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Thyrotropin-releasing hormone (TRH) and cholecystokinin octapeptide (CCK) are endogenous neuropeptides known to inhibit intake of alcohol. Although both peptides are released by alcohol consumption and are hypothesized to satiate alcohol intake, their interaction has not been examined. We deprived ad-lib-fed male (n=6) and female (n=4) Wistar rats of water for 23 h and then gave them 30 min access to 5% w/v ethanol, followed by 30 min access to water. After adaptation to this schedule, rats were randomly assigned to receive intraperitoneal injections of either saline+saline, CCK (4 μg/kg)+saline, saline+TRH (10 mg/kg) or CCK+TRH immediately before alcohol access. Analyses of variance revealed a significant (P<.05) effect of CCK, and a significant interaction of CCK and TRH in control of ethanol consumption. CCK reliably reduced alcohol intake, and TRH blocked this satiation effect of CCK, increasing intake by 88.8% and 34.6% in males and females, respectively. TRH increased water intake in females, and CCK blocked this effect of TRH. Results indicate an infra-dose-additive interaction of CCK and TRH in satiation of alcohol intake, which may reflect a natural, endogenous neuropeptide interaction in the regulation of caloric intake. [Copyright &y& Elsevier]

Cholecystokinin octapeptide (CCK-8) and bombesin tetradecapeptide (BBS-14) are brain-gut neuropeptides shown to inhibit intake and choice of alcohol solutions and foods in a variety of species. Recently, Draski and colleagues selectively bred strains descended from N/Nih outbred Norway rats that differ in sleep time after injection of ethanol. The intake of 5% w/v ethanol, food, and water was measured in these rats with high, low, and control alcohol sensitivity (HAS, US, and CAS), after intraperitoneal injection of randomized sequences of doses of CCK-8 or BBS-14 (0-8 μg/kg). During baseline adaptation to water deprivation-induced consumption of alcohol, LAS rats consumed reliably more ethanol than HAS or CAS rats. Injection of CCK-8 or BBS-14 significantly and equivalently suppressed intake of ethanol and food at 30 min after presentation in each group of rats. Water intake and food intake at 30-60 min following alcohol access was not affected by prior injection of either neuropeptide. Large differences in alcohol neurosensitivity (HAS > CAS > LAS) were observed in these rats' resting behavior for 1 hr after intraperitoneal injection of 1 g/kg of ethanol. These selectively bred alcohol neurosensitivity differences cannot be explained by corresponding differences in sensitivity to the inhibitory behavioral effects of CCK-8 or BBS-14. However, differences in alcohol intake and resting behavior do correspond to artificially selected sensitivities to ethanol's hypnotic effect. [ABSTRACT FROM AUTHOR]

An α-θ brainwave biofeedfack training program was applied as a novel treatment technique for chronic alcoholics. Following a temperature biofeedback pretraining phase, experimental subjects completed 15 30-min sessions of α-θ biofeedback training. Compared to a nonalcoholic control group and a traditionally treated alcoholic control group, alcoholics receiving brainwave training (BWT) showed significant increases in percentages of EEG record in α and θ rhythms, and increased α rhythm amplitudes. Alcoholics receiving BWT showed a gradual increase in α and θ brain rhythms across the 15 experimental sessions. These experimentally treated alcoholics showed sharp reductions in self-assessed depression (Beck's Depression Inventory) compared to the control groups. Alcoholics receiving standard medical treatment (abstinence, group psychotherapy, antidepressants) showed a significant elevation in serum β-endorphin levels at the conclusion of the experiment. This neuropeptide is an index of stress and a stimulant of caloric (e.g., ethanol) intake. Application of brainwave treatment, a relaxation therapy, appears to counteract the increase in circulating β-endorphin levels seen in the control group of alcoholics. 13-month follow-up data indicate sustained prevention of relapse in alcoholics that completed α-θ brainwave training. [ABSTRACT FROM AUTHOR]

Cholecystokinin (CCK) and bombesin (BBS) are neuropeptides of the brain and gut which have been shown to inhibit intake of ethanol. CCK octapeptide and BBS tetradecapeptide were injected intrapritoneally in both single doses and combinations of doses to determine Interactions of the two peptides in the control of consumption of ethanol. Water-deprived rats were given access to 5% w/v ethanol for 30 min, followed by a 30-min access to water, daily. One minute before presentation of ethanol, rats were injected with either saline or one of ten peptide solutions (three of CCK alone, three of BBS done, and four combinations of both). Results from the injections of single peptides were used to determine predicted inhibitions of the peptide combinations, assuming perfect additivity of doses. None of the actual values of inhibition of intake of ethanol by peptide combinations differed significantly from its predicted additive value. Endogenous CCK-like and BBS-like peptides may suppress intake of ethanol by an additive mechanism of inhibition. [ABSTRACT FROM AUTHOR]