al., 1993), Huntington's disease, nocturnal enuresis and attention deficit disorder (Ornitz et al. 1992), and Tourette's syndrome (Swerdlow et al. 1994; Castellanos et al. 1996). According to one study, people who have temporal lobe epilepsy with psychosis also show decreases in PPI, unlike those who have TLE without psychosis. Therefore, PPI deficits are not typical to specific disease, but rather tell of disruptions in a specific brain circuit. PPI deficit in schizophrenia PPI deficits represent a well-described finding in schizophrenia, with the first report dating back to 1978. The abnormalities are also noted in unaffected relatives of the patients. In one study, patients failed to show increased PPI to attended prepulses. Dopamine, which plays a major role in schizophrenia, had been shown to regulate sensorimotor gating in rodent models. These findings fit to the dopamine hypothesis of schizophrenia. In theory, PPI disruption in schizophrenia may be related to the processes of sensory flooding and cognitive fragmentation. Antipsychotic medication have been shown to increase PPI in patients, with atypical antipsychotics having more effect. Patients display the same gender difference in PPI as healthy people: males have higher PPI compared to females. One notable finding is that patients are specifically deficient in PPI with 60 ms prepulse intervals relative to intervals of other lengths; this remains so even under antipsychotic treatment. The other fact is the influence of cigarette smoking: the research suggests that smoking does indeed "calm the nerves". Non-smoking patients have lower PPI compared to smokers, and heavy smokers have the highest PPI. This finding runs in accord with the high rates of smoking among schizophrenic patients, estimated at 70%, with many patients smoking more than 30 cigarettes a day. Some studies show association of schizophrenia with the CHRNA7 and CHRFAM7A genes, which code for alpha7 subunit of nicotinic receptors, but other studies are negative. Contrary to the predictions, nicotine receptor alpha7 subunit knockout mice do not show disruptions in PPI. In rodents Murine models are widely used to test hypotheses linking genetic components of various diseases with sensorimotor gating. While some of the hypotheses stand to the test, others are not, as some mice models show unchanged or increased PPI contrary to the expectations, as in the tests of COMT-deficient mice. Certain surgical procedures also disrupt PPI in animals, helping to unravel the underlying circuitry. Many animal studies of PPI are undertaken in order to understand and model the