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Postnatal development of somatostatin‐ and vip‐immunoreactive neurons in the rabbit's visual cortex
Author(s) -
Ramón y Cajal S.,
MartinezHillán L.,
Contamina P.
Publication year - 1985
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/0736-5748(85)90262-x
Subject(s) - somatostatin , citation , cortex (anatomy) , neuroscience , psychology , computer science , library science
Somatostatin contents have been investigated in several central nervous regions of the pituitary deficient Snell dwarf mouse (dw/dw). When compared to the normal mouse, the dwarf mutant showed decreased somatostatin levels in the hypothalamus, whereas more or less increased somatostatin concentrations were found in any extrahypothalamic site studied. Higher plasmatic SRIF levels have also been evidenced. These opposite results in hypothalamus and extrahypothalamic sites provide arguments for the assumption of a primary somatostatin excess which could be related to the single recessive dwarf mutation. In the hypothalamus exposed to the stimulatory growth hormone (OH) retrocontrol, the severe defect in GH of the dwarf mutant may lead to a reduction in the presumed initially elevated hormonal somatostatin levels. In extrahypothalamic sites which are known to escape to the GH retroaction, higher sommtostatin levels can remain. Since somatostatin appears soon in ontogenesis and is involved in neuromaturation, a primary and overall excess of this neuropeptide should nave strong incidences in the pituitary development and function. Also neurotransmission impairments may be related to the high somatostatin levels found in central nervous areas of this mouse. The hypothesis of a primary somatostatin excess in the Snell dwarf mouse is discussed with regards to the central cholinergic neurotransmission deficiency we evidenced in this mutant.