Growih hormone and growth
51
SRIF has been shown to
inhibit the
vitro release of GH from tilapia pitui—
taries
(Fryer at al., 1979). More recently, we have demonstrated that intra—
peritoneal injection of synthetic mammalian SRIF decreases circulating levels
of GH in the goldfish (Cook and Peter, 1984) and inhibits GH release in a
dose-dependent manner from goldfish pituitaries maintained in an ia vitro
superfusion system (T. Marchant, R. Fraser and R. Peter, unpublished
results). The nucleus preopticus periventricularis of the preoptic region in
goldfish contains abondant neuronal cell bodies with SRIF—like immunoreacti—
vity (Kah a£ al., 1982), and destruction of the preoptic region of the
goldfish forebrain by radiofrequency lesions stimulates GH cell activity
(Fryer, 1981) and increases body growth rates and serum GH levels (Cook and
Peter, 1983). The results of the lesioning studies suggest that the preoptic
region of the goldfish brain is involved in the inhibition of GH secretion,
presumably through SRIF or a SRlF—like molecule. Therefore, evidence from in
vivo and in vitro studies provide firm support for the hypothesis that SRIF
or
a
SRIF—like molecule acts as a GH release—inhibiting peptide in the
goldfish and possibly other teleost species.
Crude hypothalamic extracts from several teleost species have been
shown to stimulate GH release (for review: Ball, 1981), providing the possi—
bility that a GRF may also be present in the teleost hypothalamus. Indirect
evidence for & GRF in teleosts is also supplied by a lesioning study in
goldfish (Cook and Peter, 1983). In this study, destruction of the nucleus
anterior
tuberis of the hypothalamus resulted in a decreased growth rate in
goldfish, suggesting that a stimulatory influence on GH secretion may have
been destroyed by the lesion. More recently, the GRF molecule isolated from
mammalian tissues
(GRF—40) has been shown to stimulate GH release ia yiyg in
the goldfish (Peter at al., l984), leading to the suggestion that a molecule
similar to
the mammalian GRF may function as a GRF in the goldfish. A mammal—
ian GRF—like molecule has not yet been shown to be present in the goldfish
brain, but a recent report has demonstrated the presence of mammalian
GRF—like immunoreactivity in the hypothalamus and pituitary of the codfish
(Pan a; al., 1985). Although theSe results suggest that the teleost GRF may
be biochemically similar to the mammalian GRF, further studies are required
to
confirm the identity of the GRF—like immunoreactivity in the codfish brain
and to verify the presence of GRF in the brain of other teleost species.
Various neurotransmitters are known to influence GH secretion in verte—
brates, primarily through effects on the release of SRIF and GRF from the
hypothalamus (Arimura and Culler, 1985). The pituitary of teleosts is
directly innervated by aminergic fibers from the hypothalamus (Ball, 1981)
and neurotransmitters
could influence GH secretion by actions within the
hypothalamus or by acting directly at the level of the somatotrophs. Very
little is known about the influence-of various neurotransmitters on GH
release in teleosts. We have conducted a preliminary study on the influence
of catecholaminergic neurotransmitters on GH release in the goldfish (Chang
gt al., 1985). In this study, evidence suggests that dopamine stimulates GH
release in the goldfish, possibly by inhibiting SRIF release from the hypo—
thalamus, whereas other results from this study indicate that the neurotransmitter norepinephrine might inhibit GH secretion by acting directly on the
somatotropbs to decrease GH release. Preliminary data also suggested that an
alpha—adrenergic system Which stimulates GH secretion may also be present in
the goldfish (Chang a£ al., 1? T). The interactions of these neurotransmitter
systems with the hypophysiotrop c
or
other neurotransmitter systems
influencing GH secretion in the goljfish are not yet known, although the
results of this study in goldfish provide a basis from Which further experi—
ments
in this area can be designed and conducted.
—
51
SRIF has been shown to
inhibit the
vitro release of GH from tilapia pitui—
taries
(Fryer at al., 1979). More recently, we have demonstrated that intra—
peritoneal injection of synthetic mammalian SRIF decreases circulating levels
of GH in the goldfish (Cook and Peter, 1984) and inhibits GH release in a
dose-dependent manner from goldfish pituitaries maintained in an ia vitro
superfusion system (T. Marchant, R. Fraser and R. Peter, unpublished
results). The nucleus preopticus periventricularis of the preoptic region in
goldfish contains abondant neuronal cell bodies with SRIF—like immunoreacti—
vity (Kah a£ al., 1982), and destruction of the preoptic region of the
goldfish forebrain by radiofrequency lesions stimulates GH cell activity
(Fryer, 1981) and increases body growth rates and serum GH levels (Cook and
Peter, 1983). The results of the lesioning studies suggest that the preoptic
region of the goldfish brain is involved in the inhibition of GH secretion,
presumably through SRIF or a SRlF—like molecule. Therefore, evidence from in
vivo and in vitro studies provide firm support for the hypothesis that SRIF
or
a
SRIF—like molecule acts as a GH release—inhibiting peptide in the
goldfish and possibly other teleost species.
Crude hypothalamic extracts from several teleost species have been
shown to stimulate GH release (for review: Ball, 1981), providing the possi—
bility that a GRF may also be present in the teleost hypothalamus. Indirect
evidence for & GRF in teleosts is also supplied by a lesioning study in
goldfish (Cook and Peter, 1983). In this study, destruction of the nucleus
anterior
tuberis of the hypothalamus resulted in a decreased growth rate in
goldfish, suggesting that a stimulatory influence on GH secretion may have
been destroyed by the lesion. More recently, the GRF molecule isolated from
mammalian tissues
(GRF—40) has been shown to stimulate GH release ia yiyg in
the goldfish (Peter at al., l984), leading to the suggestion that a molecule
similar to
the mammalian GRF may function as a GRF in the goldfish. A mammal—
ian GRF—like molecule has not yet been shown to be present in the goldfish
brain, but a recent report has demonstrated the presence of mammalian
GRF—like immunoreactivity in the hypothalamus and pituitary of the codfish
(Pan a; al., 1985). Although theSe results suggest that the teleost GRF may
be biochemically similar to the mammalian GRF, further studies are required
to
confirm the identity of the GRF—like immunoreactivity in the codfish brain
and to verify the presence of GRF in the brain of other teleost species.
Various neurotransmitters are known to influence GH secretion in verte—
brates, primarily through effects on the release of SRIF and GRF from the
hypothalamus (Arimura and Culler, 1985). The pituitary of teleosts is
directly innervated by aminergic fibers from the hypothalamus (Ball, 1981)
and neurotransmitters
could influence GH secretion by actions within the
hypothalamus or by acting directly at the level of the somatotrophs. Very
little is known about the influence-of various neurotransmitters on GH
release in teleosts. We have conducted a preliminary study on the influence
of catecholaminergic neurotransmitters on GH release in the goldfish (Chang
gt al., 1985). In this study, evidence suggests that dopamine stimulates GH
release in the goldfish, possibly by inhibiting SRIF release from the hypo—
thalamus, whereas other results from this study indicate that the neurotransmitter norepinephrine might inhibit GH secretion by acting directly on the
somatotropbs to decrease GH release. Preliminary data also suggested that an
alpha—adrenergic system Which stimulates GH secretion may also be present in
the goldfish (Chang a£ al., 1? T). The interactions of these neurotransmitter
systems with the hypophysiotrop c
or
other neurotransmitter systems
influencing GH secretion in the goljfish are not yet known, although the
results of this study in goldfish provide a basis from Which further experi—
ments
in this area can be designed and conducted.
—