Increased sediment load during a large-scale dam removal changes nearshore subtidal communities.

The coastal marine ecosystem near the Elwha River was altered by a massive sediment influx-over 10 million tonnes-during the staged three-year removal of two hydropower dams. We used time series of bathymetry, substrate grain size, remotely sensed turbidity, scuba dive surveys, and towed video observations collected before and during dam removal to assess responses of the nearshore subtidal community (3 m to 17 m depth). Biological changes were primarily driven by sediment deposition and elevated suspended sediment concentrations. Macroalgae, predominantly kelp and foliose red algae, were abundant before dam removal with combined cover levels greater than 50%. Where persistent sediment deposits formed, macroalgae decreased greatly or were eliminated. In areas lacking deposition, macroalgae cover decreased inversely to suspended sediment concentration, suggesting impacts from light reduction or scour. Densities of most invertebrate and fish taxa decreased in areas with persistent sediment deposition; however, bivalve densities increased where mud deposited over sand, and flatfish and Pacific sand lance densities increased where sand deposited over gravel. In areas without sediment deposition, most invertebrate and fish taxa were unaffected by increased suspended sediment or the loss of algae cover associated with it; however, densities of tubeworms and flatfish, and primary cover of sessile invertebrates increased suggesting benefits of increased particulate matter or relaxed competition with macroalgae for space. As dam removal neared completion, we saw evidence of macroalgal recovery that likely owed to water column clearing, indicating that long-term recovery from dam removal effects may be starting. Our results are relevant to future dam removal projects in coastal areas and more generally to understanding effects of increased sedimentation on nearshore subtidal benthic communities.

Behavioral profiling of multiple pairs of rats selectively bred for high and low alcohol intake using the MCSF test.

Genetic aspects of alcoholism have been modeled using rats selectively bred for extremes of alcohol preference and voluntary alcohol intake. These lines show similar alcohol drinking phenotypes but have different genetic and environmental backgrounds and may therefore display diverse behavioral traits as seen in human alcoholics. The multivariate concentric square field™ (MCSF) test is designed to provoke exploration and behaviors associated with risk assessment, risk taking and shelter seeking in a novel environment. The aim was to use the MCSF to characterize behavioral profiles in rat lines from selective breeding programs in the United States (P/NP, HAD1/LAD1, HAD2/LAD2), Italy (sP/sNP) and Finland (AA/ANA). The open field and elevated plus maze tests were used as reference tests. There were substantial differences within some of the pairs of selectively bred rat lines as well as between all alcohol-preferring rats. The most pronounced differences within the pairs of lines were between AA and ANA rats and between sP and sNP rats followed by intermediate differences between P and NP rats and minor differences comparing HAD and LAD rats. Among all preferring lines, P, HAD1 and HAD2 rats shared similar behavioral profiles, while AA and sP rats were quite different from each other and the others. No single trait appeared to form a common 'pathway' associated with a high alcohol drinking phenotype among all of the alcohol-preferring lines of rats. The marked behavioral differences found in the different alcohol-preferring lines may mimic the heterogeneity observed among human alcoholic subtypes.

Effects of neuropeptide Y and ethanol on arousal and anxiety-like behavior in alcohol-preferring rats.

Neuropeptide Y (NPY) is abundant in the mammalian brain and plays a prominent role in behaviors related to negative affect and alcohol. NPY suppresses anxiety-like behavior and alcohol-drinking behaviors in a wide array of rodent models and also affects changes in these behaviors produced by fearful and stressful stimuli. Rats selectively bred for high alcohol preference (P rats) appear to be particularly sensitive to the behavioral effects of NPY. The dual purpose of the present investigation was to determine the effects of intraventricular NPY on (1) the acoustic startle response (ASR) of P rats in a high-anxiety setting and (2) social interaction behavior of P rats. In experiment 1, P rats were either cycled through periods of long-term ethanol access and abstinence or they remained ethanol naive. Rats were injected with one of four NPY doses and tested for ASR before and after footshock stress. NPY suppressed ASR in all P rats regardless of shock condition or drinking history. In experiment 2, rats received intraventricular infusion of one of four NPY doses and were then injected with either ethanol (0.75 g/kg) or saline and tested for social interaction. NPY increased social interaction in P rats even at doses that suppressed locomotor activity, regardless of ethanol dose. Suppression of anxiety-like and arousal behaviors by NPY in the present study confirm a role for NPY in alcohol-related behaviors in alcohol-preferring P rats.

Neuropeptide Y (NPY)-induced reductions in alcohol intake during continuous access and following alcohol deprivation are not altered by restraint stress in alcohol-preferring (P) rats.

