Biomedical subjects

K E Moore

Publications and source records attributed to K E Moore.

At least 37 records · Page 2Linked to original sources

PubMed1996

The sigma ligand rimcazole activates noradrenergic neurons projecting to the paraventricular nucleus and increases corticosterone secretion in rats.

Intraperitoneal injection of rimcazole, a sigma ligand, into male rats increased plasma concentrations of corticosterone in a dose- and time-related fashion. Concurrently, rimcazole increased concentrations of dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) in the paraventricular nucleus (PVN) of the hypothalamus, suggesting that the drug activates noradrenergic neurons terminating in this nucleus. This latter suggestion was confirmed by the finding that rimcazole also increased concentrations of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) in the PVN. Pentazocine, a sigma ligand was without effect per se, but blocked the ability of rimcazole to increase concentrations of MHPG in the PVN and corticosterone in plasma. Taken together, these results suggest that rimcazole activates noradrenergic neurons projecting to the PVN via a mechanism involving sigma binding sites, and this action may be responsible for the ability of this drug to increase secretion of corticosterone.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1996

Evidence that D2 receptor-mediated activation of hypothalamic tuberoinfundibular dopaminergic neurons in the male rat occurs via inhibition of tonically active afferent dynorphinergic neurons.

The purpose of the present study was to determine if D2 receptor-mediated activation of hypothalamic tuberoinfundibular dopaminergic (TIDA) neurons occurs via afferent neuronal inhibition of tonically active inhibitory dynorphinergic neurons in the male rat. To this end, the effects of either surgical deafferentation of the mediobasal hypothalamus or administration of a kappa opioid receptor agonist (U-50,488) or antagonist (nor-binaltorphimine (NOR-BNI)) on D2 receptor-mediated activation of TIDA neurons were assessed. For comparison, the activity of mesolimbic DA neurons was also determined in these studies. TIDA and mesolimbic DA neuronal activities were estimated by measuring dopamine synthesis (accumulation of 3,4-dihydroxyphenylalanine (DOPA) following decarboxylase inhibition) and metabolism (concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)) in terminals of these neurons in the median eminence and nucleus accumbens, respectively. Intraperitoneal administration of the D2 receptor agonist quinelorane caused a dose-dependent increase in DOPAC in the median eminence and a decrease in DOPAC in the nucleus accumbens; surgical deafferentation of the mediobasal hypothalamus prevented the effect of quinelorane in the median eminence, but not the nucleus accumbens. Activation of kappa opioid receptors with U-50,488 had no effect per se, but blocked quinelorane-induced increases in median eminence DOPA. In contrast, U-50,488 had no effect on DOPA in the nucleus accumbens of either vehicle- or quinelorane-treated rats. Blockade of kappa opioid receptors with NOR-BNI increased median eminence DOPA, and prevented the stimulatory effects of quinelorane on dopamine synthesis. Administration of prolactin also increased median eminence DOPA, but did not alter the ability of quinelorane to stimulate dopamine synthesis. Neither NOR-BNI nor prolactin had any effect on DOPA in the nucleus accumbens of vehicle- or quinelorane-treated rats. These results suggest that D2 receptor-mediated activation of TIDA neurons occurs via an afferent neuronal mechanism involving, at least in part, inhibition of tonically active inhibitory dynorphinergic neurons in the male rat.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1996

The sigma receptor ligand rimcazole alters secretion of prolactin and alpha-melanocyte stimulating hormone by dopaminergic and non-dopaminergic mechanisms.

