The effects of a subanesthetic dose of ketamine on verbal memory in normal volunteers.

Rationale: N-methyl-D: -aspartate (NMDA) glutamate receptor antagonists have been reported to induce schizophrenia-like symptoms in humans, including memory impairments. Although the NMDA receptor has been shown to impair memory acquisition by disrupting long-term potentiation (LTP), limited research has been done on studying the effects of NMDA antagonists on the post-LTP cascade of events implicated in consolidation as measured by administering the drug after the initial learning experience.

Objective: The purpose of this experiment was to examine the effect of ketamine on mental status and to identify NMDA antagonist-induced memory deficits by comparing the recall performance of items presented both immediately before and during ketamine infusion.

Subtle effects of ketamine on memory when administered following stimulus presentation.

Rationale: N-methyl-D-aspartate (NMDA) receptor antagonists (e.g., PCP, ketamine) have been shown to impair learning/memory.

Nicotine improves delayed recognition in schizophrenic patients.

Rationale: Nicotine has been shown to enhance some aspects of memory, attention and cognition in normal subjects and in some patient populations such as Alzheimer's and Parkinson's disease groups.

Objectives: Memory disorders are consistently observed in schizophrenic patients, so it is of interest to determine whether nicotine might improve memory performance in these patients.

Methods: Delayed recognition was assessed using yes/no recognition of visuospatial designs.

Neurodevelopmental interactions conferring risk for schizophrenia: a study of dermatoglyphic markers in patients and relatives.

Schizophrenia is hypothesized to be the result of an interaction between specific genetic factors and nonspecific insults during embryonic development. Dermatoglyphic abnormalities appear to mark these putative insults--providing information about the temporal sequence of aberrant developmental events as well as the organism's vulnerability to their adverse effects. In the present study, dermatoglyphic measures thought to mark first and second trimester development were examined in patients with schizophrenia and first degree relatives and compared with those of healthy controls to examine whether genetic factors may mediate this vulnerability.

The effects of nicotine on specific eye tracking measures in schizophrenia.

Background: The role of neuronal nicotinic receptors in the etiology and pathophysiology of schizophrenia has been suggested by postmortem findings as well as by linkage analysis implicating chromosome 15q14, the region where the alpha-7 nicotinic receptor gene is located. In addition, drug probe studies show that acute nicotine administration reverses sensory gating and eye-tracking deficits associated with the genetic liability for schizophrenia. The purpose of the current study was to examine the effects of acute administration of nicotine on specific measures of smooth pursuit eye movements and visual attention.