Administration of neuropeptide Y (NPY) reduces anxiety-like behavior and alcohol intake in alcohol-preferring rats. The present experiment examined whether the effects of NPY on alcohol drinking are modulated by stress exposure during continuous access or following ethanol deprivation. Female P rats underwent 6 weeks of continuous access to 15% v/v ethanol and water prior to intracerebroventricular (ICV) cannula implantation. Deprived rats underwent two cycles of 5 days of ethanol exposure followed by 2 days of ethanol deprivation, while non-deprived rats had uninterrupted access to ethanol. Stressed rats in both ethanol access groups were exposed to restraint stress for 1h 4-6h after ethanol was removed from the deprived group in both cycles. ICV infusions of 5.0 µg NPY or aCSF were administered 48 h following the deprivation/stress procedure, after which ethanol was returned. Rats showed increased ethanol intake following ethanol deprivation compared to non-deprived controls. Food and water intake were increased, while ethanol intake was decreased, in rats infused with NPY. Stress did not increase ethanol intake or alter the response to NPY. Although no stress effects were found, the present experiment replicates previous findings regarding the effectiveness of NPY in reducing ethanol consumption. Future studies aimed at determining the extent to which stress may affect relapse to ethanol drinking and response to NPY would benefit from implementing different stress paradigms and varying the pattern of ethanol access.

Neuropeptide Y suppresses ethanol drinking in ethanol-abstinent, but not non-ethanol-abstinent, Wistar rats.

In outbred rats, increases in brain neuropeptide Y (NPY) activity suppress ethanol consumption in a variety of access conditions, but only following a history of ethanol dependence. NPY reliably suppresses ethanol drinking in alcohol-preferring rats, and this effect is augmented following a period of ethanol abstinence. The purpose of this experiment was to examine the effects of NPY on two-bottle choice ethanol drinking and feeding in Wistar rats that had undergone chronic ethanol vapor exposure, cycles of ethanol abstinence, or both. Ethanol-drinking Wistar rats were given 6 weeks of access to 15% (vol/vol) ethanol and water followed by either: two cycles of 1 week ethanol vapor exposure and 2 weeks with no ethanol; two cycles of 1 week ethanol bottle availability and 2 weeks with no ethanol; or 2 weeks of ethanol vapor exposure. Rats were infused intracerebroventricularly with one of four NPY doses (0.0, 2.5, 5.0, or 10.0 microg) following the ethanol exposure patterns described above, and tested for ethanol drinking and feeding in a two-bottle choice situation. NPY dose dependently increased food intake regardless of ethanol exposure history, but suppressed ethanol drinking only in rats that underwent cycles of ethanol access and ethanol abstinence. These results support the notion that dysregulation of brain NPY systems during chronic intermittent ethanol exposure is important in the motivational drive for subsequent relapse to ethanol drinking.

The effects of neuropeptide S on ethanol drinking and other related behaviors in alcohol-preferring and -nonpreferring rats.

BACKGROUND: Neuropeptide S (NPS) is a 20-amino-acid peptide, identified in the brain and periphery, that is reported to regulate arousal, anxiety, and feeding behavior. Studies were conducted to determine whether this peptide would alter ethanol intake, sucrose intake, anxiety, and general motor activity in alcohol-preferring (P) and -nonpreferring (NP) rats. METHODS: Experiment 1: P and NP rats were given 8 weeks of continuous access to ethanol (15% w/v) and water. All rats were implanted with a cannula aimed at either the left or right lateral ventricle and 1 week later were infused with NPS (0.075, 0.3, 1.2 nmol) or artificial cerebrospinal fluid (aCSF) and tested for ethanol, food, and water intake. Experiment 2: The same doses of NPS were administered to a group of P rats and intake of 2.5% (w/v) sucrose was measured. Experiment 3: Infusions of NPS (1.2 nmol) or aCSF were administered to P rats prior to a 5-minute test on an elevated plus maze. Experiment 4: Ethanol naive P and NP rats were infused with NPS (0.075, 0.15, 0.3, 0.6, and 1.2 nmol) or aCSF prior to a 20-minute test in activity monitors. RESULTS: NPS reduced ethanol intake in P, but not in NP rats. It did not influence sucrose solution intake in P rats. However, an increase in food intake was seen in both rat lines following lower doses of the peptide. NPS did neither alter anxiety-like behavior in the elevated plus maze test nor was there an effect on general motor activity; however, there was an increase in the amount of time spent in the center of the activity monitors following infusions of 0.6 nmol of NPS in P, but not in NP rats, indicating anxioltyic actions of the peptide. CONCLUSIONS: These data suggest a role for NPS in the modulation of ethanol drinking and possibly anxiety-like behavior in rats selectively bred for high alcohol drinking.

Neuropeptide Y administration into the amygdala suppresses ethanol drinking in alcohol-preferring (P) rats following multiple deprivations.

