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Background: Although alcohol dependence in women is an increasing problem, little is known about the effects of alcohol on the female brain. Evidence from a few structural and functional neuroimaging studies suggests that the female brain may be more susceptible than the male brain to the harmful effects of alcohol. However, no in vivo studies of the neuropharmacology of alcohol dependence in women have been carried out. The aim of this preliminary study was to test the hypothesis that alcohol dependence in women is associated with greater reduction in γ‐aminobutyric acid (GABA)‐benzodiazepine receptor levels than in men with an equivalent drinking history.

The regional distribution of the vasoactive intestinal polypeptide (VlP)-sensitive stimulation of adenylate cyclase activity was studied in homogenates of rat brain. The order of sensitivity of this peptide on enzyme activity was: olfactory bulb > hippocampus > thalamus > occipital cortex ⋍ frontal cortex ⋍ midbrain ⋍ hypothalamus > striatum > cerebellum ⋍ brain stem > spinal cord. With neurotoxin-induced lesions the possible location of VIP-sensitive adenylate cyclase within the anterior hypothalamus was investigated. Intrahypothalamic 6-hydroxydopamine blocked the stimulatory effect of VIP on hypothalmic adenylate cyclase, but neither kainic acid nor 5,7-dihydroxytryptamine lesions had any effect. Similarly, there was a 71 % reduction in the sensitivity of VIP-sensitive adenylate cyclase activity in animals whose hypothalamic noradrenergic innervation had been interrupted by transection of the ascending dorsal and ventral bundles. Biochemical analyses of the lesions suggested that loss of VIP action on adenylate cyclase was associated with loss of hypothalamic noradrenaline-containing neurons. These results may give insight into those regions of rat brain where VIP may have a neurotransmitter role, and point to a possible noradrenergic localization of the VIP-sensitive adenylate cyclase within the hypothalamus.

Since the demonstration of dopamine-containing nerve terminals within cortical regions1,2, studies have confirmed the existence of a dopaminergic projection to the medial prefrontal cortex3,4. Cortical dopamine (DA) may be a functional neurotransmitter, as there are selective high-affinity receptor binding5,6and uptake sites7,8within this area, a DA-selective adenylate cyclase system8,9, cells responsive to iontophoretically applied DA10, and a pool of DA amenable to release in vivo11or in vitro12,13. Lesions of either midbrain cell bodies in the ventral tegmental area14,15or of frontal cortical areas directly16, with subsequent loss of DA terminals from the medial prefrontal cortex, induce hyperactivity in rats16, and enhanced behavioural responses to amphetamine16,17. Lesion of subcortical DA pathways results in the opposite effects, suggesting that frontal cortical DA systems may have an inhibitory role in motor behaviour15,16. Dopamine-dependent hyperactivity and stereotypy is believed to be mediated from extrapyramidal and mesolimbic DA-innervated sites18. We previously noted that loss of catecholamine terminals within the frontal cortex of the rat results in increased DA turnover and utilization in subcortical striatal and limbic regions after one week19. We now show evidence of both enhanced pre-synaptic and post-synaptic mechanisms in the terminal regions of the ascending nigrostriatal and mesolimbic DA pathways one month after destruction of DA terminals within the medial prefrontal cortex of the rat. The increased 3H-ADTN and 3H-spiperone binding, enhanced DA-induced stimulation of adenylate cyclase and potentiated uptake capacity for DA within striatum and nucleus accumbens may demonstrate a functional basis for the observed potentiated behavioural responses.

Dopamine receptors are strong candidates for involvement in schizophrenia and are targeted by a wide variety of antipsychotics. We hypothesized that genetic variation in these neurotransmitter receptors may influence clinical response to clozapine, an antipsychotic which displays high affinity for dopamine D2 receptors in the limbic system. To test this hypothesis, we studied a functional polymorphism in the promoter region of the D2 receptor gene (-141C Ins/Del) in a sample of 151 clozapine treated patients of British origin. In addition, the influence of this polymorphism on antipsychotic response in general was investigated on a sample of 146 Han Chinese schizophrenic patients treated with a variety of antipsychotics. No association was found between this polymorphism and clinical response in either of the two samples suggesting that genetic variation in D2 receptors does not play a major role in determining clinical response to antipsychotic treatment.

