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M H Whitnall

Publications and source records attributed to M H Whitnall.

41 records · Page 3Linked to original sources

Axonal transport of lipid in goldfish optic axons.

After injection of labeled glycerol, choline, or serine into the eye of goldfish, labeled lipids were axonally transported along the optic nerve to the optic tectum. Although the different precursors were presumably incorporated into somewhat different lipid populations, all three were approximately equally effective in labeling the lipids transported to the tectum, but the amount of transported material remaining in the nerve was different, being highest with choline and lowest with serine. The labeled lipids appeared in the tectum within 6 hr of the injection, indicating a fast rate of transport, but continued to accumulate over a period of 1--2 weeks, which presumably reflects the time course of their release from the cell body. Since there was a gradual increase in the proportion of labeled lipid in the tectum during this period, some other process in addition to fast axonal transport may have affected the distribution of the lipids along the optic axons. When [3H]choline was used as precursor, the transported material included a small amount of TCA-soluble material, which was probably mainly phosphorylcholine, with labeled acetylcholine appearing in only insignificant amounts. With serine, which gave rise to a large amount of axonally transported protein in addition to lipid, a late increase in the amount of labeled lipid in the tectum was seen, accompanied by a decrease in labeling of the protein fraction.

Acetylcholine↗

Hemodynamic similarities between the trigeminal and aortic vasodepressor responses.

The hemodynamic changes associated with hypotension elicited by electrical stimulation of the spinal trigeminal complex (trigeminal depressor response, TDR) or the aortic nerve (aortic depressor reflex, ADR) were compared in rabbits anesthetized with urethan. The hypotension associated with each response was accompanied by bradycardia, a marked fall in total peripheral resistance, a small decrease in cardiac output, and a nonuniform decrease in regional vascular resistances, with the order of magnitude of the decrease being femoral greater than mesenteric greater than renal arterial resistance. In individual experiments the percent decrease in heart rate, total peripheral resistance, or regional resistances was plotted against the percent fall in arterial pressure to obtain a pair of regression lines during the TDR and ADR. There was no significant difference in the slope or y-intercept of the regression line between the TDR and ADR for all of the hemodynamic variables examined. In both responses, however, the slope of the femoral resistance/arterial pressure relationship was significantly greater than that of the renal resistance/arterial pressure relationship. We conclude that the TDR is characterized by a pattern of hemodynamic changes similar to that of the ADR.

Animals↗

Immunocytochemical identification of dynorphin-containing vesicles in Brattleboro rats.

Vasopressin and its carrier protein, vasopressin-associated neurophysin, are co-packaged together with an opioid peptide, dynorphin, into 160 nm diameter neurosecretory vesicles in the normal rat hypothalamo-neurohypophysial system. The homozygous Brattleboro rat lacks vasopressin and vasopressin-associated neurophysin, but contains substantial amounts of dynorphin in the vasopressin-deficient neurosecretory cells. We used post-embedding electron microscopic immunocytochemistry to determine the subcellular location of dynorphin in Brattleboro rats. The results show that dynorphin is present within 100 nm neurosecretory vesicles in homozygous Brattleboro cell bodies and axons, and within 160 nm vesicles in heterozygous (control) neurosecretory cell bodies and axons. Oxytocin-associated neurophysin is present in a separate population of magnocellular neurons in both homozygous and heterozygous rats, and is contained within 160 nm vesicles in both cases. Therefore, the absence of synthesis of the vasopressin prohormone results in a dramatic reduction of neurosecretory vesicle size, despite the continued synthesis and packaging of dynorphin peptides.

Animals↗

An immunochemical analysis of oxytocin and vasopressin prohormone processing in vivo.

Antisera against partially processed, unamidated forms of AVP and OT were raised and characterized by radioimmunoassay and immunocytochemistry. These antibodies, and antibodies that recognize fully processed, amidated forms of AVP and OT, were used together with various fractionation methods to study the content of prohormones, partially processed and fully processed forms of AVP and OT in the hypothalamo-neurohypophysial system of adult and fetal (E21) rats. The levels of cleaved AVP and OT in the fetus were lower than those of the adult (1 to 3 orders of magnitude for brain and pituitary, respectively), and the detection of cleaved OT in brain and pituitary was delayed compared to that of AVP. Pro-AVP cleavage efficiency in the adult and the fetus was high (99 and 95% cleavage, respectively) resulting in formation of fully processed amidated forms of AVP, with no detectable partially processed peptides. Pro-OT processing in the adult was very similar (over 99% cleavage) resulting in formation of fully processed amidated OT. However, Pro-OT processing efficiency in the fetus was very low and incomplete, resulting in 40% unprocessed precursor and the accumulation of C-terminally extended unamidated intermediate forms (OT-Gly, OT-Gly-Lys, and OT-Gly-Lys-Arg).

Animals↗

Co-localization of corticotropin-releasing factor and vasopressin in median eminence neurosecretory vesicles.

Vasopressin (VP) potentiates the effect of corticotropin-releasing factor (CRF) on the secretion of adrenocorticotropic hormone (ACTH) from anterior pituitary cells in vitro, and both CRF and VP have been found in portal blood. These data support the hypothesis that VP acts synergistically with CRF to cause the secretion of ACTH in vivo but the origin of the CRF and VP, and the physiology of their release, have not been precisely defined. Parvocellular cell bodies in the paraventricular nucleus (PVN) which project to the external zone of the median eminence can be stained for both CRF and VP after adrenalectomy, and there is light microscopic immunocytochemical evidence that neurophysin (NP) may be located within some of the CRF-containing axons. Electron microscopic immunocytochemical studies have demonstrated the presence of CRF, VP and its 'carrier' protein, VP-associated neurophysin (NP-VP) in 100-nm neurosecretory vesicles (NSVs) in axons terminating near the portal capillary plexus in the external zone of the median eminence. If these peptides are extensively co-localized in the same NSVs in the median eminence, then coordinate secretion of CRF and VP in vivo is obligatory, at least in some physiological circumstances. We demonstrate in this report, using post-embedding electron microscopic immunocytochemistry on serial ultrathin sections, that CRF, VP and NP-VP are contained not only in the same axons and terminals, but in the same 100-nm NSVs in the median eminence of both normal and adrenalectomized rats. In addition, in the normal rat median eminence 44% of the CRF-positive axons and terminals stained strongly for VP and NP-VP, whereas in the adrenalectomized rat virtually all the CRF-positive structures in the median eminence showed strong staining for VP and NP-VP, indicating a transformation of one subpopulation of CRF-positive axons and terminals by adrenalectomy.

Adrenalectomy↗