INV SUPERIOR JUBILADO
SEILICOVICH Adriana
artículos
Título:
The effect of anandamide on prolactin secretion is modulated by estrogens.
Autor/es:
C.SCORTICATI,; C.MOHN,; A. DE LAURENTIIS,; P.VISSIO,; J.FERNANDEZ SOLARI,; A. SEILICOVICH; S.M.MCCANN,; V.RETTORI,
Revista:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Editorial:
NATL ACAD SCIENCES
Referencias:
Lugar: Washington DC, USA; Año: 2003 vol. 100 p. 2134 - 2139
ISSN:
0027-8424
Resumen:
Recent research has revealed that endogenous cannabinoid receptors
(CB1 and CB2) react with the active ingredient of marijuana, 9-
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
9-
tetrahydrocannabinol. Two endogenous ligands activate these receptors.
The principal one, anandamide (AEA), activates CB1. AEA and
CB1 are localized to various neurons within the brain. Because
9-tetrahydrocannabinol inhibited prolactin (Prl) secretion following
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.
9-tetrahydrocannabinol inhibited prolactin (Prl) secretion following
its intraventricular injection into male rats,wehypothesized that AEA
would have a similar effect. Estrogen modifies many hormonal
responses and is known to increase Prl secretion. Therefore, we
hypothesized that responses to intraventricular AEA would change
depending on the gonadal steroid environment. Consequently, we
evaluated the effects of lateral cerebral ventricular microinjection of
AEA (20 ng) into male, ovariectomized (OVX), and estrogen-primed
(OVX-E) rats. AEA decreased plasma Prl in male rats, had little effect
in OVX females, and increased Prl in OVX-E rats. The results were at
least partially mediated by changes in dopaminergic turnover, altering
the inhibitory dopaminergic control of Prl release by the anterior
pituitary gland. Thus, dopamine turnover was increased in the male
rats and decreased significantly in OVX and in OVX-E rats. The
changes in Prl may be caused not only by altered dopamine input to
the anterior pituitary gland but also by effects of AEA on other
transmitters known to alter Prl release. Importantly, in OVX-E rats, the
elevated Prl release and the response toAEAwere blocked by theAEA
antagonist, indicating thatAEAis a synaptic transmitter released from
neurons that decrease inhibitory control of Prl release.