Pharmacological activation of the neurotensin receptor 1 abrogates the methamphetamine-induced striatal apoptosis in the mouse brain

  title={Pharmacological activation of the neurotensin receptor 1 abrogates the methamphetamine-induced striatal apoptosis in the mouse brain},
  author={Qingkun Liu and Ariela Hazan and Eddie Grinman and Jesus A. Angulo},
  journal={Brain Research},

Epigallocatechin Gallate Mitigates the Methamphetamine-Induced Striatal Dopamine Terminal Toxicity by Preventing Oxidative Stress in the Mouse Brain

EGCG is an effective agent that can be used to mitigate the METH-induced striatal toxicity in the mouse brain, and the reduction was prevented by EGCG pretreatment.

Long-Term Social Isolation Reduces Expression of the BDNF Precursor and Prolyl Endopeptidase in the Rat Brain.

It is found that after ten weeks of social isolation, male Wistar rats show behavioral abnormalities and cognitive deficit, accompanied by an increase in the relative expression of gene encoding serine protease prolyl endopeptidase (PREP) in the brain frontal cortex, and that neurotrophic factors and PREP are involved in the mechanisms of behavioral and cognitive impairments observed in the rats subjected to prolonged social isolation with an early life onset.

Green Tea Extract, Epigallocatechin Gallate, Protect Against Methamphetamine-Induced Striatal Neurotoxicity in Mice

The aim of this chapter is to clarify the aims and aims of the previous chapter and establish a procedure for systematic evaluation of their aims and objectives.



Neuropeptide Y Protects against Methamphetamine-Induced Neuronal Apoptosis in the Mouse Striatum

It is found that neuropeptide Y knock-out mice were more sensitive than wild-type mice to METH-induced neuronal apoptosis of both enkephalin- and nitric oxide synthase-containing neurons, suggesting that NPY plays a general neuroprotective role within the striatum.

Methamphetamine-induced neurotoxicity is attenuated in transgenic mice with a null mutation for interleukin-6.

The protective effects against METH toxicity observed in the IL-6-/- mice were not caused by differences in temperature elevation or in METH accumulation in wild-type and mutant animals, and support the proposition that IL- 6 may play an important role in the neurotoxicity of METH.

Methamphetamine induces striatal neurokinin‐1 receptor endocytosis primarily in somatostatin/NPY/NOS interneurons and the role of dopamine receptors in mice

Methamphetamine (METH) is a psychostimulant that induces long‐term deficits of dopamine terminal markers and apoptotic cell death in the striatum. Our laboratory demonstrated that pharmacological

Microdialysis assessment of methamphetamine-induced changes in extracellular neurotensin in the striatum and nucleus accumbens.

There was not a clear correlation observed between the METH effects on striatal NT tissue levels and extracellular NT concentration, and the role of DA D-1 and D-2 receptors in mediating these effects was determined by combining specific antagonists with the low dose of METH.

Further studies of the role of hyperthermia in methamphetamine neurotoxicity.

It was concluded that short- and long-term decreases in striatal DA levels depend on the degree of hyperthermia produced during METH exposure but cannot be produced byhyperthermia alone.

Methamphetamine-induced hyperthermia and dopaminergic neurotoxicity in mice: pharmacological profile of protective and nonprotective agents.

It is demonstrated that hyperthermia per se contributes to but is not solely responsible for the METH-induced neuropathology, and studies with reserpine, a compound which dramatically lowers core temperature, demonstrated that the hypothermic state produced in the reserpinized mice did not provide protection from Meth-induced toxicity.