The role of tuberoinfundibular and periventricular-hypophysial dopaminergic neurons in mediating rimcazole-induced decreases in plasma concentrations of prolactin and alpha-melanocyte stimulating hormone was assessed. Dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence and intermediate lobe of the pituitary which contain terminals of tuberoinfundibular and periventricular-hypophysial dopaminergic neurons, respectively. Rimcazole decreased plasma concentrations of both prolactin and alpha-melanocyte stimulating hormone, increased the concentration of DOPAC in median eminence, but did not alter DOPAC concentrations in the intermediate lobe of the pituitary. Pretreatment with a 'putative' sigma receptor agonist, pentazocine, prevented the rimcazole-induced increase of the concentration of DOPAC in the median eminence, but did not block the ability of rimcazole to decrease plasma concentrations of prolactin. The results of this study reveal that the ability of rimcazole to decrease alpha-melanocyte stimulating hormone secretion is not mediated by a dopaminergic mechanism, whereas the ability of rimcazole to decrease prolactin secretion appears to be mediated by both dopaminergic and non-dopaminergic mechanisms.

Animals↗

PubMed1996

Assessing client satisfaction in a psychology training clinic.

Client satisfaction with services obtained at a clinical psychology training center was assessed. A modified version of the Client Satisfaction Questionnaire was developed to obtain information about levels of satisfaction in such a setting and to evaluate training clinic-specific questions of interest, such as the impact of therapists' experience on satisfaction. Results indicated that client satisfaction is multidimensional. Consistent with other studies, satisfaction was greater among clients who were in therapy for longer periods of time, who completed treatment, and who sought therapy rather than an evaluation. Reasons for dissatisfaction included a wish for more directiveness or advice in therapy and concerns over videotaping procedures. Implications of these results for clinic administrators are discussed.

Ambulatory Care Facilities↗

PubMed1995

Efferent projections from the region of the medial zona incerta containing A13 dopaminergic neurons: a PHA-L anterograde tract-tracing study in the rat.

Potential efferent projections of A13 dopaminergic (DA) neurons were identified in the present study by examining the distribution of labelled fibers following iontophoretic injection of the anterogradely transported lectin Phaseolus vulgaris leucoagglutinin (PHA-L) into the medial zona incerta (MZI), the region of the diencephalon containing A13 DA neuronal perikarya. One week after injection, PHA-L labelled fibers were found throughout the brain with the heaviest labelling occurring ipsilateral to the injection site in the anterior hypothalamic area, lateral hypothalamus, lateral preoptic area, horizontal diagonal band of Broca, and parvocellular region of the paraventricular nucleus. Moderate labelling was observed in the ipsilateral median preoptic nucleus, lateral septum, lateral aspect of the bed nucleus of the stria terminalis, and central nucleus of the amygdala. Moderate labelling was also found in the contralateral MZI and parvocellular region of the paraventricular nucleus. Light labelling was detected in the ipsilateral medial preoptic area, supraoptic nucleus, ventromedial nucleus, arcuate nucleus, vertical limb of the diagonal band of Broca, and in the contralateral lateral hypothalamus. Few immunopositive fibers were present in the dorsomedial nucleus of the hypothalamus or the magnocellular region of the paraventricular nucleus. These results reveal that neurons located in the MZI (possibly A13 DA neurons) have ipsilateral efferent axonal projections to a variety of brain regions including the lateral hypothalamus, lateral preoptic area, and the limbic structures at the diencephalic-telencephalic juncture.

Animals↗

PubMed1995

Periventricular-hypophysial dopaminergic neurons innervate the intermediate but not the neural lobe of the rat pituitary gland.

The purpose of the present study was to determine the relative distribution of axon terminals of A14 periventricular-hypophysial dopaminergic (PHDA) neurons in the neural and intermediate lobes of the rat pituitary gland. Discrete unilateral injections of the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L) into the periventricular nucleus resulted in labelling of extensively branched terminal axonal arbors in the intermediate lobe, but not the neural lobe of the pituitary gland. In contrast, unilateral injections of PHA-L into the paraventricular nucleus revealed thick, varicose terminal arborizations containing PHA-L in the neural lobe, but not the intermediate lobe. Terminal axonal branches and varicosities containing PHA-L immunoreactivity in the intermediate lobe were also immunoreactive for tyrosine hydroxylase. These results reveal that A14 PHDA neurons originating in the periventricular nucleus of the hypothalamus project axons to the intermediate lobe of the rat pituitary gland.

Animals↗

PubMed1995

Behavioral intervention to reduce child distress during self-injection.