The present experiment examines the effects of NPY administered into the amygdala on ethanol drinking by alcohol-preferring P rats following long-term continuous ethanol access, with and without multiple periods of imposed ethanol abstinence. P rats had access to 15% (v/v) ethanol and water for 11 weeks followed by 2 weeks of ethanol abstinence, re-exposure to ethanol for 2 weeks, 2 more weeks of ethanol abstinence, and a final ethanol re-exposure. Immediately prior to the second ethanol re-exposure, 4 groups of rats received bilateral infusions NPY (0.25, 0.5, 1.0 microg) or artificial cerebrospinal fluid (aCSF) into the amygdala. Two additional groups were given uninterrupted ethanol access and were infused with a single NPY dose (1.0 microg) or aCSF. The highest NPY dose (1.0 microg) suppressed ethanol intake for 24 h in rats with a history of ethanol abstinence (i.e. deprivation) periods, but had no effect in rats with a history of continuous ethanol access. Water and food intakes were not altered. These results suggest that the amygdala mediates the suppressive effects of centrally administered NPY on ethanol drinking, and that NPY may block relapse-like drinking by opposing the anxiogenic effects of ethanol abstinence.

Neuropeptide Y modulation of ethanol intake: effects of ethanol drinking history and genetic background.

Intracerebroventricular administration of NPY suppresses ethanol intake in selectively bred alcohol-preferring rat lines, but not in rats selectively bred for low ethanol drinking or in unselected Wistar rats, when access to ethanol is limited to 2h/day. However, when rats undergo chronic (24h/day) ethanol drinking (or exposure to ethanol by vapor inhalation) and have periods of imposed ethanol abstinence, the reductions in ethanol drinking following NPY administration are enhanced in alcohol-preferring rats and are also observed in unselected Wistar rats. Thus, sensitivity to the effects of NPY on ethanol drinking appears to be altered by selective breeding for ethanol preference and by a prior history of chronic but intermittent exposure to ethanol.

Sensitized effects of neuropeptide Y on multiple ingestive behaviors in P rats following ethanol abstinence.

Neuropeptide Y (NPY) suppresses ethanol drinking in alcohol-preferring (P) rats, an effect which is augmented following a single ethanol abstinence period. The present experiment tests both ethanol drinking and feeding in P rats following multiple abstinence periods. Female P rats had continuous access to 15% (v/v) ethanol and water for 6 weeks followed by 3 ethanol access cycles of 2 weeks with no ethanol and 2 weeks with ethanol. Following intracerebroventricular cannula implantation during the third period of ethanol abstinence, groups (n=12-13/dose) were infused with NPY (2.5, 5.0, 10.0 microg) or aCSF prior to ethanol reinstatement. Two additional groups (n=11-12/dose) were treated similarly except that ethanol access was uninterrupted, and they were infused with a single NPY dose (10.0 microg) or aCSF. NPY increased food intake in all groups, and this effect was greater following ethanol abstinence. NPY suppressed ethanol intake, and this suppression lasted longer (24 h post-infusion) in rats with a history of ethanol abstinence periods than rats with a history of continuous ethanol access (4 h post-infusion). These results confirm past findings and indicate that global dysregulation of brain NPY systems during ethanol abstinence may render P rats more sensitive to the behavioral effects of NPY.

Sedative and motor-impairing effects of neuropeptide Y and ethanol in selectively bred P and NP rats.

Past findings suggest a positive association between endogenous neuropeptide Y (NPY) activity and ethanol-induced sedation, and there is evidence for additive effects of administered NPY with sedative-hypnotics. The present investigation examined the effects of intracerebroventricular NPY injection on ethanol-induced sedation and motor impairment in selectively bred alcohol-preferring (P) and -nonpreferring (NP) rats. In Experiment 1, P and NP rats were assessed for loss and recovery of righting reflex (RR) following infusion with either NPY (10.0 microg) or aCSF followed by ethanol injection (2.5 g/kg ip). NPY reduced time to lose RR and increased time to regain RR similarly in P and NP rats. Blood-ethanol levels (BELs) were lower at time of recovery in NPY-treated rats relative to aCSF controls. Thus, NPY enhanced ethanol-induced sedation. In Experiment 2, P and NP rats pretreated with either saline or ethanol (1.0 g/kg ip) were assessed for motor activity following infusion with either NPY (2.5, 5.0, or 10.0 microg) or aCSF. Ethanol alone and NPY alone suppressed motor activity, but there were no additive effects between the two. Taken together, these results provide partial support for past observations of additivity between NPY and drug-induced sedation, and suggest a role for NPY in the neurobehavioral effects of acute ethanol exposure.