1. Intrahypothalamic injection of either dopamine or 5‐hydroxytryptamine (5‐HT) in a dose volume of 1 microliters caused a fall in core temperature in lightly restrained rats maintained at an ambient temperature of 17 +/‐ 1 degree C. 2. Haloperidol (6.5 n‐mole), a dopamine antagonist, prevented the hypothermic effect of dopamine (65 n‐mole), but was ineffective against the response to either intrahypothalamic 5‐HT (114 n‐mole) or oxotremorine (6.0 n‐mole). 3. Methysergide (14 n‐mole) and cryproheptadine (17 n‐mole) blocked the effect of both 5‐HT and dopamine. However, these same doses failed to antagonise the effect of oxotremorine. 4. Rats placed on 0.65 m below a 250 W infra‐red lamp responded to the imposed heat load vasodilation of tail skin blood vessels, as indicated by an increased tail skin temperature. 5. Rats tested 2 weeks after bilateral intrahypothalamic injection of 5,6‐dihydroxytryptamine (42 n‐mole in 2 microliters) showed a significant reduction in their tail skin temperature response and were less able to withstand the imposed heat load. 6. Three serial sections (0.8 mm thick) were prepared from the preoptic area of the rat brain, one anterior, one posterior and one corresponding to the previously defined dopamine‐sensitive site. 7. Pretreatment with 5,6‐dihydroxytryptamine significantly reduced the 5‐HT concentration in the dopamine sensitive site, but had no effect on the concentration of dopamine. This pretreatment blocked dopamine but not 5‐HT‐induced hypothermia. 8. The 5‐hydroxyindoleacetic acid (5HIAA) concentration in the hypothalamus of the normal rat exposed to a heat load was found to be significantly elevated, whereas there was no change in the 5HIAA concentration in the cortex. 9. Slices of rat preoptic hypothalamus and hippocampus were incubated with [3H]5‐HT (0.2‐2 microM). These slices accumulated 5‐HT with properties characteristic of a neuronal uptake process. 10. Perfusion with either dopamine (greater than 50 microM) or apomorphine (greater than 200 microM) enhanced the release of [3H]5‐HT from the prelabelled hypothalamic slices, but failed to stimulate release from hippocampal slices. 11. The release of [3H]5‐HT from preoptic slices by dopamine and apomorphine was antagonised by the dopamine antagonists haloperidol (2 microM) and (+) isomer of butaclamol (1 microM), the (‐) isomer of butaclamol was inactive. 12. These results support the hypothesis of a dopamine‐5HT link in the hypothalamic thermoregulatory pathways of the rat.

It is probably not often that an otolaryngologist is called on to do surgical work on the blood vessels in the neck, and yet, on occasions when this becomes necessary, the importance of the outcome, dependent on a careful technic, is paramount and calls for prompt diagnosis, decision and action. It is with regard to this problem that this paper is undertaken.The location of the smaller blood vessels is not always easily ascertained, but in the case of the larger vessels not only is there a problem of which vessel to approach but there is a question as to what type of surgical procedure should be used.If one disregards the problems of aneurysmorrhaphy or anastomosis of blood vessels, wiring of an aneurysm and stripping of the adventitia, the usual condition presenting is one which calls for obstructing the flow of blood through the vessel concerned. In short, shall

ADVANCES in therapy always constitute a good reason for presenting a familiar subject. Indeed, the chronology of juvenile nasopharyngeal hemangiofibroma reflects this steplike progress in the almost cyclical reappearance of reports in the otolaryngological literature as improvements in handling this sometimes alarming condition manifest themselves.In reviewing the literature, I received the impression that a greater number of these cases were reported in the foreign journals, European and South American, than in those of this country. Part of this may be due to the depressant effect of the last war on medical literature in general, especially as regards the number of reports from this country compared with that of South America.It has been the privilege of very few men to see several of these interesting cases, most reports being limited to one, two, three, four or six. In fact, when larger numbers of cases are reported often cases are