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Albert Sattin – One of the best experts on this subject based on the ideXlab platform.

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides.
    Brain research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH(2) (EEP), pGlu-Val-Pro-NH(2) (Val(2)-TRH), Leu(2)-TRH, Phe(2)-TRH and Tyr(2)-TRH has recently been discovered. TRH (pGlu-His-Pro-NH(2)) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val(2)-TRH and Leu(2)-TRH were Analeptics, like TRH, but Phe(2)-TRH and Tyr(2)-TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC(50) values of TRH-like peptides for displacement of [3H]TRH from TRHR2 were TRH

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides
    Brain Research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    Abstract A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH 2 (EEP), pGlu-Val-Pro-NH 2 (Val 2 -TRH), Leu 2 -TRH, Phe 2 -TRH and Tyr 2 -TRH has recently been discovered. TRH (pGlu-His-Pro-NH 2 ) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val 2 -TRH and Leu 2 -TRH were Analeptics, like TRH, but Phe 2 -TRH and Tyr 2 -TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC 50 values of TRH-like peptides for displacement of [ 3 H]TRH from TRHR2 were TRH⋘(Leu 2 -, Phe 2 -TRH) 2 -, Ser 2 -TRH)≪(Val 2 -, Tyr 2 -, Arg 2 -, Thr 2 -, and Glu 2 -TRH). The IC 50 for Leu 2 -TRH was about 100 times that for TRH. When tested at the calculated IC 50 values, TRH-like peptides stimulated calcium responses in cells expressing TRHR1 and TRHR2, indicating that the peptides act as weak agonists at both receptors. These results indicate that TRHR1 and TRHR2 do not mediate the behavioral effects of TRH-like peptides.

M.a. Carino – One of the best experts on this subject based on the ideXlab platform.

  • The Analeptic effect of methamphetamine in pentobarbital-narcotized rats is mediated via a dopaminergic-cholinergic mechanism.
    The Journal of pharmacology and experimental therapeutics, 1994
    Co-Authors: Akira Horita, M.a. Carino, Y Ukai
    Abstract:

    Methamphetamine (MAP) administered in doses of 0.5 to 5 mg/kg i.p. to rats anesthetized with pentobarbital produced a shortening of the duration of loss of righting reflex. This Analeptic effect of MAP was blocked by atropine but not by atropine methylbromide, indicating the central cholinergic nature of the response. This effect was also blocked by the D1 and D2 dopamine antagonists SCH 23390 (0.2 mg/kg) and raclopride (2 mg/kg), respectively. Pentobarbital decreased sodium-dependent high-affinity choline uptake (HACU) in frontal cortex and hippocampus as measured in synaptosomes from treated rats. MAP given to pentobarbital-narcotized rats restored HACU activity to nonanesthetized levels, but this restorative effect of MAP was blocked by SCH 23390 or raclopride. These data suggest that in addition to a cholinergic mechanism, the Analeptic effect of MAP involves the dopamine system. alpha-Methyl-p-tyrosine, but not reserpine, pretreatment completely blocked the MAP Analeptic response. In reserpinzed rats, MAP produced a markedly enhanced Analeptic response. Studies of the effects of repeated administration of MAP on its Analeptic activity were also undertaken in view of the well known sensitization to the locomotor and stereotypic effects of the amphetamines that occur with repeated intermittent administration. Rats pretreated daily with MAP (5 mg/kg) for 5 or 12 days showed neither tolerance nor sensitization to the Analeptic effect of subsequent MAP administrations. 3H-quinuclidinyl benzilate-binding studies also showed no changes in muscarinic binding characteristics of membranes prepared from cortex or hippocampus of rats pretreated chronically with MAP. These and our earlier studies suggest that the Analeptic effect of MAP is mediated via a dopaminergic-cholinergic mechanism.

  • D-1 Agonist, SKF 38393, but not a D-2 agonist, produces a cholinergically mediated Analeptic effect in rabbits
    Pharmacology biochemistry and behavior, 1991
    Co-Authors: Akira Horita, M.a. Carino
    Abstract:

    Abstract SKF 38393 (2–15 mg/kg, IV), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rabbits. This effect was blocked by atropine (2–5 mg/kg, IV), but not by atropine methylbromide, suggesting that a central cholinergic mechanism was involved. The Analeptic effect was also blocked by SCH 23390 (0.1 mg/kg, IV) or raclopride (5 mg/kg, IV). These results indicate that SKF 38393 activates central cholinergic neurons, which in turn initiate the Analeptic effect. However, the fact that raclopride also blocked the SKF 38393 Analeptic effect, but quinpirole did not exert any Analeptic effect, suggests that a D-1/D-2 modulation of cholinergic systems may be involved in the SKF 38393-induced Analeptic effect. These results also support our earlier findings and view that cocaine-induced Analeptic activity is mediated by a dopaminergic cholinergic mechanism.

