Use of @entity19 with Targeted Genetic Inactivation in the Serotonergic System for the Study of XXXX

@entity1 @entity66 @entity19 @entity14200 @entity148 @entity750 @entity19472
The first knockout of a @entity750 receptor was published more than 10 years ago and since then most of the @entity750 receptors have been genetically inactivated in @entity19 . Reviewing the @entity148 -related behavior of individual receptor knockout lines, it is apparent that genetic inactivation of some receptors, including the 5-HT2A and 5-HT3 receptors, reproduced the phenotype elicited by the acute pharmacological blockade of the receptor. This indicates that signaling through some @entity750 receptors is directly involved in the regulation of @entity148 states. In other cases, however, the genetic inactivation and pharmacological blockade of the receptor resulted in different and sometimes opposing behaviors. For example, the genetic inactivation of the @entity750 transporter results in increased @entity148 whereas chronic pharmacological blockade of the @entity750 transporter by SSRIs leads to reduced @entity148 . @entity19 null for the @entity19472 show increased @entity148 , while selective pharmacological inhibitors of the receptor do not have a measurable effect on @entity148 in adult @entity19 . These are interesting findings because the genetic inactivation of the receptor could be similar to inherited conditions characterized by a loss of function mutation of the receptor/transporter. Indeed, @entity750 transporter knockout in @entity19 may reproduce the s polymorphism in @entity1 . Also, certain individuals have a reduced expression of the @entity19472 that, if present from early life, is similar to the null mutation of the receptor in @entity19 . Therefore, the @entity19472 and @entity750 transporter knock-out @entity19 strains may @entity66 models that can be used to understand how a @entity14200 leads to an @entity148 -like phenotype.
