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Would the loss of striatal neurons result in higher or lower GABA levels? 

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This secondary change in striatal GABA function is likely to contribute to the basal ganglia dysfunction produced by the striatal dopamine loss and thus may be related to certain aspects of parkinsonian symptomatology.
We conclude that GABA has a depolarizing effect on striatal cells.
These findings provide further support for direct inhibition of DA release by GABA receptors and reveal that striatal GABA operates a tonic inhibition on DA output that could critically influence striatal output.
The combination of GABA neuron loss and alterations in remaining GABA neurons provides likely, though still unproven, substrates for the epileptic state.
The present results show for the first time that the major four subpopulations of striatal neurons express GABABR1 receptor and may have a functional implication in the GABA neurotransmission in the microcircuitry of the neostriatum.
These results strongly suggest that 2 different GABA release mechanisms exist in striatal neurons.
The presence of GAD within these terminals is consistent with results of other investigations which have indicated that the striatopallidal and striatoentopeduncular pathways as well as neostriatal local circuit neurons and/or collaterals from neostriatal projection neurons, use GABA as a neurotransmitter.

Related Questions

Does GABA act as an excitatory neurotransmitter due to the high concentration of intracellular chloride in immature neurons?4 answersGABA can act as an excitatory neurotransmitter in immature neurons due to the high concentration of intracellular chloride. The depolarizing effect of GABA is mainly attributed to the high intracellular chloride levels in immature neurons, which result from the expression of chloride transporter proteins. This high intracellular chloride concentration leads to depolarizing GABAergic responses, although they are not necessarily excitatory and can also contribute to shunting inhibition. The balance between excitatory and inhibitory GABAergic responses depends on the relation between GABA reversal potential and action potential threshold, as well as other factors such as spatial confounds or voltage-dependent currents. The impact of glutamatergic co-stimulation on GABA-induced chloride fluxes can enhance or attenuate the depolarizing effect of GABA, depending on the conductance, decay kinetics, and localization of the glutamatergic inputs. These findings highlight the functional significance of neuronal chloride microdomains in modifying the impact of GABAergic inputs.
What happens to the levels of different neurotransmitters like glutamate, dopamine, gaba in schizophrenic brain?4 answersThe levels of different neurotransmitters in the schizophrenic brain are altered. Dopamine, glutamate, and gamma-aminobutyric acid (GABA) have been implicated in the pathophysiology of schizophrenia. Patients with schizophrenia have shown marked changes in dopamine receptor and neurotransmitter levels in specific brain areas, and drugs targeting dopamine receptors have been successful in reducing symptoms. Glutamate, specifically affecting NMDA receptors, has also been implicated in schizophrenia, as it can cause positive and negative symptoms associated with the disorder. GABA, when tampered with, has been shown to induce schizophrenic symptoms, and it is believed to work in conjunction with the glutamate model. In addition to dopamine, serotonin, glutamate, GABA, and norepinephrine have also been found to play a role in the pathophysiology of schizophrenia. The substantia nigra, a dopaminergic nucleus in the brain, receives glutamatergic and GABAergic inputs that regulate dopaminergic neuronal activity, and dysregulation of the substantia nigra may contribute to the increased dopamine levels observed in the striatum of patients with schizophrenia.
How do GABA and glutamate levels change after brain damage?5 answersGABA and glutamate levels change after brain damage. Traumatic brain injury (TBI) leads to an imbalance of cortical excitation and inhibition, with changes in neurotransmitter concentrations and receptor populations. Poststroke, patients show lower GABA levels in the primary motor cortex, which may contribute to motor impairment. Imbalances in GABA and glutamate homeostasis have been linked to brain disorders such as epilepsy, Alzheimer's, Parkinson's, and MS, suggesting dysregulation of GABAergic/glutamatergic neurotransmission. Activation of the GABAergic system, either directly by GABA or indirectly through GABA aminotransferase inhibition, has shown neuroprotective effects against cerebral ischemia and reperfusion-induced damage.
How 5-ht6 affects Striatal GABA interneurons?5 answersActivation of 5-HT6 receptors affects striatal GABA interneurons. Increased expression of 5-HT6 receptors in indirect pathway medium spiny neurons (iMSNs) of the nucleus accumbens shell reduces the amount of cocaine self-administered and increases the time to the first response and the length of the inter-infusion interval. Selective 5-HT6 antagonists reduce the length of primary cilia in wild-type neurons, suggesting that blocking 5-HT6 receptor activity reduces cilia length. Additionally, 5-HT6 receptors in iMSNs of the dorsomedial striatum (DMS) modulate striatal dopamine dynamics during operant learning, and pharmacological stabilization of dopamine suppresses the effects of LTSI inhibition on learning. Furthermore, 5-HT6 receptor overexpression in indirect pathway MSNs of the DLS facilitates behavioral flexibility in rats overtrained on a repetitive pressing task. These findings suggest that 5-HT6 receptors play a role in modulating the activity of striatal GABA interneurons and have implications for drug addiction and cognitive processes.
For what conditions are GABA concentrations assessed in research?3 answersGABA concentrations are assessed in research for various neurologic and psychiatric conditions, including epilepsy, mood disorders, motor disorders such as focal dystonia and stiff-person syndrome, sleep disorders, neuroplasticity, and drug and alcohol dependence. Additionally, GABA concentrations have been studied as a potential biomarker for Post-Traumatic Stress Disorder (PTSD) severity. In the presence of demyelinating disease, such as multiple sclerosis, regional GABA levels have been investigated in relation to microstructural damage, motor and cognitive performance, and local microstructural integrity. Furthermore, GABA concentrations have been studied in the context of lactic acid bacteria production and determination methods. Finally, GABA concentrations have been examined in microdialysis studies to investigate exocytotic release and the presence of GABA type B (GABA(B)) autoreceptors.
What is the relationship between GABRA2 and GABA levels?1 answersGABRA2, a gene that encodes the alpha-2 subunit of the GABA-A receptor, has been found to be associated with alcohol dependence and externalizing behavior. The GABA-A receptor is believed to mediate some of the physiological and behavioral actions of ethanol. Additionally, plasma GABA levels have been found to be decreased in some patients with depression, mania, and alcoholism. Medications that increase plasma GABA have been shown to improve symptoms of mood disorders and decrease aggression. Furthermore, elevation of brain GABA levels by GABA-T inhibition is accompanied by changes in polyamine metabolism, suggesting a regulatory interaction between GABA and polyamine metabolism. Overall, these findings suggest a relationship between GABRA2 and GABA levels, with implications for alcohol dependence, externalizing behavior, mood disorders, and aggression.

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