Central muscarinic cholinergic antagonists block wet-dog shakes produced by the TRH analog MK-771 in the rat

Sills, Matthew A.; Mellow, Alan M.; Sunderland, Trey; Jacobowitz, David M.

doi:10.1016/0006-8993(88)90184-9

Cited by 6 publications

(2 citation statements)

References 14 publications

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“…Thus, the different time-course of the biochemical and behavioural effects and the lack of the latter during the increase in ACh output elicited by local TRH infusion indicate that the two effects are not simply related to each other. Although Sills et al (1988) reported that the wet-dog shaking caused in the rat by an analogue of TRH (MK-771) is blocked, in a noncompetitive manner, by atropine or scopolamine, other evidence indicates that the stereotyped behaviour and the locomotor effects elicited by TRH rely also on other neurotransmitter systems, particularly the dopaminergic system of the nucleus accumbens (Roth et al, 1976;Kalivas et al, 1987). In this respect, TRH stimulates the release of [3H]-dopamine from slices of rat nucleus accumbens but not nucleus caudate in vitro (Kerwin & Pycock, 1979); bilateral injections of TRH into the nucleus accumbens of rats increase locomotor activity and promote behavioural activities similar to those produced by activation of the dopaminergic system (Heal & Green, 1979;Heal et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Effect of thyrotropin releasing hormone (TRH) on acetylcholine release from different brain areas investigated by microdialysis

Giovannini

Casamenti

Nistri

et al. 1991

British J Pharmacology

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The effect of thyrotropin releasing hormone (TRH) administration upon acetylcholine (ACh) release in freely moving rats was investigated by means of transversal microdialysis coupled to h.p.l.c. TRH administered either s.c. or via local perfusion increased the ACh release from the cortex and hippocampus but not from the striatum. The increase in ACh release was maintained after 7 days of s.c. administration of TRH. 2 After s.c. injection of the neuropeptide, the increase in ACh release was dose-dependent and reached a maximum at 40{min after administration. The maximal percentage increases were 18, 52, 66 and 89% at doses of 1, 2.5, 5 and lOmgkg-' and 35, 48 and 54% at doses of 2.5, 5 and lOmgkg-' in the cortex and hippocampus, respectively. The effect of TRH was dependent on neuronal activity since it was completely inhibited by perfusion with tetrodotoxin (TTX), 5 x 10-7 M.3 Perfusion with TRH, 2.5 pgpul-1, caused 198% and 150% increase in ACh release 60 and 80min after the beginning of the perfusion in the cortex and hippocampus, respectively. After this initial peak, a 100% increase in ACh release persisted throughout the perfusion. 4 Systemic TRH administration was followed by marked hyperactivity and stereotyped behaviour that showed a time course shorter than that of the increase in ACh release. 5 These findings demonstrate that TRH exerts a strong stimulant action on cortical and hippocampal cholinergic pathways.

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Section: Discussionmentioning

confidence: 99%

Effect of thyrotropin releasing hormone (TRH) on acetylcholine release from different brain areas investigated by microdialysis

Giovannini

Casamenti

Nistri

et al. 1991

British J Pharmacology

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“…Second, the animal models of memory impairment can be used directly to test new drug therapies for eventual human use in treating memory disorders. For example, the modeling capacity of scopolamine has been extensively utilized over the past few years to demonstrate the potential usefulness of serotonergic (Altman et al, 1987;Costall et a1,1989;Normile & Altman, 1988), adrenergic (Quartermain & Leo, 1988;Stone et al, 1988), dopaminergic (Levin, 1988;Yamamoto et al, 1990), peptidergic (Itoh et al, 1988;Sills et al, 1988), opiate , nootropic (Piercey et al, 1987 ;Verloes et al, 1988), ergot alkaloid (Voronina et al, 1988 ), and steroid agents (Flood et al, 1988) in reversing, or at least attenuating, some of scopolamine's acute amnestic effects. While the cholinergic model of memory impairment with scopolamine is probably the best known example of pharmacological modeling in various species Bartus & Johnson, 1982), it is also well recognized that other neurotransmitter systems are involved in the memory process in animals (Haroutunian et al, 1986;Sidel, 1988;Vanderwolf, 1987).…”

Section: Discussionmentioning

confidence: 99%

A Strategy of “Combination Chemotherapy” in Alzheimer's Disease: Rationale and Preliminary Results with Physostigmine plus Deprenyl

Sunderland

Molchan

Lawlor

et al. 1992

Int. Psychogeriatr.

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Although the central cholinergic deficits are still considered to be of primary importance in Alzheimer's disease, there is great need for an expansion of the pharmacological approach in this illness beyond the simple cholinergic replacement hypothesis. This report focuses on the concept of “combination chemotherapy” in Alzheimer's disease as the next generation of therapeutic strategies. Based on earlier positive findings in Alzheimer patients with the monoamine oxidase B inhibitor, 1-deprenyl, the authors speculate that a combination of physostigmine, the short-acting cholinesterase inhibitor, and 1-deprenyl might be more beneficial than either agent alone. The authors outline a sample paradigm for such combination studies, report preliminary data on the first 16 Alzheimer subjects to have received an initial combination of physostigmine and deprenyl, and point to other possible “combination chemotherapy” strategies for future study.

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Effect of injection of thyrotropin-releasing hormone into nucleus accumbens on pain discharges in nucleus parafascicularis of the thalamus in rats

Nie

Liu

1991

Journal of Tongji Medical University

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Glass microelectrode recording method was used to investigate the effect of injection of thyrotropin-releasing hormone (TRH) into nucleus accumbens, nucleus amygdalae or nucleus caudatus on unit discharges from pain-excitation neurons (PEN) in nucleus parafascicularis of the thalamus in rats. The results showed that: 1) Injection of TRH into the nucleus accumbens resulted in a significant inhibition of pain discharges from PEN in nucleus parafascicularis, while injection of TRH into nucleus amygdalae, nucleus caudatus exerted no significant effect. 2) Pretreatment with atropine abolished the above-mentioned effect of TRH. 3) Pretreatment with haloperidol also abolished the above-mentioned inhibitory effect of TRH. 4) Pretreatment with naloxone, propranolol or phentolamine did not affect the inhibitory effect of TRH. These results suggested that nucleus accumbens might be a special area in response to TRH and the effect of TRH seems to be involved in both cholinergic M-receptor and dopaminergic receptor.

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Central muscarinic cholinergic antagonists block wet-dog shakes produced by the TRH analog MK-771 in the rat

Cited by 6 publications

References 14 publications

Effect of thyrotropin releasing hormone (TRH) on acetylcholine release from different brain areas investigated by microdialysis

Effect of thyrotropin releasing hormone (TRH) on acetylcholine release from different brain areas investigated by microdialysis

A Strategy of “Combination Chemotherapy” in Alzheimer's Disease: Rationale and Preliminary Results with Physostigmine plus Deprenyl

Effect of injection of thyrotropin-releasing hormone into nucleus accumbens on pain discharges in nucleus parafascicularis of the thalamus in rats

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