Short communicationAmphetamine lowers extracellular GABA concentration in the ventral pallidum☆
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Ventral pallidum and alcohol addiction
2019, Neuroscience of Alcohol: Mechanisms and TreatmentThe ventral pallidum: Subregion-specific functional anatomy and roles in motivated behaviors
2015, Progress in NeurobiologyCitation Excerpt :The number of GABAergic synapses on VP neurons has been estimated to be greater than 80% (Zahm et al., 1985), most likely reflecting Acb and local GABAergic connections. Neurochemical studies have shown that the VP contains high concentrations of extracellular GABA (Bourdelais and Kalivas, 1990, 1992; Xi and Stein, 2000; Lawrence et al., 2003; Tang et al., 2005; Li et al., 2009; Wydra et al., 2013) and intense immunoreactivity for the GABA synthesizing enzyme, GAD (Oertel and Mugnaini, 1984; Margeta-Mitrovic et al., 1999). AcbSh and AcbC projections synapse onto both GABAergic and cholinergic VP cells (Grove et al., 1986; Zaborszky et al., 1991; Zaborszky and Cullinan, 1992).
The Physiological Basis of Brain Stimulation
2014, The Stimulated Brain: Cognitive Enhancement Using Non-Invasive Brain StimulationFormation and reverberation of sequential neural activity patterns evoked by sensory stimulation are enhanced during cortical desynchronization
2013, NeuronCitation Excerpt :For example, amphetamine-induced desynchronization is also accompanied by increased extracellular levels of neuromodulators, such as dopamine (Creese, 1983), which are implicated in the facilitation of memory consolidation in neocortex (Schicknick et al., 2012). Amphetamine also reduces extracellular gamma-aminobutyric acid (GABA) concentrations (Bourdelais and Kalivas, 1990) and stimulates glutamate release (Karler et al., 1994; Kelley and Throne, 1992). These mechanisms are believed to be responsible for enhanced cortical plasticity after amphetamine injection (Boroojerdi et al., 2001; Tegenthoff et al., 2004).
One day of motor training with amphetamine impairs motor recovery following spinal cord injury
2012, Experimental NeurologyCitation Excerpt :Although amphetamine is an indirect agonist of the monoamines: norepinephrine, dopamine, and serotonin (Seiden et al., 1993), studies have specifically implicated the noradrenergic system in mediating the enhancement of locomotor recovery following brain injury (Boyeson and Feeney, 1990; Feeney and Westerberg, 1990). It has been proposed that amphetamine may enhance activity or use-dependent plasticity by unmasking already existing circuitry, decreasing GABAergic inhibition (Bourdelais and Kalivas, 1990; Tegenthoff et al., 2004). However, the precise mechanisms underlying this enhancement of functional recovery remain to be elucidated.
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This research was supported in part by USPHS Grants MH-40817 and DA-03906.
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We would like to thank Yonas Habte for his care in making the dialysis probes, and Jenny Baylon for her assistance in preparing the manuscript.