Some Jurassic Trigoniids from Peru

In 1973 and 1979, the geological and palaeontological reconnaissance surveys on the Mesozoic group of Los Andes Cordillera, Central Peru were carried out by the members of Palaeontological Party of Chiba University and of Instituto de Geologico, Minero y Metalurgico, Ministerio de Energia y Minas, INGEMMET, as the cooperative study supported by the Overseas Scientific Research Funds, Ministry of Education, Government of Japan. The Jurasso•Triassic marine sediments are distributed widely on the western foot and the midst of Los Andes Cordillera in the southern part of Peru. Some Jurassic trigoniids from this part are described in this paper as one of the results obtained by the cooperative study. The fossils treated in this paper were collected by the geologists of INGEMMET through the geological survey for making the geological sheet map of the southern part of Peru. Their fossils are buried generally in the light or dark gray, medium-grained sandstone or in the dark impure hard limestone. The fossil localities are shown in text-figure 1

Cardiovascular responses to chemical stimulation of the hypothalamic arcuate nucleus in the rat: role of the hypothalamic paraventricular nucleus.

The mechanism of cardiovascular responses to chemical stimulation of the hypothalamic arcuate nucleus (ARCN) was studied in urethane-anesthetized adult male Wistar rats. At the baseline mean arterial pressure (BLMAP) close to normal, ARCN stimulation elicited decreases in MAP and sympathetic nerve activity (SNA). The decreases in MAP elicited by ARCN stimulation were attenuated by either gamma-aminobutyric acid (GABA), neuropeptide Y (NPY), or beta-endorphin receptor blockade in the ipsilateral hypothalamic paraventricular nucleus (PVN). Combined blockade of GABA-A, NPY1 and opioid receptors in the ipsilateral PVN converted the decreases in MAP and SNA to increases in these variables. Conversion of inhibitory effects on the MAP and SNA to excitatory effects following ARCN stimulation was also observed when the BLMAP was decreased to below normal levels by an infusion of sodium nitroprusside. The pressor and tachycardic responses to ARCN stimulation at below normal BLMAP were attenuated by blockade of melanocortin 3/4 (MC3/4) receptors in the ipsilateral PVN. Unilateral blockade of GABA-A receptors in the ARCN increased the BLMAP and heart rate (HR) revealing tonic inhibition of the excitatory neurons in the ARCN. ARCN stimulation elicited tachycardia regardless of the level of BLMAP. ARCN neurons projecting to the PVN were immunoreactive for glutamic acid decarboxylase 67 (GAD67), NPY, and beta-endorphin. These results indicated that: 1) at normal BLMAP, decreases in MAP and SNA induced by ARCN stimulation were mediated via GABA-A, NPY1 and opioid receptors in the PVN, 2) lowering of BLMAP converted decreases in MAP following ARCN stimulation to increases in MAP, and 3) at below normal BLMAP, increases in MAP and HR induced by ARCN stimulation were mediated via MC3/4 receptors in the PVN. These results provide a base for future studies to explore the role of ARCN in cardiovascular diseases

Effect of baseline MAP on cardiovascular responses elicited by microinjections of NMDA into the ARCN.

*<p>Significantly smaller compared with ‘†’ (P<0.01). **Significantly greater compared with ‘‡’ (P<0.01). ***Significantly greater compared with ‘§’ (P<0.05). ARCN, the hypothalamic arcuate nucleus; HR, heart rate (beats/min); MAP, mean arterial pressure, NMDA, N-methyl-D-aspartic acid (10 mM, 20 nl); SNP, sodium nitroprusside (150–300 µg/kg/hr).</p

Concentration-response for microinjections of NMDA into the ARCN.

<p>ARCN: the hypothalamic arcuate nucleus; bpm: beats/min; HR: heart rate; MAP: mean arterial pressure; NMDA: N-methyl-D-aspartic acid. **Significantly greater compared with ‘‡’ (P<0.01). *Significantly greater compared with ‘†’ (P<0.05). The volume of all microinjections was 20 nl.</p

Histological identification of microinjection sites in the PVN.

<p>A: A typical microinjection site in the PVN marked with green retrobeads IX (30 nl). B-D: Composite diagrams of PVN sections at levels 1.72 mm, 1.80 mm, 1.92 mm caudal to the bregma showing microinjection sites (n = 10). Each dark spot represents one microinjection site in one animal. Calibration bar in panel A = 500 µm. Abbreviations: AH, the anterior hypothalamic area; Pe, the hypothalamic periventricular nucleus.</p

Tracings showing the effect of iGLUR blockade in the PVN on ARCN responses.

<p>A: In barodenervated rat, unilateral microinjection of aCSF into the ARCN elicited no changes in MAP, GSNA or HR. B: 2 min later, unilateral microinjection of NMDA (10 mM, 20 nl) into the ARCN elicited increases in MAP, GSNA and HR. C: 20 min later, ipsilateral PVN site was identified by a microinjection of NMDA (10 mM, 30 nl); increases in MAP, HR and GSNA were elicited. D: 20 min later, mixed solution (30 nl) of NBQX (4 mM, 15 nl) and D-AP7 (10 mM, 15 nl) was microinjected into the ipsilateral PVN; no changes in baseline MAP, HR or GSNA were elicited. E: After an interval of 3 min, NMDA (10 mM, 20 nl) was again microinjected into the ARCN; decreases (instead of increases) in MAP and GSNA were elicited and tachycardic response was attenuated. D-AP7 (NMDA receptor antagonist); NBQX (non-NMDA receptor antagonist); iGLURs, ionotropic glutamate receptors.</p

Group data showing the effect of melanocortin receptor blockade in the PVN on ARCN responses.

<p>A: In barodenervated rats, microinjections of NMDA (10 mM, 20 nl) into the ARCN before the blockade of MC 3/4 receptors in the ipsilateral PVN by SHU9119 (open bar) elicited increases in MAP (n = 5). Microinjections of SHU9119 (2 mM, 30 nl) into the ipsilateral PVN elicited no changes in baseline MAP, GSNA or HR (not shown). Microinjections of NMDA (10 mM, 20 nl) into the ARCN after the blockade of MC 3/4 receptors in the ipsilateral PVN (dark bar) elicited smaller increases in MAP than those before microinjections of SHU9119 (**P<0.01). B: Increases in GSNA elicited by microinjections of NMDA into the ARCN were attenuated by the blockade of melanocortin 3/4 receptors in the PVN (*P<0.05). C: Increases in HR elicited by the ARCN stimulation were attenuated by the blockade of melanocortin 3/4 receptors in the PVN (*P<0.05).</p