No description available.

No description available.

No description available.

No description available.

No description available.

Alcohol dependence causes disruption to both work and family life and the associated costs are £150+ million in the UK alone. Stressful life events play a role in initiation of uncontrolled (dependent) drinking and can precipitate relapse to high ethanol consumption after treatment / abstinence. The primary neurological substrate for ethanol reward is the mesolimbic dopamine system of the medial forebrain bundle. Activation of the hypothalamopituitaryadrenal axis (the hormonal response to many stresssors) plays a role in the control of ethanol consumption and relapse, and modulation of neuronal activity by chronic calcium channel blockade decreases ethanol intake, tolerance and withdrawal. The stress system and calcium channel blockade both affect the dopaminergic reward pathways. Hypothesis: Stress and the stress hormone, corticosterone, play a crucial role in the modulation of ethanol consumption and the long term changes resulting from chronic ethanol intake. This hypothesis was tested by investigating the effects of:• social status and calcium channel blockade on chronic ethanol intake (free choice 5, 10, 20% ethanol and water) of group housed rats.• social stress from defeat by an aggressive resident on ethanol preference of low ethanol preference C57 mice.• 6 days abstinence from chronic ethanol intake (liquid diet) on NMDA-stimulated firing of dopaminergic, ventral tegmental area, cells and the role of corticosterone in modulation of this response to NMDA. The main findings from these studies indicate that, while the social stress of group housing under laboratory conditions may be insufficient to elevate ethanol intake, repeated defeat significantly increases ethanol intake. However, neither chronic ethanol consumption nor corticosterone seemd to have any effect on NMDA-stimulated dopamine cell firing. These results indicate a significant role for social stress in the modulation of ethanol intake but possibly not via the action of corticosterone on NMDA-stimulation of the mesolimbic dopamine system.

Typescript (photocopy). / Digitized by Kansas Correctional Industries

Vasopressin, or antidiurectic hormone, has long been known to have peripheral antidiuretic and vasoconstrictor properties. However, more recently a body of research has shown that vasopressin (AVP) affects central nervous system functions by to influencing memory processes. In light of the growing evidence for the role of vasopressin (AVP) in memory, my dissertation research was designed to test the hypothesis that AVP acts as a neuromodulator in the CNS. To test this hypothesis criteria used to establish neurotransmitter status was applied to AVP. Thus, a series of experiments were carried out to investigate (1) AVP brain levels; (2) release of AVP in the CNS; (3) existence of specific AVP binding sites in brain and finally, (4) existence of AVP metabolite peptide, AVP (4-9), binding sites in brain. Results of these experiments indicate that AVP meets some of the criteria for neuromodulator status in the CNS. The detection of AVP in brain, elucidation of the modulatory influence of a CNS depressant upon the content and release of AVP in brain, demonstration and characterization of the regional distribution for putative AVP receptors in brain along with binding sites for a metabolite peptide of AVP, all suggest that AVP acts through receptors within the CNS to influence memory processes.

No description available.

No description available.