Oxytocin und Autismus

Interessante Forschung zur Wirkung von Oxytocin:

Oxytocin is the focus of intense scrutiny for its apparent roles in establishing trust between people, and has been administered to children with autism spectrum disorders in clinical trials. The new study, to be published Sept. 12 in Nature, pinpoints a unique way in which oxytocin alters activity in a part of the brain that is crucial to experiencing the pleasant sensation neuroscientists call „reward.“ The findings not only provide validity for ongoing trials of oxytocin in autistic patients, but also suggest possible new treatments for neuropsychiatric conditions in which social activity is impaired. „People with autism-spectrum disorders may not experience the normal reward the rest of us all get from being with our friends,“ said Robert Malenka, MD, PhD, the study’s senior author. „For them, social interactions can be downright painful. So we asked, what in the brain makes you enjoy hanging out with your buddies?“ Some genetic evidence suggests the awkward social interaction that is a hallmark of autism-spectrum disorders may be at least in part oxytocin-related. Certain variations in the gene that encodes the oxytocin receptor – a cell-surface protein that senses the substance’s presence – are associated with increased autism risk.

Oxytocin wäre also dafür zuständig, soziale Interaktionen zu belohnen. Interessant auch die weiteren Ausführung zur Bindung:

In the 1970s, biologists learned that in prairie voles, which mate for life, the nucleus accumbens is replete with oxytocin receptors. Disrupting the binding of oxytocin to these receptors impaired prairie voles‘ monogamous behavior. In many other species that are not monogamous by nature, such as mountain voles and common mice, the nucleus accumbens appeared to lack those receptors. „From this observation sprang a dogma that pair bonding is a special type of social behavior tied to the presence of oxytocin receptors in the nucleus accumbens. But what’s driving the more common group behaviors that all mammals engage in – cooperation, altruism or just playing around – remained mysterious, since these oxytocin receptors were supposedly absent in the nucleus accumbens of most social animals,“ said Dölen. The new discovery shows that mice do indeed have oxytocin receptors at a key location in the nucleus accumbens and, importantly, that blocking oxytocin’s activity there significantly diminishes these animals‘ appetite for socializing. Dölen, Malenka and their Stanford colleagues also identified, for the first time, the nerve tract that secretes oxytocin in the region, and they pinpointed the effects of oxytocin release on other nerve tracts projecting to this area.

Und zu der Wirkungsweise:

As the Stanford team found, oxytocin acting at the nucleus accumbens wasn’t simply squirted into general circulation, as hormones typically are, but was secreted at this spot by another nerve tract originating in the hypothalamus, a multifunction midbrain structure. Oxytocin released by this tract binds to receptors on the dorsal Raphe projections to the nucleus accumbens, in turn liberating serotonin in this key node of the brain’s reward circuitry. The serotonin causes changes in the activity of yet other nerve tracts terminating at the nucleus accumbens, ultimately resulting in altered nucleus accumbens activity – and a happy feeling. „There are at least 14 different subtypes of serotonin receptor,“ said Dölen. „We’ve identified one in particular as being important for social reward. Drugs that selectively act on this receptor aren’t clinically available yet, but our study may encourage researchers to start looking at drugs that target it for the treatment of diseases such as autism, where social interactions are impaired.“

Demnach wäre Autismus eine Folge davon, dass man nicht hinreichend für soziale Interaktionen belohnt wird, was mal wieder zeigt, wie biochemisch unser Gehirn arbeitet:  Funktioniert eines der Systeme nicht, dann verändert es das gesamte Denken

Frau-zu-Mann-Transsexuelle und Autismus

Eine interessante Studie beschäftigt sich mit Frau-zu-Mann-Transsexuellen und Autismus:

The ‘extreme male brain’ theory suggests females with Autism Spectrum Conditions are hyper-masculinized in certain aspects of behavior. We predicted that females with Gender Identity Disorder (who are masculinized) would have elevated Autism Spectrum Quotient (AQ) scores. AQ scores from five groups were compared: (1) n = 61 transmen (female-to-male transsexual people); (2) n = 198 transwomen (male-to-female transsexual people); (3) n = 76 typical males; (4) n = 98 typical females; and (5) n = 125 individuals with Asperger Syndrome (AS). Transmen had a higher mean AQ than typical females, typical males and transwomen, but lower than individuals with AS. Transmen have more autistic traits and may have had difficulty socializing with female peers and thus found it easier to identify with male peer groups.

Quelle: Brief Report: Female-To-Male Transsexual People and Autistic Traits (PDF)

Das ist interessant, weil die Theorie des „extrem männlichen Gehirns“ Autismus als eben eine solche Ausprägung ansieht, weswegen Männer wesentlich häufiger von Autismus betroffen sind als Frauen. Nach dieser Theorie wären solche extrem männlichen Gehirne eher auf Sachen und weniger auf Personen bezogen, weswegen Autisten mit Menschen gar nicht zurecht kommen und ihre Handlungen wesentlich schwerer verstehen. Der Schluss daraus ist, dass Frauen mit einem solchen extrem männlichen Gehirn sich dann eben eher als Männer sehen und auf deren Art denken, zumindest auf diese Weise eher mit Männern zurechtkommen als mit Frauen.

Die Forscher dazu:

We found there was no difference between transwomen and control males on the AQ: transwomen have a mean AQ score that lies in the average range for both control males and females, and is not significantly different from either. Similarly, the proportion of transwomen with BAP and MAP also lies between control males and control females. Interestingly, within the 198 transwomen group, there were 6 individuals (i.e. 3%) with a diagnosis of AS. This rate is about 3 times as many as in the general population (Baird et al. 2006), although we have not calculated confidence intervals for this, it is consistent with previous studies (de Vries et al. 2010). Interestingly, among the transwomen sexual preference influenced AQ scores, consistent with findings that there are different typologies among transwomen based upon their sexual orientation (Lawrence 2010). Future research should explore this connection, as it appears that the association between GID and ASC in transwomen is complex

Aus der Besprechung am Ende:

In closing, this study provides evidence that transmen have an elevated number of autistic traits. This may be a reflection of elevated FT levels since both normative amniotic testosterone studies (Chapman et al. 2006; Knickmeyer et al. 2005) and studies of rare genetic conditions in which FT levels are abnormally high (such as in females with Congenital Adrenal Hyperplasia) (Knickmeyer et al. 2006a) indicate that higher FT is correlated with reduced empathy, reduced social interest, reduced social skills, and higher AQ scores. Quite how this is expressed in terms of neural masculinization (Baron-Cohen et al. 2005) is an important question for further study, which we are currently seeking to answer using MRI in children whose amniotic FT levels are known. The causation of GID and its development is complex and this paper is a contribution regarding a particular association between GID and ASC.