  • D1 agonist SKF 38393 antagonizes pentobarbital-induced narcosis and depression of hippocampal and cortical cholinergic activity in rats.
    Life sciences, 1991
    Co-Authors: Akira Horita, M.a. Carino, Y. Nishimura
    Abstract:

    SKF 38393 (5 mg/kg), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rats. This effect was blocked by atropine (2 mg/kg), but not by atropine methylbromide, suggesting involvement of central cholinergic mechanisms. The Analeptic effect was also blocked by SCH 23390 (0.2 mg/kg) or raclopride (2 mg/kg). SKF 38393 also increased sodium dependent high affinity choline uptake (HACU) in cortical and hippocampal synaptosomes that had been depressed by pentobarbital. SCH 23390 or raclopride prevented the SKF 38393 reversal of the depressed HACU, indicating that both D1 and D2 mechanisms were involved mediating the Analeptic effect. These results provide neurochemical evidence that cortical and hippocampal D1-mediated cholinergic activation results in a behavioral arousal (Analeptic) response. They also suggest that DA mechanisms may be involved in regulation of cortical and hippocampal cholinergic neurons.

Patricia M Hinkle – One of the best experts on this subject based on the ideXlab platform.

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides.
    Brain research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH(2) (EEP), pGlu-Val-Pro-NH(2) (Val(2)-TRH), Leu(2)-TRH, Phe(2)-TRH and Tyr(2)-TRH has recently been discovered. TRH (pGlu-His-Pro-NH(2)) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val(2)-TRH and Leu(2)-TRH were Analeptics, like TRH, but Phe(2)-TRH and Tyr(2)-TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC(50) values of TRH-like peptides for displacement of [3H]TRH from TRHR2 were TRH

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides
    Brain Research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    Abstract A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH 2 (EEP), pGlu-Val-Pro-NH 2 (Val 2 -TRH), Leu 2 -TRH, Phe 2 -TRH and Tyr 2 -TRH has recently been discovered. TRH (pGlu-His-Pro-NH 2 ) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val 2 -TRH and Leu 2 -TRH were Analeptics, like TRH, but Phe 2 -TRH and Tyr 2 -TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC 50 values of TRH-like peptides for displacement of [ 3 H]TRH from TRHR2 were TRH⋘(Leu 2 -, Phe 2 -TRH) 2 -, Ser 2 -TRH)≪(Val 2 -, Tyr 2 -, Arg 2 -, Thr 2 -, and Glu 2 -TRH). The IC 50 for Leu 2 -TRH was about 100 times that for TRH. When tested at the calculated IC 50 values, TRH-like peptides stimulated calcium responses in cells expressing TRHR1 and TRHR2, indicating that the peptides act as weak agonists at both receptors. These results indicate that TRHR1 and TRHR2 do not mediate the behavioral effects of TRH-like peptides.

Akira Horita – One of the best experts on this subject based on the ideXlab platform.

  • The Analeptic effect of methamphetamine in pentobarbital-narcotized rats is mediated via a dopaminergic-cholinergic mechanism.
    The Journal of pharmacology and experimental therapeutics, 1994
    Co-Authors: Akira Horita, M.a. Carino, Y Ukai
    Abstract:

    Methamphetamine (MAP) administered in doses of 0.5 to 5 mg/kg i.p. to rats anesthetized with pentobarbital produced a shortening of the duration of loss of righting reflex. This Analeptic effect of MAP was blocked by atropine but not by atropine methylbromide, indicating the central cholinergic nature of the response. This effect was also blocked by the D1 and D2 dopamine antagonists SCH 23390 (0.2 mg/kg) and raclopride (2 mg/kg), respectively. Pentobarbital decreased sodium-dependent high-affinity choline uptake (HACU) in frontal cortex and hippocampus as measured in synaptosomes from treated rats. MAP given to pentobarbital-narcotized rats restored HACU activity to nonanesthetized levels, but this restorative effect of MAP was blocked by SCH 23390 or raclopride. These data suggest that in addition to a cholinergic mechanism, the Analeptic effect of MAP involves the dopamine system. alpha-Methyl-p-tyrosine, but not reserpine, pretreatment completely blocked the MAP Analeptic response. In reserpinzed rats, MAP produced a markedly enhanced Analeptic response. Studies of the effects of repeated administration of MAP on its Analeptic activity were also undertaken in view of the well known sensitization to the locomotor and stereotypic effects of the amphetamines that occur with repeated intermittent administration. Rats pretreated daily with MAP (5 mg/kg) for 5 or 12 days showed neither tolerance nor sensitization to the Analeptic effect of subsequent MAP administrations. 3H-quinuclidinyl benzilate-binding studies also showed no changes in muscarinic binding characteristics of membranes prepared from cortex or hippocampus of rats pretreated chronically with MAP. These and our earlier studies suggest that the Analeptic effect of MAP is mediated via a dopaminergic-cholinergic mechanism.