We investigated the effects of a cognitive-behavioral treatment package on reduction of anticipatory fear of pain during self-administered insulin injections. Two patients diagnosed with insulin-dependent diabetes mellitus participated. An ABAB design was employed; the intervention conditions consisted of cue-controlled breathing, filmed modeling, pacing, and reinforcement. A substantial reduction in the mean time for injection and a reduction in behaviors indicative of anticipatory distress were achieved under intervention conditions. The clinical importance of the study is discussed and areas for future research are identified.

Adolescent↗

PubMed1994

Histaminergic neurons mediate restraint stress-induced activation of central 5-hydroxytryptaminergic neurons in the rat.

The role of histamine in mediating restraint stress-induced increases in the activity of central 5-hydroxytryptaminergic neurons was evaluated in male rats. 5-Hydroxytryptaminergic neuronal activity was estimated by measuring concentrations of the 5-hydroxytryptamine (5-HT) metabolite 5-hydroxyindoleacetic acid (5-HIAA) in the nucleus accumbens and suprachiasmatic nucleus which contain terminals of these neurons. Placement of rats within restraining tubes rapidly increased (within 10 min) 5-HIAA concentrations in the nucleus accumbens and suprachiasmatic nucleus. Depletion of neuronal histamine by alpha-fluoromethylhistidine or antagonism of histamine H1 receptors by mepyramine prevented stress-induced increases in 5-HIAA concentrations, whereas blockade of histamine H2 receptors by zolantidine was without effect. Neither alpha-fluoromethylhistidine, mepyramine nor zolantidine affected basal 5-HIAA concentrations in either brain region. These results indicate that histaminergic neurons mediate stress-induced increases in the activity of central 5-hydroxytryptaminergic neurons via an action at histamine H1 receptors.

Animals↗

PubMed1994

Neurochemical evidence that AMPA receptor-mediated tonic inhibition of hypothalamic dopaminergic neurons occurs via activation of inhibitory interneurons.

Blockade of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors with 6-nitro-7-sulfamoyl-benzo-[f]quinoxaline-2,3(1H,4H)-dione (NBQX) activates tuberoinfundibular (TIDA) and periventricular-hypophysial dopaminergic (PHDA) neurons suggesting that these neurons are tonically inhibited by endogenous excitatory amino acid neurotransmitters acting at AMPA receptors. The purpose of the present study was to identify prospective inhibitory neurotransmitters mediating this effect by examining the ability of gamma-aminobutyric acid (GABA)A and kappa-opioid receptor agonists to reverse the stimulatory effects of NBQX on the activity of these neurons (estimated from concentrations of 3,4-dihydroxyphenylacetic acid [DOPAC] in the median eminence and intermediate lobe of the pituitary). The GABAA receptor agonist isoguvacine prevented the NBQX-induced increase in DOPAC concentrations in the median eminence but not in the intermediate lobe. The kappa-opioid receptor agonist U-50,488 had no effect in the median eminence, but attenuated the NBQX-induced increase of DOPAC concentrations in the intermediate lobe. These results suggest that excitatory amino acid neurotransmitters activate AMPA receptors and increase release of GABA, which by acting at GABAA receptors tonically inhibits TIDA neurons. On the other hand, AMPA receptor-mediated tonic inhibition of PHDA neurons occurs, at least in part, by a mechanism involving endogenous kappa-opioids.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

GABAergic regulation of tuberoinfundibular dopaminergic neurons in the male rat.

