Nitrous oxide and xenon prevent amphetamine-induced carrier-mediated dopamine release in a memantine-like fashion and protect against behavioral sensitization

in Biological Psychiatry (2006), 60(1), 49-57

Background. Amphetamine administration induces stimulation-independent dopainine release in the nucleus accumbens (NAcc) through reverse dopamine transport, a critical neurochemical event involved in its ... [more ▼]

Background. Amphetamine administration induces stimulation-independent dopainine release in the nucleus accumbens (NAcc) through reverse dopamine transport, a critical neurochemical event involved in its psycbostimulant action, and, furthermore decreases stimulation-dependent vesicular dopamine release. These effects may involve possible indirect glutamateigic mechanisms. Methods: We investigated the effiects of nitrous oxide and xenon, which possess antagonistic action at the N-methyl-D-aspartate (NMDA) receptor, on brain slices ex vivo on aniphetamine-induced changes in carrier-mediated and KCI-evoked dopamine release in the NAcc, and in vivo on ampbetamine-induced locomotor sensitization Results: Like the low-affininity NMDA receptor antagonist memantine, but not the prototypical compound MK-801, nitrous oxide and xenon at appropriate concentrations blocked both the increase in carrier-mediated dopamine release and locomotor sensitization produced by amphetamine. Conclusions: In contrast to what has generally been found using prototypical NMDA receptor antagonists, these data regarding the effect qf memantine, nitrous oxide, and xenon support the hypothesis that activation qf certain NMDA receptors (possibly those qf containing the NR1a/NR2D subunit) in the NAcc is involved in the ampbetamine-induced increase in carrier-mediated dopamine release and the development qf behavioral sensitization to amphetamine. Nitrous oxide, xenon, and memantine may be of therapeutic interest for treating drug dependence. [less ▲]

Harm avoidance dimension of the Tridimensional Personality Questionnaire and serotonin-1A activity in depressed patients.

in Biological Psychiatry (1997), 42(10), 959-61

Brain hypometabolism of glucose in anorexia nervosa: Normalization after weight gain

in Biological Psychiatry (1996), 40(8), 761-768

Using positron emission tomography and (18-F)-fluorodeoxyglucose, we studied cerebral glucose metabolism in 10 anorectic girls within their underweight state and after weight gain. Ten age- and sex ... [more ▼]

Using positron emission tomography and (18-F)-fluorodeoxyglucose, we studied cerebral glucose metabolism in 10 anorectic girls within their underweight state and after weight gain. Ten age- and sex-matched healthy volunteers were used as controls. Both groups were scanned during rest, eyes closed and with low ambient noise. In absolute values, the underweight anorectic patients, when compared to control subjects, showed a global (p = 0.002) and regional (p ≤ 0.001) hypometabolism of glucose which normalized with weight gain. In relative values, no global difference could be assessed between underweight anorectic patients and controls but a trend can, nevertheless, be observed toward parietal and superior frontal cortex hypometabolism associated with a relative hypermetabolism in the caudate nuclei and in the inferior frontal cortex. After weight gain, all regions normalized for absolute and relative values, although a trend appears toward relative parietal hypometabolism and inferior frontal cortex hypermetabolism in weight gain anorectic patients. Absolute brain glucose hypometabolism might result from neuroendocrinological or morphological aspects of anorexia nervosa or might be the expression of altered neurotransmission following deficient nutritional state. As some differences exists in relative values in underweight patients and tend to persist in weight gain states, this could support a potential abnormal cerebral functioning, a different reaction to starvation within several regions of the brain or different restoration rates according to the region. [less ▲]

Growth hormone response to clonidine in nondepressed patients with a history of suicide attempts.

in Biological Psychiatry (1995), 38(3), 201-3

Suicidal behavior and growth hormone response to apomorphine test.

in Biological Psychiatry (1992), 31(12), 1213-9

Several cerebrospinal fluid (CSF) studies have provided support for a possible role for the dopaminergic system as a biological correlate of suicidal behavior. Indeed, low CSF levels of the dopamine ... [more ▼]

Several cerebrospinal fluid (CSF) studies have provided support for a possible role for the dopaminergic system as a biological correlate of suicidal behavior. Indeed, low CSF levels of the dopamine metabolite homovanillic acid (HVA) have been described in depressed patients with a history of suicide attempts. In this study, we assessed the dopamine receptor sensitivity in relationship to suicidal behavior by measuring growth hormone (GH) response to apomorphine 0.5 mg subcutaneously (sc) in 15 DSM-III-R (APA 1987) major depressive inpatients with a history of suicide attempts, compared to age-matched and gender-matched major depressive inpatients without a history of suicide. Patients with a history of suicidal behavior exhibited a significantly lower GH response to apomorphine than patients who never attempted suicide (t = 3.60, df = 1.28, p = 0.0012). Therefore, these results suggest that a blunted GH response to apomorphine could represent a biological marker of suicidal behavior. [less ▲]