1 This study examined whether activation of group II metabotropic glutamate (mGlu) receptors in the substantia nigra pars reticulata (SNr) could reverse akinesia in a rodent model of Parkinson's disease (PD). 2 Male Sprague Dawley rats, stereotaxically cannulated above either the SNr or third ventricle, were rendered akinetic by injection of reserpine (5 mg kg 71 s.c.). Eighteen hours later, the rotational behaviour induced by unilateral injection of the group II mGlu receptor agonist, (2S,2'R,3'R)-2-(2',3'-dicarboxycyclopropyl)glycine (DCG-IV), was examined. 3 Following intranigral injection, DCG-IV (0.125 ± 0.75 nmol in 0.1 ml) produced a dose-dependent increase in net contraversive rotations (n=6 ± 8 animals per dose), reaching a maximum of 395+51 rotations 60 min 71 after 0.75 nmol. The eects of DCG-IV (0.5 nmol) were inhibited by 63.0+9.0% following 30 min pre-treatment with the group II mGlu receptor antagonist, (2S)-a-ethylglutamic acid (EGLU; 100 nmol in 0.2 ml; n=6). 4 Following intraventricular injection, DCG-IV (0.125 ± 1.5 nmol in 2 ml) produced a dosedependent increase in bilateral locomotor activity (n=6 ± 7 animals per dose), reaching a maximum of 180+21 locomotor units 30 min 71 after 0.5 nmol. Pre-treatment with EGLU (200 nmol in 2 ml) inhibited the eects of DCG-IV (0.5 nmol) by 68.2+12.3% (n=5). 5 These data show that activation of group II mGlu receptors in the SNr provides relief of akinesia in the reserpinized rat model of PD. The reversal seen following intraventricular administration supports the likely therapeutic bene®t of systemically-active group II mGlu receptor agonists in PD.

1 This study examined whether activation of 5HT 1B receptors in the rodent globus pallidus (GP) could reduce GABA release in vitro and reverse reserpine-induced akinesia in vivo. 2 Microdissected slices of GP from male Sprague Dawley rats (300 ± 350 g) were preloaded with [ 3 H]-GABA. During subsequent superfusion, 4 min fractions were collected for analysis of release. The eects of the 5HT 1B receptor agonist, 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one (CP-93129), on 25 mM KCl-evoked release were examined using a standard dual stimulation paradigm. 3 Male Sprague Dawley rats (270 ± 290 g), stereotaxically cannulated above the GP, were rendered akinetic by injection of reserpine (5 mg kg 71 s.c.). Eighteen hours later, the rotational behaviour induced by unilateral injection of CP-93129 was examined. 4 CP-93129 (0.6 ± 16.2 mM) produced a concentration-dependent inhibition of 25 mM KCl-evoked [ 3 H]-GABA release reaching a maximum inhibition of 52.5+4.5%. The eect of a submaximal concentration of CP-93129 (5.4 mM) was fully inhibited by the 5HT 1B receptor antagonist, isamoltane (10 mM). 5 Following intrapallidal injection, CP-93129 (30 ± 330 nmol in 0.5 ml) produced a dose-dependent increase in net contraversive rotations reaching a maximum of 197+32 rotations in 240 min at 330 nmol. Pre-treatment with isamoltane (10 nmol in 1 ml) inhibited the eects of a submaximal dose of CP-93129 (220 nmol) by 84+6%. 6 These data suggest that at least some 5HT 1B receptor function as heteroreceptors in the GP, reducing the release of GABA. Moreover, CP-93129-mediated activation of these receptors in the GP provides relief of akinesia in the reserpine-treated rat model of PD.

No abstract

A 19-year-old woman was referred for nasal breathing and aesthetic concerns regarding her nose. A computed tomography scan revealed a massive osseous shield anterior to the piriform aperture. Furthermore, there was a submucosal median alveolar cleft, and the posterior arch of C1 was missing. The magnetic resonance imaging brain scan revealed a curvilinear lipoma of corpus callosum. The ectopic nasal bone was removed by open rhinoplast,y and nasal function and aesthetics were restored. The described features defy conventional clinical diagnosis and severity classifications and present a diagnostic conundrum somewhere between a mild form of frontonasal dysplasia, oculoauriculofrontonasal syndrome, and Pai syndrome.

When the University of Oxford developed guidelines for medical students' examination of children, three areas were particularly problematic Medical students are expected to examine patients as an integral part of their clinical education, raising the issue of what should be the proper conduct of students and their teachers, and what guidelines should be provided. These questions, in the specific setting of "intimate" examinations, were raised by the publication in 2003 of a survey of students in the medical school in Bristol.1 This survey found that in a quarter of examinations the consent procedures seemed inadequate. The authors pointed to a potential conflict between the educational needs of the students and the ethical requirements of protecting individual patients, and commentary and correspondence highlighted disagreement over the right balance.2 3 One vital component of medical students' training involves gaining experience in examining children. We report the development in another UK medical school of guidelines for students in examining child patients and highlight three areas that were particularly problematic.