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Epidemiological studies have identified high prevalence rates of anxiety and depression in North America [e.g., J. of Nerv. Ment. Dis. 182 (1994) 290]. However, only a small percentage of these individuals access effective treatment. The undertreatment of anxiety and depression is a major public health issue and is associated with significant personal, social, and economic burden. This article describes the existing discrepancy between prevalence of anxiety and depression and access to effective treatment for adults and children, the contributors to this discrepancy, and suggests various means through which access to effective treatment may be enhanced. We begin with a brief overview of the prevalence and associated personal, societal, and systemic burdens of anxiety and depression. This is followed by a review of current rates of access to treatment and possible individual, provider, and systemic barriers to accessing treatment. Recommendations for bridging the gap between the high rates of these disorders and limited accessibility of effective care are then presented.

Readiness for change is increasingly cited as an important variable in the health behaviours literature, yet there remains a dearth of research related to this construct in mental health. This study examined the psychometric properties of the University of Rhode Island Change Assessment (URICA) scale in two samples. In Study 1 (n = 252), undergraduates completed the URICA and were administered measures of hopelessness, the consequences of worry, self-esteem, anxious symptomatology, and social desirability. The reliability and validity of the URICA were generally supported, although the goodness-of-fit with the intended subscales was only moderate. The Precontemplation, Contemplation and Maintenance subscales correlated as expected with ancillary measures, but the Action subscale did not. In Study 2 (n = 81), individuals with panic disorder were administered the URICA at initial assessment and following cognitive behavioural therapy. The URICA demonstrated excellent reliability, significantly predicted treatment retention and dropout, and showed modest utility for predicting treatment outcome. Confirmatory factor analysis, however, revealed an inadequate fit to the intended subscales. The implications of these findings are discussed and directions for future research highlighted.

We have previously demonstrated that the antinociception induced by morphine and beta-endorphin given intracerebroventricularly (i.c.v.) is mediated by the stimulation of respective mu- and epsilon-opioid receptors. The effects of i.c.v. pretreatment with pertussis toxin on the antinociception induced by morphine and beta-endorphin given i.c.v. were studied in male ICR mice. Antinociception was assessed by the tail-flick and hot-plate tests. Pretreatment with pertussis toxin (0.5 microgram) given i.c.v. 96 h earlier blocks the antinociception induced by i.c.v. administered morphine in both tail-flick and hot-plate tests. The same pretreatment did not affect the antinociception induced by i.c.v. administered beta-endorphin. Our results indicate that morphine-, but not beta-endorphin-induced antinociception is mediated by pertussis toxin sensitive G-proteins.

The antinociception induced by beta-endorphin given supraspinally has been previously demonstrated to be mediated by the release of [Met5]enkephalin acting on delta-opioid receptors in the spinal cord. The present study was designed to determine what type of opioid receptors in the spinal cord is involved in beta-endorphin-induced antinociception in the rat. Antinociception was induced by beta-endorphin (0.6 nmol) given into nucleus raphe obscurus and was assessed by the tail-flick test in pentobarbital-anesthesized rats. Naltriben (0.6-6.0 nmol), a selective delta 2-opioid receptor antagonist, given intrathecally dose-dependently attenuated beta-endorphin-induced inhibition of the tail-flick response. On the other hand, 7-benzylidene naltrexone (2.1-64.3 nmol), CTOP (D-Phe-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2, 0.09-2.8 nmol), or nor-binaltorphimine (1.4-40.8 nmol), selective delta 1-, mu-, and kappa-opioid receptor antagonists, respectively, did not block beta-endorphin-induced antinociception. The results of present study in rats are consistent with previous experiments in mice indicating that spinal delta 2-, but not delta 1-, mu- or kappa-opioid receptors are involved in beta-endorphin-induced inhibition of the tail-flick response.

