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PPI or pre-pulse inhibition is the measure of startle response. PPI is reflective of cognitive and other responses, and is indicative in patients suffering Schizophrenia, obsessive/compulsive disorders and Huntingtons disease.
This paper looks at how humans respond to PPI tests after various pre-treatments followed by MDMA. What is very interesting is that humans are affected in the opposite way to rodents which seem to have reduced PPI when given MDMA.
Effects of MDMA (Ecstasy) on Prepulse Inhibition and Habituation of Startle in Humans after pretreatment with Citalopram, haloperidol, or Ketanserin
This paper looks at how humans respond to PPI tests after various pre-treatments followed by MDMA. What is very interesting is that humans are affected in the opposite way to rodents which seem to have reduced PPI when given MDMA.
Effects of MDMA (Ecstasy) on Prepulse Inhibition and Habituation of Startle in Humans after pretreatment with Citalopram, haloperidol, or Ketanserin
[From the Introduction]
Startle
The startle reflex is a contraction of the skeletal and facial musculature in response to a sudden intense stimulus, such as a loud noise. In humans, the eyeblink component of the startle reflex is measured using electromyography of the orbicularis oculi muscle. In rodents, a stabilimeter is used to register a whole-body flinch response. The startle reflex exhibits several forms of behavioral plasticity, such as prepulse inhibition
(PPI) and habituation, which are consistent phenomena across species. PPI refers to the normal suppression ofthe startle response when the startling stimulus is precededby a weak prestimulus. PPI is regarded as an operational measure of sensorimotor gating reflecting the ability to filter cognitive or sensory information. Habituation refers to the decrement of the startle response observed with repeated presentation of the stimulus and is considered to be the simplest form of learning and a prerequisite of selective attention. Both PPI and habituation deficits have been found in patients with schizophrenia (Bolino et al. 1994; Braff et al. 1992; Geyer and Braff 1982) and schizotypal personality disorder (Cadenhead et al. 1993). Deficits in PPI are also seen in obsessive–compulsive disorder(Swerdlow et al. 1993) and Huntington’s disease (Swerdlow et al. 1995).
....Little is known about the pharmacology of PPI in humans. Surprisingly, a recent study from our laboratory found that MDMA (1.7 mg/kg PO) increased PPI in healthy volunteers, thus having an opposite effect on sensorimotor gating in humans versus animals (Vollenweider et al. 1999a). Whether procedural or species-specific differences, including a different mechanism of action of MDMA, account for these findings is unclear. Therefore, the aims of the present study were several. First, the previous findings of an MDMA-induced increase in PPI should be confirmed. Second, three pretreatments—the highly selective serotonin uptake inhibitor citalopram,the D2antagonist haloperidol, and the 5-HT 2A/C antagonist ketanserin—were used in order to prevent MDMA effects on PPI to the extent that they depend on:
(1) MDMA-induced carrier-mediated release of presynaptic serotonin,
(2) D2 stimulation, or
(3)5-HT 2A/C stimulation.
It was hypothesized that citalopram would attenuate the effect of MDMA on PPI, based on the fact that selective serotonin uptake inhibitors reduce MDMA-induced serotonin release (Gudelsky and Nash 1996; Hekmatpanah and Peroutka 1990; Koch and Galloway 1997) and behavioral effects in animals (Callaway et al. 1990). Third, correlations should be assessed between differences in MDMA-induced psychological changes and changes in %habituation or %PPI.