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Neurons that accompany the stria terminalis as it loops over the internal capsule have been termed collectively the supracapsular bed nucleus of the stria terminalis (BSTS). They form two cell columns, a lateral column and a considerably smaller medial column. The lateral column merges rostrally with the lateral bed nucleus of the stria terminalis and caudally with the central amygdaloid nucleus (central extended amygdala components). The medial column is continuous with the medial bed nucleus of the stria terminalis and the medial amygdaloid nucleus (medial extended amygdala districts). The connections of the BSTS were investigated in the rat by placing injections of Phaseolus vulgaris-leucoagglutinin (PHA-L) or retrograde tracers in different parts of the extended amygdala or in structures related to the extended amygdala. BSTS inputs and outputs were identified, respectively, by the presence of varicose fibers and retrogradely labeled neurons within the stria terminalis. The results suggest that the medial-to-lateral compartmentalization of BSTS neurons reflects their close alliance with the medial and central divisions of the extended amygdala. The medial BSTS contains primarily elements that correspond to the posterodorsal part of the medial amygdaloid nucleus and the medial column of the posterior division of the medial bed nucleus of the stria terminalis, and the lateral BSTS contains elements that correspond to the medial and lateral parts of the central amygdaloid nucleus and lateral bed nucleus of the stria terminalis. These results add strong support to the concept of the extended amygdala as a ring-like macrostructure around the internal capsule, and they are of theoretical interest for the understanding of the organization of the basal forebrain.

A monoclonal antibody produced against the human erythrocyte plasma membrane calcium pump (PMCA) was shown to react immunohistochemically with an epitope of the PMCA in avian and mammalian cerebellum. Western blot analysis of purified synaptosomes and homogenates from avian cerebellum revealed major immunoreactive proteins with molecular masses (130 kDa and 138 kDa) similar to those of purified erythrocyte PMCA. Dual-imaging confocal immunofluorescence microscopy of avian cerebellum showed that the PMCA antibody stained the periphery of the soma whereas calbindin-D2sk was located in the cytosol. PMCA heavily stained the more distal dendrites of the Purki' e cells and, within the resolution of the fluorescence procedure, colocalized with calbindin-D%sk. By using alkaline phosphatase-conjugated second antibody, PMCA was again localized to the peripheral soma, to a segmental pattern in dendrites, and to presumed spiny elements. The soma periphery and dendrites of Purkiaje cells of the rat cerebellum were also prominently stained with anti-PMCA antibody and compared to parvalbumin localization. Dendritic depolarization and dendritic spiking behavior are significant Ca2+-dependent events of Purki je cells. The rapid decline of intracellular free Ca2+ after the rapid rise time of Ca2+ transients is considered to be due to sequestration by Ca2+ buffers, uptake by intracellular stores, and Cae+ extrusion mechanisms, the latter a function of PMCA now shown immunohistochemically to be a prominent feature of Purkinje cell dendrites.The only output from the cerebellar cortex arises from Purkinje cells whose GABAergic axons terminate in deep cerebellar nuclei and other regions of the central nervous system (1) (GABA is y-taminobutyric acid). The Purkinje cells receive two types of excitatory input from the periphery by way of the granule-cell-derived parallel fibers that invest the more distal dendrites and from climbing fibers that make contact with the Purkinje cell soma and proximal dendrites. GABAergic inhibitory inputs to these cells originate from the interneurons, the basket and stellate cells, resident in the cerebellar molecular layer.The excitatory neurotransmitters from parallel fibers and climbing fibers are considered to be glutamate and aspartate, respectively, and activate both ionotropic and metabotropic receptors on the Purkinje-cell surface (1-4). Activation of Purkinje-cell dendrites is characterized initially by a slow Ca2+-dependent depolarization and, when of sufficient magnitude, all-or-none Ca2+-dependent spikes are generated (5, 6). The Ca2+ contributing to the Ca2+-dependent spiking might be both from the influx of Ca2+ from the extracellularThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.fluid through activation of voltage-and agonist-dependent Ca2+ channels and from the release of Ca2+ from the intracellular stores shown to cont...

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The effect of stimulation of the bed nucleus of the stria terminalis (BNST) on ovulation and LH release was studied in unanesthetized, freely moving rats. Electrochemical stimulation (anodic d.c, 100 µA/30 sec) was applied at i 1.30 h through chronically implanted monopolar, stainless steel electrodes. Serial blood samples were obtained by way of a plastic cannula implanted in the jugular vein. Stimulation on the day of proestrus prevented ovulation and the preovulatory discharge of LH when the stimulus was applied to the lateral part of the BNST but advanced the surge of LH in those rats stimulated in the medial part of the nucleus. In ovariectomized estrogen-primed rats stimulation in the medial part of the BNST produced LH release but no effect was seen when the stimulus was applied in the lateral part. It is concluded that the BNST is part of a dual system with antagonistic effects on LH secretion.

The rise in the concentration of LH in the serum that takes place in ovariectomized, estrogen-primed rats exposed to the odors from a cage with bedding soiled by a male rat was completely prevented by bilateral lesions destroying the ventral premammillary (PMv) nuclei. These results suggest that the pheromonal stimuli generate stimuli that course through a pathway which involves the PMv nuclei before they reach the hypothalamus. In addition, the chemosensory information is apparently transmitted centrally by an uncrossed pathway in view of the fact that removal of one vomeronasal organ combined with lesions of the contralateral PMv nucleus, but not of the ipsilateral nucleus, suppressed the release of LH in rats exposed to male odors. Since pheromonal stimuli are known to activate the accessory olfactory system, of which the medial (Me) amygdaloid nucleus and the bed nucleus of the stria terminalis (BNST) are parts, the effect of stimulating these nuclei in rats bearing lesions of the PMv nucleus was also investigated. Unilateral lesions of the PMv nucleus prevented the release of LH in ovariectomized, estrogen-primed rats and the advancement of LH surge in proestrous rats induced by electrochemical stimulation (anodic d.c. 100 µA/30 s) of the ipsilateral Me amygdaloid nucleus but not those induced by stimulation of the contralateral Me amygdaloid nucleus. Similar results were obtained stimulating the medial part of the BNST in proestrous rats. It is concluded that the impulses evoked by pheromonal stimuli inducing LH release in the rat are conveyed by an uncrossed pathway and relay in the PMv nucleus before they reach the medial basal hypothalamus.