Herring body

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Herring bodies are very large swellings in the axons of the neurosecretory neurons that innervate the posterior pituitary gland. They are named after Percy Theodore Herring (1872-1967), who first observed them from histological studies of the pituitary gland that he conducted at The University of Edinburgh. Herring published his findings in the first volume of the ‘’Quarterly Journal of Experimental Physiology’’, whose principal editor, Edward Albert Sharpey-Schafer held the Chair of Physiology at the University. [1]

In Herring’s words the posterior lobe is found to contain small hyaline bodies, highly refractive when unstained. He noted that sometimes they have a distinctly granular appearance, and speculated that they were involved in secretion, and that they might contain the physiologically active principle of the posterior lobe.

We now know that there are two "physiologically active principles" in the posterior pituitary – the hormones oxytocin and vasopressin. These hormones are stored in neurosecretory vesicles that are made in the cell bodies of neurosecretory neurons in the hypothalamus, and transported down the neuronal axons to their storage sites in the posterior pituitary. When newly formed vesicles first arrive at the pituitary gland, they are first targeted to the many small neurosecretory endings from which they can be readily released, and are then relocated to larger axonal swellings. Secretion can also occur from these swellings, but less readily and accordingly the small swellings seem to represent a reserve store [2] Each axon gives rise to about 2,000 of these endings and small swellings, and exocytosis of vesicles from them has been studied at the electron-microscopic level using the texchnique of tannic acid perfusion to capture images of the vesicles underoing exocytosis [3]. These studies showed that exocytotic events occurred at nerve endings, small axonal swellings, and even from undilated axons, and at each of these sites the probability of an exocytotic event occurring apparently reflects the number of vesicles close to the plasma membrane. Accordingly, the many neurosecretory endings, with relatively small numbers of vesicles but which are all close to the membrane, contain the most readily-releasable vesicles. Axonal swellings are less abundant and contain more vesicles, but fewer of these are adjacent to the plasma membrane so these are less easily releasable but provide a reserve store that can be accessed by intense stimulation.

When viewed under the electron microscope, the Herring bodies stand out as very occasional, exceptionally large axonal swellings that contain very large numbers of aged neurosecretory vesicles. However, the Herring bodies are not a site of secretion of these vesicles, but are involved in their disposal by an autophagic process. [4]

. Neurohypophysial axons often terminate as Herring bodies [5] , but these ”end bulbs” lack the ultrastructural characteristics of release sites – in particular, they are typically engulfed by glial processes and do not directly contact the basal lamina lining the perivascular space [6]

Dellman and Rodriguez (1970) proposed that Herring bodies in the bovine neurohypophysis could be classified into three types according to distinct ultrastructural features. The type I Herring body is rare; it contains an accumulation of neurosecretory vesicles, but should not be confused with the very numerous, small, axonal swellings which also contain neurosecretory vesicles and which are sites of secretion. The type II Herring body is frequently observed, and has a varying number of normal, moderately electron dense and empty vesicles, autophagic vacuoles, multilamellate bodies and occasional mitochondria. These features all suggest that the type II Herring body is associated with a degenerating phase. The type III Herring body has dense vesicles connected to tubular formations which contain material of variable electron density, filaments, and many long, slender mitochondria, and (they suggested) that this type is "in a regenerative process", possibly being an axonal growth site.

[7]

References

  1. Herring PT (1908) The histological appearances of the mammalian pituitary body. Q J Exp Physiol 121-60
  2. Tweedle CD (1983) Ultrastructural manifestations of increased hormone release in the neurohypophysis. Prog Brain Res 60:259-72
  3. Morris JF, Pow DV (1988) Capturing and quantifying the exocytotic event J Exp Biol 139:81-103
  4. Krsulovic J et al. (2005) The destination of the aged, nonreleasable neurohypophyseal peptides stored in the neural lobe is associated to the remodeling of the neurosecretory axon. Microsc Res Tech 68:347-59
  5. Bodian D (1951) Nerve endings, neurosecretory substance and lobular organization of the neurohypophysis. Bull Johns Hopkins Hosp 89: 354-376
  6. Tweedle CD et al. (1989) Neurosecretory endings in the rat neurohypophysis are en passant Exp Neurol 106:120-26
  7. Dellman H-D, Rodriguez EM (1970)Herring bodies; an electron microscopic study of local degeneration and regeneration of neurosecretory axons Cell Tissue Res 111:293-315