1. Evoked potentials restricted to the magnocellular portion of the mediodorsal nucleus (MDmc) of the thalamus were recorded after stimulation of the olfactory bulb (OB) and the posterior orbital cortex of the frontal lobe (OFC). Potentials evoked by stimulation of OB were probably trans-synaptically elicited, while potentials evoked by stimulation of OFC were probably a result of antidromic activation. 2. The area in which stimulation could elicit antidromic evoked potentials in MDmc was located in the centroposterior portion of OFC (CPOF). This area corresponds approximately to Walker's (80) area 13 and to von Bonin and Bailey's (9) area FF, and is situated medial and just anterior to a previously identified olfactory area, the lateroposterior portion of OFC (LPOF), which receives olfactory impulses through the hypothalamus. 3. Using extracellular microelectrodes, 58 neurons that responded with short latencies to OFC stimulation were identified in MDmc. To determine whether these neurons were activated antidromically by CPOF stimulation, three conventional neurophysiological criteria were applied; 20 of 58 neurons satisfied all the three criteria. Hence, they were concluded to be thalamocortical relay (TCR) neurons. 4. Intracellular recording of MDmc neurons disclosed that CPOF stimulation elicits an antidromic spike potential accompanied by an afterhyperpolarization. This hyperpolarization was presumed to be due to concurrent stimulation of inhibitory orbitothalamic fibers. It was also shown that EPSP-like depolarizations with superimposed spike potentials often occurred in the middle of the afterhyperpolarization. 5. Intracellular recording of MDmc neurons strongly suggested that the remaining 38 neurons that did not satisfy one of the three criteria were also TCR neurons. 6. These studies provide electrophysiological evidence for a transthalamic olfactory pathway from OB through MDmc to CPOF. 7. Using an extracellular recording technique, responses of neurons to eight odors were examined in CPOF and MDmc of unanesthetized awake monkeys. When these results were compared with the responses of neurons to the same odors in OB, prepyriform-amygdaloid area, and LPOF, it was concluded that the newly found transthalamic olfactory pathway to CPOF is very different in function from the previously demonstrated transhypothalamic olfactory pathway to LPOF.

An olfactory projection area was studied in monkeys anesthetized with Nembutal. 1. Evoked potentials were recorded when the olfactory bulb (OB) was electrically stimulated in the lateroposterior portion of the orbitofrontal cortex (LPOF). However, those potentials disappeared when the anterior pyriform cortex (AP) (probably together with the medial portion of the amygdala (MA)) was aspirated or electrically destroyed. 2. In nearly the entire hypothalamic region, evoked potentials were recorded by the same stimulation of the OB. When the hypothalamic region was stimulated, evoked potentials were recorded in the LPOF. 3. The evoked potentials in the LPOF due to the OB stimulation never disappeared even when the thalamus was extensively aspirated or destroyed electrically, but they did disappear when the anterolateral and dorsoposterior portions of the hypothalamus were absorbed or electrocoagulated. 4. Evoked potentials in the mediodorsal nucleus (MD) of the thalamus were recorded when the OB was stimulated. When this nucleus was stimulated, evoked potentials were observed in the broad extent of the orbitofrontal cortex anterior to the LPOF, but never in the LPOF itself. 5. Monkeys were conditioned to discriminate two odors. When the LPOF was removed, such ability strikingly decreased; but when other areas in the prefrontal cortex were removed, the ability decreased only slightly. 6. It was concluded that there exists an olfactory pathway from the OB to the LPOF through the AP (and probably the MA) and the hypothalamus, but none through the thalamus, and that the LPOF plays an important role in the discrimination of odors. 7. It was proved that the entorhinal cortex (ER) is neither located as an intermediate olfactory area nor is it situated as a higher area than the LPOF in the newly found olfactory pathway stated above. It may be a link between the high olfactory area and the limbic system.

Effects of various gustatory stimulants upon the olfactory epithelia were examined in the olfactory bulb of the bullfrog and the carp.

The new screening method for the detection of VLCAD deficiency using an immunohistochemical technique identified 13 new Japanese patients with VLCAD deficiency.

A 55 year old man with isolated ACTH deficiency is reported. The lesion would appear to be located in the pituitary gland since plasma ACTH and cortisol did not respond to lysine vasopressin and corticotrophin releasing factor (CRF). A fall in T4, a rise in basal values of TSH, prolactin (Prl), LH and FSH, excessive responses of TSH and Prl to TRH, and hyperreactive responses of LH and FSH to LRH were observed. These hormonal changes were examined before and after administration of cortisol. The abnormality in these hormones might be caused by deficiency of long-term glucocorticoid.Isolated ACTH deficiency (Steinberg et al. 1954;Stacpoole et al. 1982) is rare but variable in its manifestions. Some patients present with anorexia, vomiting, fever and emaciation and others with neuropsychiatrie symptoms. In this study to deter¬ mine whether a primary lesion lay in the pituitary gland or the hypothalamus tests using hypoglycae¬ mia, lysine vasopressin and CRF were performed. Hormonal changes before and after administration of cortisol were studied in this case, and a fall in T4, elevated basal values for TSH and Prl and hyperresponsive responses to TRH and LRH were de¬ monstrated. Case ReportA 55 year old man was admitted with the complaints of anorexia, emaciation and disturbance of gait. At the beginning of January, 1982, he noticed fatigability. In February of the same year, his appetite diminished and nausea and vomiting occurred occasionally and his weight decreased ; slight fever and night sweats were also noted. Early in March, he had difficulty in standing and a disturbance of gait appeared. On April 17, he was admitted to hospital and investigations included serum biochemistry, CT scan of the head, lumbar puncture and electroencephalography. He was discharged with no ab¬ normality found. From the middle of May, pain in the left elbow joint and morning stiffness of the fingers began to appear. On July 2, he was admitted for an intensive check-up.Physical examination on admission: emaciation was conspicuous. The level of consciousness was normal but he appeared apathetic and pallid. The skin was dry and coarse, and turgor was decreased markedly. His blood pressure was 88/58 mmHg; pulse 68/min and regular.Vision and visual fields were normal. Ocular movement was normal. The mouth was normal. There was no enlargement of lymph nodes or thyroid. Gynaecomastia was observed. The chest and abdomen were not remark¬ able, and there was no oedema. Axillary and pubic hair was present. He was unable to stand on tiptoe or on his heels. There was no paralysis in the upper and lower extremities, but the muscle was lean with decreased muscular strength. Tendon reflexes were normal. There were no pathological reflexes. There was no sensory disturbance. The function of cerebellum was normal.Urinalysis and stool examination were normal. Exa¬ mination of peripheral blood disclosed mild hypochromic and microcytic anaemia with moderate eosinophilia and lymphocytosis. All routine laboratory examinations, including serum enzymes and ...