Amphetamine stimulates movement through thalamocortical glutamate release

Abstract

The ventrolateral thalamus (VL) is a primary relay point between the basal ganglia and the primary motor cortex (M1). Using dual probe microdialysis and locomotor behavior monitoring, we investigated the contribution of VL input into M1 during amphetamine (AMPH)-stimulated monoamine release and hyperlocomotion in rats. Tetrodotoxin (TTX) (10 uM) perfusion into the VL significantly lowered hyperactivity induced by AMPH (1 mg/kg i.p.). This behavioral response corresponded to reduced cortical glutamate and monoamine release. To determine which glutamate receptors the thalamocortical projections acted upon, we perfused either the AMPA/kainate receptor antagonist NBQX (10 μM) or the NMDA receptor antagonist (MK-801) intracortically followed by systemic AMPH. The results show that AMPA/kainate, and to a lesser extent NMDA receptors, mediated the observed effects. Since glutamate-monoamine interactions could possibly occur through local or circuit-based mechanisms, we isolated and perfused M1 tissue ex vivo to determine the extent of local glutamate-dopamine interactions. Taken together, these results demonstrate that AMPH generates hyperlocomotive states via thalamocortical signaling and that cortical AMPA receptors are an important mediator of these effects.

Low-frequency stimulation of the pedunculopontine nucleus affects gait and the neurotransmitter level in the ventrolateral thalamic nucleus in 6-OHDA Parkinsonian rats

“…In the present work, a significant decrease in ACh concentration was observed in the lesioned animals, which may potentially resulted from DA depletion as suggested in other studies [23]. Indeed, the thalamus receives a variety of neurochemical inputs, including DA, Ach and NA inputs [24].…”

PKCβ Inhibitors Attenuate Amphetamine-Stimulated Dopamine Efflux

“…50,51 Webcams were connected via USB ports to analysis PCs running Matlab 2009 (Mathworks, Natick, MA, USA) software. Using the image acquisition toolbox in Matlab, data were collected via a custom designed motion monitoring program (Mark Dow, University of Oregon).…”

Neonatal propofol anesthesia modifies activity‐dependent processes and induces transient hyperlocomotor response to d‐amphetamine during adolescence in rats

“…in the dose of 1.5 mg/kg. The drug was chosen to test the integrity of cortico–striato–thalamo–cortical loops, considering novel data about the importance of thalamocortical signaling for amphetamine‐induced motor activity (Mabrouk et al, 2014).…”

“…We have also examined TrkB as mBDNF receptor and synaptophysin, GAP‐43 and drebrin as well known markers of synaptic plasticity. In order to establish whether transient propofol treatment have a long‐term consequences on the integrity of cortico‐subcortical circuits, and to what extent these changes remain, we assessed psychomotor response of adolescent and adult animals (propofol pretreated at P7) to d ‐amphetamine as a challenge, considering the importance of thalamocortical signaling for amphetamine‐induced motor activity (Mabrouk et al, 2014).…”