The purpose of the present study was to examine the effects of gamma-aminobutyric acid (GABA)A and GABAB receptor blockade and activation on the activity of tuberoinfundibular dopaminergic (TIDA) neurons in male rats. The activity of TIDA neurons was estimated by measuring the concentration of the primary dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence. Administration of the GABAA receptor antagonist SR 95531 increased DOPAC concentrations in the median eminence, and decreased plasma concentrations of prolactin, in a dose- and time-related manner. Administration of the GABAA receptor agonist isoguvacine had no effect per se on DOPAC concentrations in the median eminence, but produced a delayed decrease in plasma prolactin concentrations. Isoguvacine pre-treatment prevented the increase in DOPAC concentrations in the median eminence produced by SR 95531. In contrast, administration of the GABAB receptor agonist baclofen decreased DOPAC concentrations in the median eminence, and increased plasma prolactin concentrations in a dose-dependent manner. Administration of the GABAB receptor antagonist 2-hydroxysaclofen had no effect on TIDA neurons per se, but blocked baclofen-induced decreases in DOPAC concentrations in the median eminence and increases in plasma prolactin concentrations. These results indicate that while activation of GABAB receptors inhibits TIDA neurons, these neurons are tonically inhibited by endogenous GABA acting at GABAA but not GABAB receptors.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Neurochemical identification of A13 dopaminergic neuronal projections from the medial zona incerta to the horizontal limb of the diagonal band of Broca and the central nucleus of the amygdala.

Studies utilizing fluorescent histochemical techniques first revealed that A13 dopaminergic (DA) perikarya located in medial zona incerta (MZI) project to various regions within the hypothalamus; accordingly, these DA neurons were designated the 'incertohypothalamic' DA neuronal system. More recently, it has been shown that the anterograde neuronal tract tracer Phaseolus vulgaris leucoagglutinin, after injection into MZI, is identified in nerve terminals outside of the hypothalamus; for example, in horizontal limb of the diagonal band of Broca (HDB) and central nucleus of the amygdala (cAMY). The purpose of the present study was to determine, using neurochemical techniques, if A13 DA neurons project to the HDB and cAMY. Concentrations of dopamine and one of its metabolites 3,4-dihydroxyphenylacetic acid (DOPAC) were determined in HDB and cAMY following: (1) electrical stimulation of MZI, (2) electrolytic lesion or knife ablation of MZI, and (3) administration of gamma-hydroxybutyric acid (GHBA) into MZI. For comparison, similar measurements were made in nucleus accumbens (N. Acc.), a terminal region of A10 DA neurons in the ventral tegmental area (VTA). Electrical stimulation of MZI increased DOPAC concentrations in HDB and cAMY, whereas electrolytic or ablative lesions of MZI decreased dopamine concentrations in both of these regions. By contrast, neither stimulation nor lesion of MZI had any effect on DOPAC or dopamine concentrations in N. Acc. Intracerebral injection of GHBA into MZI increased dopamine concentrations in MZI and HDB, but not in cAMY or N. Acc. Intracerebral administration of GHBA into VTA increased dopamine concentrations in HDB and N. Acc., but not in MZI or cAMY.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Differential role of histamine in mediating stress-induced changes in central dopaminergic neuronal activity in the rat.

The role of histamine in mediating restraint stress-induced alterations in dopaminergic neuronal activity and alpha-melanocyte-stimulating hormone (alpha MSH) secretion was evaluated in male rats. Dopaminergic neuronal activity was estimated by measuring concentrations of the dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in brain regions containing terminals of these neurons. Physical restraint increased DOPAC concentrations in nucleus accumbens and decreased DOPAC concentrations in the intermediate lobe of the pituitary, but was without effect on DOPAC concentrations in either the striatum or median eminence. These data indicate that restraint stress increases mesolimbic, decreases periventricular-hypophysial, and is without effect on nigrostriatal or tuberoinfundibular dopaminergic neuronal activity. Neither depletion of neuronal histamine by alpha-fluoromethylhistidine, blockade of H1 receptors by mepyramine, nor blockade of H2 receptors by zolantidine prevented the stress-induced increase in DOPAC concentrations in the nucleus accumbens suggesting that histaminergic neurons are not major contributors to stress-induced increases in mesolimbic dopaminergic neuronal activity. In contrast, alpha-fluoromethylhistidine- and mepyramine-, but not zolantidine-treatment prevented the stress-induced decrease in DOPAC concentrations in the intermediate lobe. Restraint stress increased alpha MSH secretion; this increase was not prevented by alpha-fluoromethylhistidine, mepyramine, or zolantidine. These data indicate that histaminergic neurons mediate the stress-induced decrease in periventricular-hypophysial dopaminergic neuronal activity through an action at H1 receptors, but do not effect stress-induced alpha MSH secretion.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Histaminergic neurons mediate restraint stress-induced increases in the activity of noradrenergic neurons projecting to the hypothalamus.

