Phencyclidine (PCP)-induced disruption in cognitive performance is gender-specific and associated with a reduction in brain-derived neurotrophic factor (BDNF) in specific regions of the female rat brain.

Phencyclidine (PCP), used to mimic certain aspects of schizophrenia, induces sexually dimorphic, cognitive deficits in rats. In this study, the effects of sub-chronic PCP on expression of brain-derived neurotrophic factor (BDNF), a neurotrophic factor implicated in the pathogenesis of schizophrenia, have been evaluated in male and female rats. Male and female hooded-Lister rats received vehicle or PCP (n=8 per group; 2 mg/kg i.

Testing the validity of c-fos expression profiling to aid the therapeutic classification of psychoactive drugs.

Rationale: Different stimuli, including pharmacological stimuli, induce different neuroanatomical profiles of c-fos expression. Can these profiles be used in classifying psychoactive drugs and predicting therapeutic utility?

Objective: To test the validity of c-fos expression profiling to aid therapeutic classification.

Methods: Anxiolytics, antidepressants, antipsychotics and psychostimulants were compared.

Activation of p44/p42 MAP kinase in striatal neurons via kainate receptors and PI3 kinase.

The members of the mitogen-activated protein (MAP) kinase family -- p44/p42 MAP kinase (ERK), c-jun N-terminal kinase (JNK) and p38 MAP kinase (p38) are known to be important mediators of the physiological plasticity or neurotoxicity induced in the striatum by activation of ionotropic glutamate receptors. However, our knowledge of the class of glutamate receptor and the intracellular pathways involved derives totally from studies on embryonic neurons, where the mechanisms are likely to be totally different from those operating in mature neurons. In superfused striatal slices from adult rats, NMDA and kainate, but not AMPA, were found to activate ERK.

Mammalian thermoregulation: species differences.

An understanding of the variation between species is a basic requirement if one is to give proper care to laboratory animals, select an appropriate animal to find answers to a specific question, and/or appreciate the limits in interpreting experimental results as they may apply to humans.

Kainate receptors activate NF-kappaB via MAP kinase in striatal neurones.

The transcription factor NF-kappaB has been implicated in the synaptic plasticity and neurotoxicity mediated by ionotropic glutamate receptors in the striatum. However, the class of glutamate receptor and the intracellular pathways involved have not been determined. Kainate, but not AMPA or NMDA, was found to activate NF-kappaB in superfused slices of rat striatum.