Overlapping peptide control of alcohol self-administration and feeding.

This article represents the proceedings of a symposium at the 2003 annual meeting of the Research Society on Alcoholism in Fort Lauderdale, FL. The organizers and chairpersons were Mark Egli and Todd E. Thiele. The presentations were (1) Voluntary alcohol consumption is modulated by central melanocortin receptors, by Todd E. Thiele; (2) Central infusion of neuropeptide Y reduces alcohol drinking in alcohol-preferring P rats, by Robert B. Stewart and Nancy E. Badia-Elder; (3) The gut peptide cholecystokinin controls alcohol intake in Sardinian alcohol-preferring rats, by Nori Geary and Maurizio Massi; and (4) Hypothalamic galanin: a possible role in excess alcohol drinking, by Sarah F. Leibowitz and Bartley G. Hoebel.

A role for neuropeptide Y in alcohol intake control: evidence from human and animal research.

This article is based on proceedings of a symposium presented at the 2002 meeting of the Society for the Study of Ingestive Behavior and provides a brief overview of recent research suggesting a role for neuropeptide Y (NPY) in the modulation of ethanol drinking. The discussion focuses mainly on recent studies with genetic animal models including mutant mice lacking specific NPY receptor and selectively bred rodents, namely the Indiana alcohol-preferring (P) and alcohol-nonpreferring (NP) rats and the Indiana high alcohol drinking (HAD) and low alcohol drinking (LAD) rats. It is concluded that abnormal or low central NPY activity can promote high alcohol drinking and that NPY modulates alcohol consumption via the NPY Y1 and Y2 receptors.

Neuropeptide Y reduces oral ethanol intake in alcohol-preferring (P) rats following a period of imposed ethanol abstinence.

BACKGROUND: Intracerebroventricular infusion of NPY has been shown to reduce ethanol intake in alcohol-preferring (P) rats in a limited access procedure. The purpose of the present investigation was to extend this finding to a two-bottle free-choice continuous access procedure in groups of rats that either did or did not undergo a period of imposed ethanol abstinence and ethanol reinstatement. METHODS: In experiment 1, female P rats were given 6 weeks of continuous access to ethanol (8% w/v) and water. Ethanol was removed for a period of 2 weeks during which the rats were surgically implanted with a cannula into the lateral ventricle. Following the ethanol abstinence period and immediately before ethanol reinstatement, rats received a single infusion of either artificial cerebrospinal fluid or NPY (10 microg). Ethanol and water intake was measured at both 4 hr and 24 hr after infusion, and 24-hr intake measures were taken daily for 13 postinfusion days. Experiment 2 was run in parallel with experiment 1, with the exception that rats did not undergo a period of imposed ethanol abstinence. Also, food intake was measured 4 and 24 hr after infusion. RESULTS: Following 2 weeks of imposed ethanol abstinence (experiment 1), NPY suppressed ethanol intake through postinfusion day 2. After uninterrupted continuous access to ethanol (experiment 2), NPY suppressed ethanol intake to a lesser extent and this effect lasted only 24 hr. NPY increased food intake at the 4-hr but not the 24-hr measure. CONCLUSIONS: Previous findings that central administration of NPY suppresses ethanol intake in P rats are extended by this study to a continuous access procedure, and the effect is amplified following a period of imposed ethanol abstinence. This effect of NPY compares favorably to results obtained with other treatments tested in similar animal models and provides support for a role of NPY in an allostasis model of addiction.

Phenotypic and genotypic characterization of the Indiana University rat lines selectively bred for high and low alcohol preference.

The Indiana lines of selected rats, the HAD and LAD replicates and the P and NP lines, were bred for high and low alcohol preference. The P and HAD lines have met criteria for an animal model of alcoholism in that they voluntarily consume sufficient ethanol to achieve significant blood alcohol concentrations, and their alcohol-seeking behavior is reinforced by the pharmacological effects of ethanol rather than its taste, caloric content, or other properties. These lines have been characterized extensively for associated behavioral and physiological phenotypes. The P and HAD rats show an enhanced responsiveness to the stimulatory effects of ethanol and reduced sensitivity to the aversive sedative effects of ethanol. Consistent findings with the selected lines include differences in the mesolimbic dopamine reward system, as well as differences in serotonin, GABA, endogenous opioid, and neuropeptide Y systems. Genetic mapping studies have identified quantitative trait loci influencing alcohol preference on chromosomes 3, 4, and 8 in the inbred P/NP rats and on chromosomes 5, 10, 12, and 16 in the noninbred HAD1/LAD1 rats. The elucidation of the genotypes and phenotypes that result in excessive alcohol intake may lead to a better understanding of alcohol abuse and alcoholism and could guide strategies for potential treatment and prevention.