The antinociceptive effects induced by beta-endorphin and morphine given supraspinally have been previously demonstrated to be mediated by the activation of different neural mechanisms. The present experiments were to examine the effects of intraventricular administration of beta-endorphin and morphine in mechanical paw-withdrawal and thermal tail-flick nociceptive tests in rats of 2-28 days of age. 2-4-day-old neonates were not responsive to i.c.v. injection of beta-endorphin or morphine for the inhibition of the tail-flick response. The thermal antinociceptive responses induced by beta-endorphin and morphine started to develop in 7-14-day-old rats and continued to increase at 21-28 days. The inhibition of the mechanical paw-withdrawal response to beta-endorphin was already present in 2-day-old rats and morphine in 4-day-old rats. The mechanical antinociception progressively increased and reached a plateau at 7 days of age for beta-endorphin and 28 days of age for morphine. beta-Endorphin was found to be more efficacious than morphine in producing mechanical antinociception. The results demonstrate that beta-endorphin- and morphine-induced antinociception to mechanical and thermal stimuli develops differently and are consistent with the hypothesis that two descending pain inhibitory systems activated by beta-endorphin and morphine are differentially developed.

An antisense oligodeoxynucleotide (A-oligo) to delta-opioid receptor mRNA was utilized to block the expression of mouse delta-opioid receptor in the spinal cord of male ICR mice. Intrathecal treatment with A-oligo (1.6-163 pmol) dose-dependently attenuated the antinociception induced by i.t. administered DPDPE ([D-Pen2,5]enkephalin) or [D-Ala2]deltorphin II, delta-opioid receptor agonist, without affecting the antinociception induced by DAMGO ([D-Ala2-MePhe4,Gly(ol)5]enkephalin) or U50,488H, respective mu- or kappa-opioid receptor agonists. Scrambled sense oligodeoxynucleotide (163 pmol) was ineffective against the tail-flick inhibition induced by DPDPE,[D-Ala2]deltorphin, DAMGO or U50,488H. The studies confirm previous pharmacological studies at the molecular level indicating a distinct delta-opioid receptor for antinociception in the spinal cord.

The effects of subcutaneous morphine pellet-implantation on antinociception induced by intracerebroventricular (i.c.v.) administration of beta-endorphin or morphine and intrathecal (i.t.) administration of morphine, [D-Pen2,D-Pen5]enkephalin (DPDPE), [D-Ala2,NMePhe4,Gly5-ol]enkephalin (DAMGO), serotonin or norepinephrine were studied in male ICR mice. The tail-flick and hot-plate responses were used for antinociceptive tests. The ED50 values for i.c.v. administered morphine for antinociception in morphine pellet-implanted mice were increased from 3.3- and 2.2-fold at 0 h to 14.2- and 19.0-fold at 4 h and declined to 4.8- and 3.0-fold at 8 h after pellet removal in the tail-flick and hot-plate tests, respectively. On the other hand, the ED50 values for i.c.v. administered beta-endorphin for antinociception were only slightly increased (1.7- to 5.1-fold increases) throughout the same time course. The inhibition of the tail-flick response induced by i.t. injection of morphine, DPDPE and serotonin, but not norepinephrine or DAMGO, was attenuated in morphine pellet-implanted mice. These findings are consistent with previous studies indicating that different neuronal mechanisms are involved in morphine- and beta-endorphin-induced antinociception.

The inhibition of the tail-flick response induced by beta-endorphin given i.c.v. has been demonstrated to be mediated by the stimulation of epsilon- but not mu-, delta- or kappa-opioid receptors. beta-Endorphin given i.t. also inhibited the tail-flick response. The present studies were designed to determine what types of opioid receptors in the spinal cord were involved in i.t. beta-endorphin-induced tail-flick inhibition. Blockade of kappa-opioid receptors by coadministration of nor-binaltorphimine or Win 44,441-3 with beta-endorphin given i.t. dose dependently inhibited i.t. beta-endorphin-induced inhibition of the tail-flick response. Blockade of mu-opioid receptors by i.t. coadministration of D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 with beta-endorphin blocked i.t. beta-endorphin-induced inhibition of the tail-flick response. I.t. injection of delta-opioid receptors antagonists, ICI 174,864 and naltrindole, or epsilon-opioid receptor antagonist, beta-endorphin-(1-27), did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. Blockade of alpha 2-adrenoceptors and 5-HT receptors by i.t. injection of yohimbine and methysergide, respectively, also did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. The results indicate that the inhibition of the tail-flick response induced by beta-endorphin given i.t. is mediated by the stimulation of kappa- and mu-opioid receptors but not delta- and epsilon-opioid receptors, alpha 2-adrenoceptors or 5-HT receptors.