The role of histamine in mediating restraint stress-induced increases in the activity of noradrenergic neurons projecting to the hypothalamus was evaluated in male rats. Noradrenergic neuronal activity was estimated by measuring concentrations of the norepinephrine metabolite 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) in the paraventricular and medial preoptic nuclei which contain terminals of these neurons. Placement of rats within restraining tubes rapidly increased MHPG but not norepinephrine concentrations in the paraventricular and medial preoptic nuclei. Depletion of neuronal histamine by alpha-fluoromethylhistidine and antagonism of H1 receptors by mepyramine attenuated, whereas blockade of H2 receptors by zolantidine did not prevent the stress-induced increases in MHPG concentrations. Neither mepyramine nor zolantidine affected MHPG concentrations in hypothalamic regions of nonstressed rats. These results indicate that histaminergic neurons contribute to the stress-induced increase the activity of noradrenergic neurons projecting to the hypothalamus via an action at H1 receptors.

Animals↗

PubMed1994

MDL-101,562 blocks the stimulatory effects of bombesin and gastrin-releasing peptide on hypothalamic dopaminergic neurons.

The effects of central administration of bombesin, gastrin-releasing peptide (GRP) and a putative bombesin/GRP receptor antagonist [Phe8 psi[CH2S]Leu9]litorin (MDL-101,562) were determined on the activities of hypothalamic tuberoinfundibular and periventricular-hypophysial dopaminergic neurons in male rats. Dopaminergic neuronal activity was estimated by measuring concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence and the intermediate lobe of the posterior pituitary which contain terminals of these neurons. Intracerebroventricular injections of bombesin and GRP increased DOPAC concentrations in both the median eminence and intermediate lobe. MDL-101,562 had no effect on median eminence or intermediate lobe DOPAC concentrations per se, but blocked the stimulatory actions of bombesin and GRP on DOPAC concentrations in these regions. These results suggest that MDL-101,562 may be a useful pharmacologic tool in the study of the central actions of bombesin and related peptides.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Effects of histamine on 5-hydroxytryptaminergic neuronal activity in the rat hypothalamus.

Effects of pharmacological manipulations which mimic or enhance histaminergic neuronal transmission were determined on the activity of 5-hydroxytryptaminergic neurons projecting to the hypothalamus of male rats. Intracerebroventricular administration of histamine decreased 5-hydroxytryptamine (5-HT) and increased 5-hydroxyindoleacetic acid (5-HIAA) concentrations in several hypothalamic nuclei; these effects were blocked by the histamine H1 receptor antagonist mepyramine but not the histamine H2 receptor antagonist zolantidine. Blockade of the 5-HT reuptake system by fluoxetine did not prevent histamine-induced decreases in 5-HT concentrations suggesting that histamine is not transported into nerve terminals via the 5-HT reuptake system to subsequently displace 5-HT stores. These data suggest that exogenous histamine increases 5-hydroxytryptaminergic neuronal activity through an action at histamine H1 receptors. In contrast, neither the histamine H3 receptor antagonist thioperamide, the histamine-N-methyltransferase inhibitor metoprine, nor combined thioperamide-metoprine treatment affected concentrations of 5-HT or 5-HIAA suggesting these agents, which purportedly enhance endogenous histaminergic transmission, do not affect 5-hydroxytryptaminergic neuronal activity. These results reveal that procedures commonly employed to study central actions of histamine differentially affect 5-hydroxytryptaminergic neuronal activity in the rat hypothalamus.

Animals↗

PubMed1994

Non-NMDA receptor-mediated regulation of hypothalamic dopaminergic neurons in the rat.

