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Several lines of evidence have shown that traumatic events during the early postnatal stage might precipitate long-lasting alteration in the functional properties underlying emotional expression. The aim of the present study was to examine whether the early postnatal stress alters the 5-HTergic mechanism underlying regulation of emotional stress, focusing on the 5-HT(1A) receptor-mediated synaptic responses in adult rats. Pups were exposed to aversive stimulus, footshock (FS) at the postnatal period of the second (2W) and the third week (3W). At postadolescent period (10-12-week-old), electrophysiological and behavioral studies were performed. The 5-HT(1A) receptor agonist tandospirone (10 mg/kg body wt, i.p.) blocked the long-term potentiation (LTP) in the hippocampal CA1 field of 3W-FS, as well as non-FS control, whereas this inhibition was not observed in 2W-FS group. Fear-related freezing behavior observed during exposure to contextual fear conditioning markedly attenuated in 2W-FS, but not in 3W-FS. These data suggest that aversive stress exposed at 2W is attributable to changes in the 5-HT(1A) receptor-mediated synaptic plasticity, which may be responsible for the attenuation of freezing behavior. Thus, 5-HT(1A) receptors appear to play a key role in the 5-HTergic mechanism underlying regulation of emotional stress on the postnatal development of the brain. In other words, the second postnatal week may be the "critical period" for establishing proper behavioral responses to emotional stress in adult rats. (c) 2005 Wiley-Liss, Inc.

The present study was undertaken to examine the possible involvement of cortical gamma-aminobutyric acid (GABA) neuronal mechanisms in the regional differences of dopamine (DA) response to psychological stress: contextual fear conditioning (CFC) in the rat prefrontal cortex (PFC) and dorsolateral striatum (DLS). Rats that received five footshocks (shock intensity, 0.5 mA; shock duration, 2 sec) were subjected to CFC and dynamic changes in DA and GABA in both PFC and DLS were examined using dual-probe microdialysis. Extracellular levels of DA in the PFC were enhanced during exposure to CFC, whereas the levels in the DLS were not affected by this stimulus. Extracellular levels of GABA in the PFC, but not in the DLS, were markedly enhanced by CFC. Freezing behavior observed during exposure to CFC was attenuated by the GABA(A) receptor antagonist bicuculline (10(-3) M), which was perfused into the PFC. Intracortical application of bicuculline (10(-3) M) furthermore caused sustained increases in DA levels in the DLS by CFC. These data suggest that cortical GABA(A) receptors contribute to modulation of DA release in the DLS in response to CFC. Thus, the GABAergic neuronal system in the PFC appears to play a key role in the regional differences of the DAergic response to psychological stress.

Abstract. Repetitive transcranial magnetic stimulation (rTMS) changes the function of the cortex. This study clarified the effects of acute rTMS treatment on extracellular serotonin (5-HT) concentrations in the rat prefrontal cortex (PFC) by using in vivo microdialysis methods. Each rat received acute rTMS treatment of the frontal brain at 500 stimuli from twenty trains applied at 25 Hz for 1 s at 1-min intervals between trains. Sham-treated rats received the same handling procedure and sound of the stimulator. Sham treatment increased the extracellular 5-HT levels compared with the non-treated group. However, rTMS treatment using the stimulation intensity of 110% motor threshold eliminated the increase in 5-HT levels induced by the sham treatment. Acute rTMS treatment of the frontal brain is related to the serotonergic neuronal system in the rat PFC, and it may have therapeutic implications for emotional disorders.

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We present the case of a 39-year-old man with bilateral sclerochoroidal calcification with primary hyperparathyroidism. Both the calcium and parathyroid hormone levels were elevated. Funduscopic examination revealed slightly elevated, multiple yellow lesions in both eyes. Fluorescein angiography showed filling defects of the choroid. Ultrasonography showed elevated, highly reflective lesions, and a computed tomography scan of the globe disclosed sclerochoroidal lesions with high density. We discuss the mechanism of sclerochoroidal calcification.