  • D-1 Agonist, SKF 38393, but not a D-2 agonist, produces a cholinergically mediated Analeptic effect in rabbits
    Pharmacology biochemistry and behavior, 1991
    Co-Authors: Akira Horita, M.a. Carino
    Abstract:

    Abstract SKF 38393 (2–15 mg/kg, IV), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rabbits. This effect was blocked by atropine (2–5 mg/kg, IV), but not by atropine methylbromide, suggesting that a central cholinergic mechanism was involved. The Analeptic effect was also blocked by SCH 23390 (0.1 mg/kg, IV) or raclopride (5 mg/kg, IV). These results indicate that SKF 38393 activates central cholinergic neurons, which in turn initiate the Analeptic effect. However, the fact that raclopride also blocked the SKF 38393 Analeptic effect, but quinpirole did not exert any Analeptic effect, suggests that a D-1/D-2 modulation of cholinergic systems may be involved in the SKF 38393-induced Analeptic effect. These results also support our earlier findings and view that cocaine-induced Analeptic activity is mediated by a dopaminergic cholinergic mechanism.

  • D1 agonist SKF 38393 antagonizes pentobarbital-induced narcosis and depression of hippocampal and cortical cholinergic activity in rats.
    Life sciences, 1991
    Co-Authors: Akira Horita, M.a. Carino, Y. Nishimura
    Abstract:

    SKF 38393 (5 mg/kg), but not quinpirole, shortened the duration of loss of righting reflex produced in pentobarbital-narcotized rats. This effect was blocked by atropine (2 mg/kg), but not by atropine methylbromide, suggesting involvement of central cholinergic mechanisms. The Analeptic effect was also blocked by SCH 23390 (0.2 mg/kg) or raclopride (2 mg/kg). SKF 38393 also increased sodium dependent high affinity choline uptake (HACU) in cortical and hippocampal synaptosomes that had been depressed by pentobarbital. SCH 23390 or raclopride prevented the SKF 38393 reversal of the depressed HACU, indicating that both D1 and D2 mechanisms were involved mediating the Analeptic effect. These results provide neurochemical evidence that cortical and hippocampal D1-mediated cholinergic activation results in a behavioral arousal (Analeptic) response. They also suggest that DA mechanisms may be involved in regulation of cortical and hippocampal cholinergic neurons.

Shayani Senanayaki – One of the best experts on this subject based on the ideXlab platform.

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides.
    Brain research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH(2) (EEP), pGlu-Val-Pro-NH(2) (Val(2)-TRH), Leu(2)-TRH, Phe(2)-TRH and Tyr(2)-TRH has recently been discovered. TRH (pGlu-His-Pro-NH(2)) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val(2)-TRH and Leu(2)-TRH were Analeptics, like TRH, but Phe(2)-TRH and Tyr(2)-TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC(50) values of TRH-like peptides for displacement of [3H]TRH from TRHR2 were TRH

  • Role of TRH receptors as possible mediators of Analeptic actions of TRH-like peptides
    Brain Research, 2002
    Co-Authors: Patricia M Hinkle, A Eugene Pekary, Shayani Senanayaki, Albert Sattin
    Abstract:

    Abstract A large family of TRH-like peptides in the limbic region of rat brain including pGlu-Glu-Pro-NH 2 (EEP), pGlu-Val-Pro-NH 2 (Val 2 -TRH), Leu 2 -TRH, Phe 2 -TRH and Tyr 2 -TRH has recently been discovered. TRH (pGlu-His-Pro-NH 2 ) has antidepressant, neuroprotective, Analeptic, anticonvulsant, antiamnesic and euphoric properties, and other TRH-like peptides such as EEP exert several of these effects. A new TRH receptor (TRHR2) has been reported which is highly expressed in regions of rat brain that regulate attention and learning, arousal, sleep and processing of sensory information. The TRHR1 predominates in limbic structures involved in regulation of mood and in pituitary. This study examined the possibility that some of the newly discovered TRH-like peptides bind with high affinity to TRHR2, and that this receptor acts as the transducer for some of the CNS effects of this new class of neuropeptides. EEP, Val 2 -TRH and Leu 2 -TRH were Analeptics, like TRH, but Phe 2 -TRH and Tyr 2 -TRH were not. The affinity and efficacy of TRH-like peptides for TRHR1 and TRHR2 were measured in HEK293 cells stably expressing these receptors. The IC 50 values of TRH-like peptides for displacement of [ 3 H]TRH from TRHR2 were TRH⋘(Leu 2 -, Phe 2 -TRH) 2 -, Ser 2 -TRH)≪(Val 2 -, Tyr 2 -, Arg 2 -, Thr 2 -, and Glu 2 -TRH). The IC 50 for Leu 2 -TRH was about 100 times that for TRH. When tested at the calculated IC 50 values, TRH-like peptides stimulated calcium responses in cells expressing TRHR1 and TRHR2, indicating that the peptides act as weak agonists at both receptors. These results indicate that TRHR1 and TRHR2 do not mediate the behavioral effects of TRH-like peptides.