The effects of TRH analogues on cerebral ischaemia produced by middle cerebral artery occlusion in the rat

Shrewsbury-Gee, J.; Lye, R. H.; Latham, A.; Slater, P.

doi:10.1007/bf00248359

Cited by 15 publications

(2 citation statements)

References 49 publications

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“…For example, TRH has been shown to improve recovery after traumatic injuries to the cervical spine [92] and the brain [93]. It has also been reported that TRH analogs also provide significant beneficial effects against cerebral ischemia [94], [95]. TRH also provides neuroprotection against N-methyl-D-aspartate (NMDA)-induced cell death in rat hippocampal slices [96].…”

Section: Discussionmentioning

confidence: 99%

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

et al. 2009

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Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse.

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Section: Discussionmentioning

confidence: 99%

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

et al. 2009

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“…A large amount of experimental pharmacological data and clinical experience justify the conclusion that protirelin tartrate and its analogues [30] may have a possible beneficial action in the treatment of various central nervous system diseases [1, 9, 10, 12-15, 19, 25, 28, 31-33]. At least in part, our results appear to support the general trend in the international literature in favour of the use of protirelin tartrate in hyposthenie-spastic upper motoneuron syndrome due to hemispheric ischemia [ I, 9, I0, 15, 33].…”

Section: Discussionmentioning

confidence: 99%

Protirelin tartrate (TRH-T) in upper motoneuron syndrome: a controlled neurophysiological and clinical study

et al. 1994

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This randomised, single-blind, placebo-controlled study involved 20 patients with chronic upper motoneuron syndrome due to ischemic cerebrovascular lesions, selected in order to ensure the greatest possible homogeneity in terms of the severity of the syndrome. All of them were treated with protirelin tartrate 4 mg/die i.m. The study included semiquantitative clinical evaluations of neurological examinations, with particular attention being paid to weakness and spasticity. These were accompanied by neurophysiological evaluations (F-waves, magnetic motor evoked potentials). Extended biohumoral investigations of possible side effects were also carried out. The results indicate a slight but statistically significant absolute improvement in spasticity and muscular strength following protirelin tartrate, especially in the lower limbs; at the same time, the drug also proved to be capable as favourably modifying the response of the biceps femoris muscle to transcranial magnetic stimulation (reappearance, increased amplitude and a reduction in the threshold of motor evoked potentials). The drug was generally well tolerated.

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Central nervous system effects of thyrotropin-releasing hormone and its analogues: opportunities and perspectives for drug discovery and development

Prókai

2002

Progress in Drug Research

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The effects of TRH analogues on cerebral ischaemia produced by middle cerebral artery occlusion in the rat

Cited by 15 publications

References 49 publications

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

Protirelin tartrate (TRH-T) in upper motoneuron syndrome: a controlled neurophysiological and clinical study

Central nervous system effects of thyrotropin-releasing hormone and its analogues: opportunities and perspectives for drug discovery and development

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