizophrenia diagnosis. We compared the affected and the non-affected siblings and compared all of them to twin sets where none of the siblings suffered from schizophrenia. We found that the neurons derived from the schizophrenia patients were less arborized, were hypoexcitable with immature spike features, and exhibited a significant reduction in synaptic activity with dysregulation in synapse-related genes. Interestingly, the neurons derived from the co-twin siblings who did not have schizophrenia formed another distinct group that was different from the neurons in the group of the affected twin siblings but also different from the neurons in the group of the control twins. The neurons in the unaffected co-twin group were also less arborized than the neurons from controls but more arborized than those from affected siblings. Some of their spike features were immature (but less immature than neurons derived from the affected siblings). Importantly, their synaptic activity was not affected. Since schizophrenia is a genetically complex disorder, our twin study allows the measurement of neuronal phenotypes with a similar genetic background. The differences between the siblings may arise due to changes that occurred after the split of the egg into twins. Therefore, our study confirms that dysregulation of synaptic pathways, as well as changes in the rate of synaptic events, distinguishes between individuals affected with schizophrenia and unaffected individuals, even in those having a very similar genetic background.

neuroscience↗