CHAPTER 2 – ANIMAL MODELS
5. Animal models:
5.a. Neurotoxic Models:
5.a.1. 6- Hydroxydopamine model:
One of the most frequently used toxin-based animal model is 6-OHDA. It was first isolated in 1950. It is frequently used in rats. It shows affinity for catecholaminergic transporter. For example, norepinephrine transporter and dopamine transporter. Though the structure of 6-OHDA is similar to dopamine but the existence of excess amount of hydroxyl group makes it toxic to dopaminergic neurons. Catecholaminergic neurons are damaged by a combined effect of 6-OHDA, ROS and quinones. This effect leads inflammation in the brain which exists over time. All the features of Parkinson Disease are not mimic by this model. Reduced amount of dopamine, …show more content…
It is a neurotoxin found in tropical plant. It can be administered by using a variety of routes however the chronic publicity to this neurotoxin through intravenously, even at low doses, reasons degeneration of neurons in nigrostriatal location along with the aggregation of alpha-synuclein, formation of Lewy like body. These results result in the change of motor motion which is one of the most important elements of this disease. We know long-term imposition of rotenone (Rot) to Lewis rats reproduces many symptoms of Parkinson disease. Rot (3 mg/kg/day) was once placing subcutaneously to male Lewis rats for 6 days for the utilization of Alzet minipumps. Control rats obtained the auto only. If we found 0.1% bovine serum albumin for the period of the isolation approach truly remove rotenone sure to the mitochondria. Therefore, every effective change that is observed have been aftereffects of rotenone toxicity in vivo. In Rot rat intelligence mitochondria (Rot-RBM) there was once a 35-40% inhibition of respiration in State 3 and State 3U with the Complex of I (Co-I) substrates and succinate. It was found that Rot did not have any influence on the State 4Δψ of RBM and which is present in the rat liver mitochondria (RLM). However, Rot-RBM required two cases which means a good deal much less Ca2+ to provoke the permeability transition (mPT). There was present a 2-fold expand in the Formula or H2O2 generation in Rot-RBM which oxidizing …show more content…
Not only atypical but also typical antipsychotic causes drug induced parkinsonism. Typical antipsychotics include chlorpromazine, promazine, fluphenazine, pimozide gives drug induced parkinsonism. Typical antipsychotics show their effect on the dopamine receptors that are widely distributed in the stratum of the brain. For this reason, all the patients who are taking drugs of this class may have a risk for developing Parkinson. Atypical antipsychotic such as Risperidone causes parkinsonism as it binds to D2 receptors in a dose dependent
5. Animal models:
5.a. Neurotoxic Models:
5.a.1. 6- Hydroxydopamine model:
One of the most frequently used toxin-based animal model is 6-OHDA. It was first isolated in 1950. It is frequently used in rats. It shows affinity for catecholaminergic transporter. For example, norepinephrine transporter and dopamine transporter. Though the structure of 6-OHDA is similar to dopamine but the existence of excess amount of hydroxyl group makes it toxic to dopaminergic neurons. Catecholaminergic neurons are damaged by a combined effect of 6-OHDA, ROS and quinones. This effect leads inflammation in the brain which exists over time. All the features of Parkinson Disease are not mimic by this model. Reduced amount of dopamine, …show more content…
It is a neurotoxin found in tropical plant. It can be administered by using a variety of routes however the chronic publicity to this neurotoxin through intravenously, even at low doses, reasons degeneration of neurons in nigrostriatal location along with the aggregation of alpha-synuclein, formation of Lewy like body. These results result in the change of motor motion which is one of the most important elements of this disease. We know long-term imposition of rotenone (Rot) to Lewis rats reproduces many symptoms of Parkinson disease. Rot (3 mg/kg/day) was once placing subcutaneously to male Lewis rats for 6 days for the utilization of Alzet minipumps. Control rats obtained the auto only. If we found 0.1% bovine serum albumin for the period of the isolation approach truly remove rotenone sure to the mitochondria. Therefore, every effective change that is observed have been aftereffects of rotenone toxicity in vivo. In Rot rat intelligence mitochondria (Rot-RBM) there was once a 35-40% inhibition of respiration in State 3 and State 3U with the Complex of I (Co-I) substrates and succinate. It was found that Rot did not have any influence on the State 4Δψ of RBM and which is present in the rat liver mitochondria (RLM). However, Rot-RBM required two cases which means a good deal much less Ca2+ to provoke the permeability transition (mPT). There was present a 2-fold expand in the Formula or H2O2 generation in Rot-RBM which oxidizing …show more content…
Not only atypical but also typical antipsychotic causes drug induced parkinsonism. Typical antipsychotics include chlorpromazine, promazine, fluphenazine, pimozide gives drug induced parkinsonism. Typical antipsychotics show their effect on the dopamine receptors that are widely distributed in the stratum of the brain. For this reason, all the patients who are taking drugs of this class may have a risk for developing Parkinson. Atypical antipsychotic such as Risperidone causes parkinsonism as it binds to D2 receptors in a dose dependent