Autism is a devastating developmental disorder which is one of five disorders that are termed Pervasive Developmental Disorder (PDD). Autism is commonly associated with qualitative impairment in social interaction and communication as well as repetitive and stereotyped patterns of interest. These types of impairments may manifest themselves in the inability to form peer relationships, problems with verbal or nonverbal communication, and exhibition of repetitive motor mannerisms (Hollander et al. 2003). These debilitating symptoms have profound consequences when it comes to forming normal relationships. The anguish of autistic patients as well as their parents has served as motivation for current research of the underlying mechanisms behind autism. Much of this research has used such techniques as gene scanning, pharmacological and neurobiological approaches, yet the lack of concrete neurochemical, neurophysiological and neuroanatomical evidence leaves autism on the forefront of psychopathology (Insel et al. 1999
[...] Each of these knockout models was produced by selectively removing all or a combination of the three exons used to code for oxytocin production. Although each model varied in the collateral effects it produced, each model had a few things in common. For one, knocking out oxytocin production did not affect the density or the distribution of oxytocin receptors in comparison to wild type mice. From this observation, the researchers inferred that oxytocin receptor expression occurs independently of presynaptic oxytocin production. [...]
[...] It also seems more than likely that a defect in these neural networks may account for the communication and cognition impairment as well as the repetitive motor behavior that is associated with autism. Whether deficits in the oxytocin and vasopressin systems are a consequence of receptor mutation or developmental gene mutation still remains unclear. Further investigation with animal models and clinical trials should be done to gain more knowledge of the particular mechanisms behind the oxytocin and vasopressin systems. With continued persistence, research will elucidate small pieces of information that may be useful in developing treatment for autism. [...]
[...] Oxytocin and vasopressin may affect social behavior in mice, but their action may be specific to the olfactory system. If this were the case, then the data obtained from social recognition studies in mice can not be directly applied to humans. Instead, it might be able to used as a model to see how oxytocin and vasopressin act on a molecular level; a bottom up type approach. Another precautionary step that should be taken when using animal models is to evaluate the environment in which they studies are conducted. This is especially important when studying social behavior. [...]
[...] A particularly useful model for naturally studying the effects of oxytocin and vasopressin on social behavior is the rat model. Oxytocin is responsible for the onset of maternal behavior in female rats. Female rats, unlike other animals, show very little interest in infants until shortly before they give birth. Within a day of giving birth, female rats change their behavior dramatically. They show much more interest in pups from other litters as can be seen by their increase in grooming, nest building and protection of the pups. [...]
[...] Using autoradiography techniques in the rat hypothalamus, receptors for vasopressin have been found in the suprachiasmatic, sigmoid and arcuate nuclei, while oxytocin receptors are found in the ventromedial nucleus (Dreifuss et al. 1992). Single cell recordings show that oxytocin receptors in the ventromedial nucleus of the hypothalamus act as functional neuronal receptors. It is also interesting to note that the expression of these oxytocin receptors depends on gonadal steroid hormones (Dreifuss et al. 1992). Further immuno reactive studies in male and female marmosets (Callithrix jacchus) found a sexually dimorphic distribution of vasopressin neurons in the bed nucleus of the stria terminalis. [...]
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