The Effect of Chronic PCP on Behavioral Indices of Schizophrenia in the Rat
Maria Barile  (Neuroscience, 1999)
Advisor: John Kelsey

Previous research suggests that PCP induces both positive and negative symptoms of schizophrenia in humans and exacerbates schizophrenic symptoms in schizophrenic patients (Lubey et al, 1959), indicating that PCP administration may produce analogous effects in the rat. In this study, the effects of chronic PCP administration on several behavioral measures of schizophrenia were explored. In Experiment 1 and 2, rats were chronically treated with PCP (5 mg/kg) for 7 and 12 days and assessed for changes in locomotor activity, a putative positive symptom, and social interaction, a putative negative symptom, several days after cessation of the injections. Although chronic PCP failed to produce long term augmentation of locomotor activity or a reduction of social interaction, chronically PCP-injected rats exhibited locomotor sensitization following acute administration of 2.5 mg/kg PCP. In experiment 3, chronic PCP failed to effect spatial reference memory as measured by the ability to find a platform hidden in a Morris water tank. However, Experiments 3 and 4 indicated that chronic PCP administration induced perseveration in a the Morris Water Maze test and augmentation of swimming immobility as assessed by a forced swimming test, both of which may serve as putative indices of negative symptomatology. Moreover, chronic clozapine administration (10 mg/kg for 12 days) tended to reverse the PCP-induced swimming immobility, further validating this measure as an index of negative symptomatology. Thus, the results of this study suggest that chronic PCP administration does produce long term effects on perseveration and swimming immobility, and these effect may constitute valid measures of schizophrenic symptomatology which therefore lends support to the PCP model of schizophrenia.

Academic and Athletic Stress Selectively Influence the HPA axis Regulation of Cortisol in College Student-Athletes and Non-Athletes
Christian A. Oberle  (Psychology, 1999)
Advisor: Cheryl McCormick

Five college students were used to evaluate the differential effects of academic and athletic stress on the hypothalamic-pituitary-adrenal axis (HPA) secretion of cortisol (CORT). Depending upon their athletic and academic responsibilities for the semester, subjects were divided into groups of either high academic, low athletic stress (n=3), or low academic, high athletic stress (n=2). Salivary CORT samples were submitted twice daily (AM/PM) along with information concerning mood state, emotional well-being, academic stress, and activity or training. Following the 3 week observation period, factors were analyzed and interpreted using Z-scores in a time series design covering the study’s duration. High academic stress subjects showed a sensitive HPA axis response to academic stress. Similarly, mood and emotional state were extremely responsive to academic stress and there was a high level of correspondence between CORT values and mood-emotional disturbance scores. The high athletic stress group did not demonstrate a close relationship between mood state and CORT secretion. However, changes in training strongly influenced the release of CORT by the HPA axis.

Androgens, But Not Estrogens, in the Medial Preoptic Area (MPOA) Affect Corticosterone Release in Response to Stress
Bethany Sallinen  (Neuroscience, 1999)
Advisor: Cheryl McCormick

The hypothalamic-pituitary-adrenal (HPA) axis is one of the main systems involved in an organism’s response to stress. Sex hormones influence many levels of the HPA axis. Estrogens tend to have excitatory effects on HPA function and androgens tend to have inhibitory effects. Previous research has implicated the medial preoptic area (MPOA) of the brain to be a site of action for the effects of testosterone. The present study investigates whether estrogen in the MPOA affects HPA function, and whether testosterone exerts its effects on the MPOA via its reduction to 5Ct-dihydrotestosterone (DHT). Cannulae were implanted into the MPOA of gonadectomized male rats, and filled with either testosterone propionate (TP), the non-aromatizable androgen DHT, estradiol benzoate (EB), or control cannulae (CTRL). One week following surgery, rats were stressed for 20 minutes in a Plexiglas restrainer. Trunk blood was collected to measure plasma corticosterone (CORT) levels as an indication of stress responsiveness. Histological analysis and plasma luteinizing hormone (LH) levels were used to verify cannulae placement. A significant main effect of hormone replacement was found F(3, 31) = 4.79, ~ = .0074: Post hoc  analysis indicated that DHT-treated rats had significantly lower CORT levels than TP, EB, and CTRL rats whose CORT levels did not differ significantly. These results suggest that the actions of testosterone at the MPOA may involve the metabolites of testosterone.

Effects of MK-801 on Nicotine Locomotor Sensitization
Andrew Wagner (Neuroscience,1999)
Advisor: John Kelsey

The coadministration of the non-competive NMDA receptor antagonist, MK-801 has been shown to attenuate nicotine locomotor sensitization. Two experiments were conducted to determine if the coadministration of MK-801 and nicotine attenuated the development of nicotine locomotor sensitization or blocked the expression of nicotine locomotor sensitization by producing state dependency. Experiment 1 was a 2 x 2 design in which rats receive either saline/saline, saline/nicotine (.4 mg/kg, s.c.), MK-801 (.075 mg/kg, i.p.)/saline, or MK-80 1/nicotine for the acquisition period (5 sessions over 10 days) followed by 5 test sessions of nicotine treatment (over 10 days). The MK-80 1/nicotine and saline/saline group expressed similar rates of locomotor sensitization in response to repeated injections (every other day) of nicotine, which suggests that the MK-80 1/nicotine group did not sensitize to nicotine (blocked the development of nicotine locomotor sensitization) during the acquisition period. However, the saline/saline group’s rate of nicotine locomotor sensitization during the test phase was suppressed in comparison to the saline/nicotine group’s rate of nicotine locomotor sensitization, even though both groups received five nicotine injections. Thus, latent inhibition, and not coadministration of MK-801 could be causing the apparent blockade of development of nicotine sensitization. Experiment 2 is a 2×2 design in which after the acquisition phase four test sessions followed; every group received MK801 (test session 1), nicotine (test session 2), MK-801/nicotine (test session 3), and MK80 1/nicotine (test session 4). The MK-80 1/nicotine group’s activity in response to MK-801 alone was similar to its activity on the last acquisition session, which suggests that the sensitization observed during coadministration of MK-80 1 and nicotine is solely due to MK-80 1. This comparison coupled with the fact that the MK-80 1/nicotine group’s activity was suppressed when challenged with nicotine suggests that the coadministration of MK-801 blocked of development of nicotine sensitization. While both experiments do not unequivocally support the blockade of development of sensitization theory, the data from this study is more consistent with it.

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