High frequency stimulation of the subthalamic nucleus improves treadmill locomotion in unilateral 6-hydroxydopamine lesioned rats

Chang, Jing‐Yu; Shi, Lihong; Luo, Fei; Woodward, Donald J.

doi:10.1016/s0006-8993(03)03053-1

Cited by 65 publications

(58 citation statements)

References 61 publications

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“…In most DBS experiments (both clinical and preclinical), many parameters are fixed and uniform across studies. We used alternating current with biphasic symmetrical pulses (60 s pulse width and a 160 Hz frequency), parameters that are consistent with previous work in this field (Chang et al, 2003;Mayberg et al, 2005). Stimulation intensities, in contrast, are often varied within and between studies, usually in the range of 50 -200 A (Benazzouz and Hallett, 2000;Chang et al, 2003;Mayberg et al, 2005).…”

Section: Animals and Housing Male Sprague Dawley Rats (Rattus Norvegmentioning

confidence: 83%

“…We used alternating current with biphasic symmetrical pulses (60 s pulse width and a 160 Hz frequency), parameters that are consistent with previous work in this field (Chang et al, 2003;Mayberg et al, 2005). Stimulation intensities, in contrast, are often varied within and between studies, usually in the range of 50 -200 A (Benazzouz and Hallett, 2000;Chang et al, 2003;Mayberg et al, 2005). We previously reported that 150 A of current is an effective stimulation intensity in our reinstatement paradigm (Vassoler et al, 2008).…”

Section: Animals and Housing Male Sprague Dawley Rats (Rattus Norvegmentioning

confidence: 83%

“…Moreover, optogenetic inhibition of the prelimbic cortex or accumbens core impaired the reinstatement of cocaine seeking (Stefanik et al, 2013). The reinstatement of cocaine seeking also is associated with increased glutamate release in the accumbens core (McFarland et al, 2003) and enhanced surface expression of GluA2-lacking AMPA receptors in the core (Conrad et al, 2008;McCutcheon et al, 2011). Importantly, attenuation of AMPA-mediated transmission in the core attenuated the reinstatement of cocaine seeking (Conrad et al, 2008;.…”

Section: Mechanism Of Dbsmentioning

confidence: 99%

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Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Reinstatement through Local and Antidromic Activation

et al. 2013

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Accumbal deep brain stimulation (DBS) is a promising therapeutic modality for the treatment of addiction. Here, we demonstrate that DBS in the nucleus accumbens shell, but not the core, attenuates cocaine priming-induced reinstatement of drug seeking, an animal model of relapse, in male Sprague Dawley rats. Next, we compared DBS of the shell with pharmacological inactivation. Results indicated that inactivation using reagents that influenced (lidocaine) or spared (GABA receptor agonists) fibers of passage blocked cocaine reinstatement when administered into the core but not the shell. It seems unlikely, therefore, that intrashell DBS influences cocaine reinstatement by inactivating this nucleus or the fibers coursing through it. To examine potential circuit-wide changes, c-Fos immunohistochemistry was used to examine neuronal activation following DBS of the nucleus accumbens shell. Intrashell DBS increased c-Fos induction at the site of stimulation as well as in the infralimbic cortex, but had no effect on the dorsal striatum, prelimbic cortex, or ventral pallidum. Recent evidence indicates that accumbens DBS antidromically stimulates axon terminals, which ultimately activates GABAergic interneurons in cortical areas that send afferents to the shell. To test this hypothesis, GABA receptor agonists (baclofen/ muscimol) were microinjected into the anterior cingulate, and prelimbic or infralimbic cortices before cocaine reinstatement. Pharmacological inactivation of all three medial prefrontal cortical subregions attenuated the reinstatement of cocaine seeking. These results are consistent with DBS of the accumbens shell attenuating cocaine reinstatement via local activation and/or activation of GABAergic interneurons in the medial prefrontal cortex via antidromic stimulation of cortico-accumbal afferents.

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Section: Animals and Housing Male Sprague Dawley Rats (Rattus Norvegmentioning

confidence: 83%

Section: Animals and Housing Male Sprague Dawley Rats (Rattus Norvegmentioning

confidence: 83%

Section: Mechanism Of Dbsmentioning

confidence: 99%

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Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Reinstatement through Local and Antidromic Activation

et al. 2013

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“…A common DBS target in human OCD patients is the ventral anterior internal capsule Abelson et al, 2005;Greenberg et al, 2006); however, recently therapeutic responses have been achieved by targeting the NAc (Sturm et al, 2003;Aouizerate et al, 2005), supporting the validity of our stimulation target in the rat. Although difficult to precisely replicate human parameters, current intensities were modeled after the human literature, and in the range used effectively in animal models of Parkinson's disease (Chang et al, 2003;Degos et al, 2005). Moreover, these stimulation parameters produced profound effects on neuronal firing without observable tissue trauma.…”

