Protein expression changes in the nucleus accumbens and amygdala of inbred alcohol-preferring rats given either continuous or scheduled access to ethanol.

Chronic ethanol (EtOH) drinking produces neuronal alterations within the limbic system. To investigate changes in protein expression levels associated with EtOH drinking, inbred alcohol-preferring (iP) rats were given one of three EtOH access conditions in their home-cages: continuous ethanol (CE: 24h/day, 7days/week access to EtOH), multiple scheduled access (MSA: four 1-h sessions during the dark cycle/day, 5 days/week) to EtOH, or remained EtOH-naïve. Both MSA and CE groups consumed between 6 and 6.5g of EtOH/kg/day after the 3rd week of access. On the first day of EtOH access for the seventh week, access was terminated at the end of the fourth MSA session for MSA rats and the corresponding time point (2300h) for CE rats. Ten h later, the rats were decapitated, brains extracted, the nucleus accumbens (NAcc) and amygdala (AMYG) microdissected, and protein isolated for 2-dimensional gel electrophoretic analyses. In the NAcc, MSA altered expression levels for 12 of the 14 identified proteins, compared with controls, with six of these proteins altered by CE access, as well. In the AMYG, CE access changed expression levels for 22 of the 27 identified proteins, compared with controls, with 8 of these proteins altered by MSA, as well. The proteins could be grouped into functional categories of chaperones, cytoskeleton, intracellular communication, membrane transport, metabolism, energy production, or neurotransmission. Overall, it appears that EtOH drinking and the conditions under which EtOH is consumed, differentially affect protein expression levels between the NAcc and AMYG. This may reflect differences in neuroanatomical and/or functional characteristics associated with EtOH self-administration and possibly withdrawal, between these two brain structures.

Factors influencing in vivo trabecular cell replication as determined by 3H-thymidine labelling; an autoradiographic study in cats.

Because trabecular cell loss is thought to play a role in the pathogenesis of some forms of glaucoma, identification of factors which influence trabecular cell division may provide some insight into the mechanisms and potential treatment of this disease. We studied several commonly encountered clinical situations which may affect the trabecular meshwork: phagocytosis of debris, hyphema, and argon laser trabeculoplasty. The effect of these factors on trabecular cell division was determined using 3H-thymidine autoradiography. Laser trabeculoplasty induced a 307% increase in 3H-thymidine labelling of trabecular cells while phagocytosis and hyphema had no effect on cell labelling. In addition, subgroups of eyes with a loss of trabecular cells or with inflammation did not have increased labelling. Thus laser trabeculoplasty, known to increase outflow facility, was associated with increased trabecular cell labelling while factors often associated with decreased outflow facility and glaucoma were not.