The purpose of the present study was to examine the effects of non-NMDA receptor blockade and activation on the activity of tuberoinfundibular dopaminergic (TIDA), periventricular-hypophysial dopaminergic (PHDA) and, for comparison, nigrostriatal dopaminergic (NSDA) neurons in male and female rats. The activity of TIDA, PHDA and NSDA neurons was estimated by measuring the concentration of the primary dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence, intermediate lobe of the posterior pituitary and striatum, respectively. Systemic administration of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-selective antagonist 6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3(1H,4H)-dione (NBQX) increased DOPAC concentrations in the median eminence and intermediate lobe, and decreased plasma concentrations of prolactin and alpha-MSH, in a dose- and time-related manner. In contrast, NBQX had no effect on DOPAC concentrations in the striatum, suggesting that non-NMDA receptors are not involved in the tonic regulation of NSDA neurons. The increase in DOPAC concentrations in the median eminence and intermediate lobe, and the decrease in plasma concentrations of prolactin and alpha-MSH, produced by NBQX were prevented by AMPA but not by kainic acid. Taken together, the results demonstrate that endogenous excitatory amino acid neurotransmitters, acting at AMPA receptors, tonically inhibit both TIDA and PHDA neurons, and thereby increase the secretion of prolactin and alpha-MSH in male and female rats.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1994

Activation of noradrenergic neurons projecting to the diencephalon following central administration of histamine is mediated by H1 receptors.

The effect of histamine on the activity of noradrenergic neurons terminating in discrete regions of the diencephalon was examined in male rats. Noradrenergic neuronal activity was estimated by measuring the concentration of norepinephrine and its metabolite 3-methoxy-4-hydroxyphenylethyleneglycol [MHPG] in the medial zona incerta [MZI] and in the dorsomedial [DMN], periventricular [PeVN] and medial preoptic hypothalamic nuclei [MPN]. The intracerebroventricular administration of histamine effected a time-related increase in MHPG concentrations in the MZI, DMN, PeVN and MPN; these effects were blocked by the H1 antagonist mepyramine but not the H2 antagonist zolantidine. Neither mepyramine nor zolantidine affected basal MHPG concentrations in any of the brain regions examined. These results indicate that central administration of histamine increases the activity of noradrenergic neurons projecting to the diencephalon via an action at H1 but not H2 receptors.

Animals↗

PubMed1994

Neurochemical evidence that estrogen-induced suppression of kappa-opioid-receptor-mediated regulation of tuberoinfundibular dopaminergic neurons is prolactin-independent.

The purpose of the present study was to examine the role of estrogen and prolactin in determining the responsiveness of tuberoinfundibular dopaminergic (TIDA) neurons to kappa-opioid receptor blockade in female rats. TIDA neuronal activity was estimated by measuring either dopamine synthesis [accumulation of 3,4-dihydroxyphenylalanine (DOPA) 30 min after the administration of the decarboxylase inhibitor NSD-1015] or metabolism [concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)] in terminals of these neurons in the median eminence. Blockade of kappa-opioid receptors with the selective kappa-antagonist norbinaltorphimine (NOR-BNI) increased the concentrations of DOPAC in the median eminence of ovariectomized rats but had no effect in gonadally intact rats, suggesting that loss of endogenous ovarian hormones following ovariectomy results in an increase in kappa-opioid-receptor-mediated inhibition of TIDA neurons. Estrogen administration ot ovariectomized rats blocked NOR-BNI-induced increases in median eminence DOPAC concentrations, whereas treatment of gonadally intact or ovariectomized, estrogen-treated rats with prolactin antiserum had no effect on the insensitivity of these neurons to NOR-BNI. Administration of antiserum to dynorphin A1-8 increased DOPA accumulation in the median eminence of ovariectomized but not estrogen-treated ovariectomized rats. Taken together, these results reveal that estrogen, acting via a prolactin-independent mechanism, suppresses kappa-opioid-receptor-mediated inhibition of the activity of TIDA neurons, possibly by decreasing the release of endogenous dynorphin.

3,4-Dihydroxyphenylacetic Acid↗