Section: Discussionmentioning

confidence: 99%

“…An additional 5 min of baseline activity was then collected before recording with DBS-on for 30 min. The DBS parameters used (0.1-0.4 mA, 100 S pulse duration, 130 Hz) have been shown to be efficacious in rat Parkinson's models (Chang et al, 2003;Degos et al, 2005) and are reported to cause negligible trauma to the stimulated area. This DBS protocol produced no visible lesions in the NAc under 25ϫ light microscopy with cresyl violet staining.…”

Section: Methodsmentioning

confidence: 99%

High-Frequency Deep Brain Stimulation of the Nucleus Accumbens Region Suppresses Neuronal Activity and Selectively Modulates Afferent Drive in Rat Orbitofrontal CortexIn Vivo

McCracken

Grace²

2007

J. Neurosci.

178

131

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High-frequency deep-brain stimulation (DBS) of the nucleus accumbens (NAc) region is an effective therapeutic avenue for patients with treatment-resistant obsessive-compulsive disorder (OCD). Imaging studies suggest that DBS acts by suppressing the aberrant metabolism in the orbitofrontal cortex (OFC) that is a hallmark of OCD; however, little is known about the mechanisms by which this occurs. We examined the effects of 30 min NAc DBS at 130 Hz on spontaneously active OFC neurons and local field potentials (LFPs) in addition to evoked responses elicited by single-pulse stimulation of the NAc or mediodorsal thalamus (MD) in urethane-anesthetized rats. NAc DBS reduced the mean firing rate of OFC neurons, although neurons receiving monosynaptic input from MD were less affected and some putative interneurons were excited by DBS. Single-pulse stimulation of the NAc produced a robust inhibition in OFC neurons that was attenuated after DBS, whereas excitatory responses were unchanged. In contrast, after DBS inhibitory responses evoked from MD were unchanged, whereas excitatory responses were enhanced. NAc-evoked LFP responses were potentiated after DBS, whereas MD-evoked LFP responses were unchanged. NAc DBS also enhanced OFC spontaneous LFP oscillatory activity in the slow (0.5-4 Hz) frequency band. These results suggest that DBS of the NAc region may alleviate OCD symptoms by reducing activity in subsets of OFC neurons, potentially by driving recurrent inhibition though antidromic activation of corticostriatal axon collaterals. Moreover, selective potentiation of input to these inhibitory circuits may also contribute to the therapeutic effects produced by DBS in OCD patients.

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High‐frequency stimulation of the subthalamic nucleus restores neural and behavioral functions during reaction time task in a rat model of Parkinson's disease

Wang

Gao

et al. 2009

J of Neuroscience Research

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Deep brain stimulation (DBS) has been used in the clinic to treat Parkinson’s disease (PD) and other neuropsychiatric disorders. Our previous work has shown that DBS in the subthalamic nucleus (STN) can improve major motor deficits, and induce a variety of neural responses in rats with unilateral dopamine (DA) lesions. In the present study, we examined the effect of STN DBS on reaction time (RT) performance and parallel changes in neural activity in the cortico-basal ganglia regions of partially bilateral DA- lesioned rats. We recorded neural activity with a multiple-channel single-unit electrode system in the primary motor cortex (MI), the STN, and the substantia nigra pars reticulata (SNr) during RT test. RT performance was severely impaired following bilateral injection of 6-OHDA into the dorsolateral part of the striatum. In parallel with such behavioral impairments, the number of responsive neurons to different behavioral events was remarkably decreased after DA lesion. Bilateral STN DBS improved RT performance in 6-OHDA lesioned rats, and restored operational behavior-related neural responses in cortico-basal ganglia regions. These behavioral and electrophysiological effects of DBS lasted nearly an hour after DBS termination. These results demonstrate that a partial DA lesion-induced impairment of RT performance is associated with changes in neural activity in the cortico-basal ganglia circuit. Furthermore, STN DBS can reverse changes in behavior and neural activity caused by partial DA depletion. The observed long-lasting beneficial effect of STN DBS suggests the involvement of the mechanism of neural plasticity in modulating corticobasal ganglia circuits.

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High frequency stimulation of the subthalamic nucleus improves treadmill locomotion in unilateral 6-hydroxydopamine lesioned rats

Cited by 65 publications

References 61 publications

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Reinstatement through Local and Antidromic Activation

Deep Brain Stimulation of the Nucleus Accumbens Shell Attenuates Cocaine Reinstatement through Local and Antidromic Activation

High-Frequency Deep Brain Stimulation of the Nucleus Accumbens Region Suppresses Neuronal Activity and Selectively Modulates Afferent Drive in Rat Orbitofrontal CortexIn Vivo

High‐frequency stimulation of the subthalamic nucleus restores neural and behavioral functions during reaction time task in a rat model of Parkinson's disease

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