We thank Etiévant et al. (
1
) for their comments and the opportunity to discuss our data. In response, we should
first consider some of the concepts involving deep brain stimulation (DBS) at high
frequencies (e.g., >100 Hz). One of the mechanisms commonly described is a depolarization
block. This mechanism is characterized by a state in which cells undergo depolarization
with an almost complete abolishment of spontaneous action potentials (functional inactivation)
(
2
). In addition, DBS excites fiber pathways in the vicinity of the electrodes (efferent
and afferent projections from and to the targeted region as well as fibers en passant)
(
2
,
3
); this is important, as the anterograde and retrograde propagation of action potentials
may influence the functioning of brain regions projecting to or receiving projections
from the stimulated site. Finally, DBS has been shown to modulate activity of glial
cells and induce plastic changes, such as long-term potentiation, increases in neurotrophin
levels, and neurogenesis (
3
,
4
,
5
,
6
). In contrast to the complexity of the above-described mechanisms, optogenetics,
which is often delivered for short periods of time at much lower frequencies, is a
very clean technique that allows the precise distinction of the neural elements involved
in mechanisms of behavioral and physiologic processes.To read this article in full you will need to make a payment
Purchase one-time access:
Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online accessOne-time access price info
- For academic or personal research use, select 'Academic and Personal'
- For corporate R&D use, select 'Corporate R&D Professionals'
Subscribe:
Subscribe to Biological PsychiatryAlready a print subscriber? Claim online access
Already an online subscriber? Sign in
Register: Create an account
Institutional Access: Sign in to ScienceDirect
References
- Deep brain stimulation for depression: Is it a gray or white “matter”?.Biol Psychiatry. 2016; 80: e43-e44
- Deep brain stimulation: More complex than the inhibition of cells and excitation of fibers.Neuroscientist. 2016; 22: 332-345
- Deep brain stimulation for psychiatric disease: Contributions and validity of animal models.Sci Transl Med. 2012; 4 (142rv148)
- Neuroplasticity-dependent and -independent mechanisms of chronic deep brain stimulation in stressed rats.Transl Psychiatry. 2015; 5: e674
- Deep brain stimulation reverses anhedonic-like behavior in a chronic model of depression: Role of serotonin and brain derived neurotrophic factor.Biol Psychiatry. 2012; 71: 30-35
- Preclinical studies modeling deep brain stimulation for depression.Biol Psychiatry. 2012; 72: 916-923
- Antidepressant-like effects of medial prefrontal cortex deep brain stimulation in rats.Biol Psychiatry. 2010; 67: 117-124
- Antidepressant effect of optogenetic stimulation of the medial prefrontal cortex.J Neurosci. 2010; 30: 16082-16090
- Prolonged survival of axons terminating within lesions of cat visual cortex.Neurosci Lett. 2001; 311: 66-68
Article info
Publication history
Published online: January 26, 2016
Identification
Copyright
© Society of Biological Psychiatry, 2016.
ScienceDirect
Access this article on ScienceDirectLinked Article
- Deep Brain Stimulation for Depression: Is It a Gray or White “Matter”?Biological PsychiatryVol. 80Issue 6
- PreviewDeep brain stimulation (DBS) within the subcallosal cingulate gyrus was shown to impressively improve depressive symptoms in patients with refractory depression (1). Despite these exciting results, the neurobiological bases underlying the therapeutic action of DBS remain largely unknown. Based on its anatomic connections and cytoarchitectural features, the rodent ventromedial prefrontal cortex (vmPFC) is considered as the equivalent of the subcallosal cingulate gyrus in humans. Hence, in their article in Biological Psychiatry, Hamani et al.
- Full-Text
- Preview
- ErratumBiological PsychiatryVol. 80Issue 6
- PreviewErratum to: “Reply to: Deep Brain Stimulation for Depression: Is It a Gray or White “Matter”?” by Clement Hamani and José N. Nobrega (Biol Psychiatry corrected article-in-press, available online Jan 26, 2016). This article is being corrected between the corrected proof and final print version stages of publication. It came to the authors’ attention that the last four sentences of the article needed to be altered to correct a misunderstanding of the prior literature. The original text and corrected text are both provided here for clarity.
- Full-Text
- Preview