How Adenosine Bridges Rapid Antidepressant Therapies: Insights from Ketamine and ECT Research - #36 - Nov 11, 2025

Speaker: 00:00:10

Welcome to the Neurostimulation podcast.

2

: 00:00:12

I'm Michael Passmore, clinical

Associate professor in the Department of

3

: 00:00:16

Psychiatry at the University of British

Columbia in beautiful Vancouver Canada.

4

: 00:00:21

The Neurostimulation podcast is

all about exploring the fascinating

5

: 00:00:25

world of neuroscience and in

particular clinical neurostimulation.

6

: 00:00:30

I'd like to also start to expand the scope

of this podcast to really end up being

7

: 00:00:35

an interventional mental health podcast.

8

: 00:00:38

So in addition to non-invasive clinical

neurostimulation, I'm going to start

9

: 00:00:43

expanding this into other areas such as

psychedelic assisted therapy, particularly

10

: 00:00:48

ketamine and other such interventional

mental health strategies to help improve

11

: 00:00:54

wellness functioning and quality of life.

12

: 00:00:58

What we're gonna do here is continue

to have discussions with leaders

13

: 00:01:02

in the field, both researchers,

clinicians, and other people that

14

: 00:01:06

have value to add in terms of helping

to share knowledge that will impact

15

: 00:01:12

people and help to improve lives.

16

: 00:01:14

We're gonna look at the latest research

breakthroughs, and most importantly,

17

: 00:01:18

how that research is being translated

into real world treatments that

18

: 00:01:22

can improve health and wellbeing.

19

: 00:01:24

So if you're a healthcare professional,

a student, a clinician, a researcher, a

20

: 00:01:30

person that's interested in helping to

improve mental health, or if you have

21

: 00:01:34

a friend or a relative that you think

might be interested and might benefit

22

: 00:01:38

from gaining some knowledge by listening

to or watching this podcast, I would

23

: 00:01:42

really encourage you to stay tuned and

also share the podcast with anyone that

24

: 00:01:47

you think might benefit from the content.

25

: 00:01:50

My mission here is to make the

science accessible, inspiring,

26

: 00:01:54

and relevant to your life.

27

: 00:01:56

I would also emphasize again that this

podcast is separate from my clinical and

28

: 00:02:00

academic roles but really is part of my

personal effort to bring neuroscience and

29

: 00:02:05

mental health education to the general

public, and so it's important to recognize

30

: 00:02:10

that the information shared here is for

educational purposes only, and is not

31

: 00:02:14

intended as medical advice or a substitute

for professional medical guidance.

32

: 00:02:19

So I really would encourage everyone to

consult with your individual healthcare

33

: 00:02:23

providers to discuss your specific

health needs and treatment options.

34

: 00:02:28

And so by listening to or watching

this podcast, it's implicit that

35

: 00:02:32

you acknowledge and agree that any

decisions related to your health are

36

: 00:02:35

your responsibility and should be

made in con are your responsibility

37

: 00:02:39

and should be made in consultation

with a qualified medical professional

38

: 00:02:43

or allied health professional.

39

: 00:02:47

Today we're gonna have a look at a

recent study that has highlighted some

40

: 00:02:51

really interesting findings in terms

of commonalities in the underpinnings

41

: 00:02:55

of the neurophysiological correlates

to improvement in depression.

42

: 00:03:00

One is with a relatively recent treatment

that has shown a lot of promise and

43

: 00:03:06

is part of the psychedelic integration

therapy field, which is ketamine

44

: 00:03:11

for treatment of severe depression

treatment, refractory depression,

45

: 00:03:15

And this study seeks to compare that in

terms of the underpinnings of how it's

46

: 00:03:19

working with a legacy treatment that

is well known to be very effective for

47

: 00:03:24

patients who have severe depression,

particularly with psychotic features,

48

: 00:03:28

namely electroconvulsive therapy or

ECT, and the common underpinning that

49

: 00:03:32

these researchers found relates to

a neurotransmitter called adenosine.

50

: 00:03:57

If you've ever needed coffee to wake up,

you've met adenosine, a natural brain

51

: 00:04:01

signaling chemical that builds up while

we're awake and makes us feel sleepy.

52

: 00:04:07

Caffeine works by blocking adenosine.

53

: 00:04:10

This study in the journal Nature suggests

that adenosine may be the common language

54

: 00:04:15

behind two of the fastest antidepressant

treatments that we have, ketamine

55

: 00:04:19

and electroconvulsive therapy or ECT.

56

: 00:04:23

In this study when scientists blocked

adenosine effects in mice, and that's

57

: 00:04:28

important, we'll come back to that, the

antidepressant benefits disappeared.

58

: 00:04:33

Activate that pathway, and

the benefits reappeared.

59

: 00:04:36

So today we're going to unpack what

that means and later what it implies

60

: 00:04:40

for caffeine, say around treatment

days, if someone is considering ketamine

61

: 00:04:45

for treatment refractory depression.

62

: 00:04:47

So why does this research matter?

63

: 00:04:49

Let's look at the big picture.

64

: 00:04:51

Classic antidepressants can take weeks,

if not months, to start working fully.

65

: 00:04:56

Ketamine and ECT are different.

66

: 00:04:58

They can help within hours to

days, especially when other options

67

: 00:05:01

haven't worked, and therefore someone

would be presenting with so-called

68

: 00:05:06

treatment refractory depression.

69

: 00:05:08

What's been unclear though, is how

ketamine and ECT act so quickly.

70

: 00:05:13

So this paper is really important

because it points to adenosine

71

: 00:05:16

signaling, especially in the medial

prefrontal cortex, which is a mood

72

: 00:05:20

control hub, as a shared switch

that these treatments seem to flip.

73

: 00:05:26

You can see the prefrontal and

hippocampal recordings in Figure 1,

74

: 00:05:29

and I'm gonna be putting up figures

from the study for viewers to see on

75

: 00:05:33

the YouTube side, but I would encourage

listeners to look it up later and

76

: 00:05:38

the links will be in the show notes.

77

: 00:05:41

Now, if this adenosine pathway is a

shared target that helps to account for

78

: 00:05:45

the effectiveness of ketamine and ECT

for treatment refractory depression,

79

: 00:05:50

we might be able to design cleaner

drugs, we might be able to time the

80

: 00:05:54

stimulation therapies to be more effective

and critically, we might be able to

81

: 00:05:59

control everyday variables that might

seem innocuous, like caffeine intake.

82

: 00:06:04

These are important factors because,

for example, with caffeine, they

83

: 00:06:09

act on the same adenosine receptors.

84

: 00:06:13

So let's take a few minutes and consider

what these scientists actually did.

85

: 00:06:18

Now again, it's really important to

emphasize that this is a study in mice,

86

: 00:06:21

and so while it's important, it does not

necessarily translate into humans, but

87

: 00:06:26

this is where the basic research often

starts in animal models, and then the

88

: 00:06:31

drug development can proceed from there.

89

: 00:06:33

Drug development, neurostimulation

development, therapeutic development,

90

: 00:06:36

in other words, proceeds from

there into clinical trials.

91

: 00:06:40

So these researchers used a tiny light

up sensor to watch in real time what

92

: 00:06:45

adenosine systems were doing in living

mouse brains while giving ketamine.

93

: 00:06:51

And the result that they found

was fascinating: a rapid adenosine

94

: 00:06:55

surge in the medial prefrontal

cortex and hippocampus, but

95

: 00:06:59

not in the nucleus accumbens.

96

: 00:07:02

And so they found that the signal started

about 100 to 150 seconds after ketamine

97

: 00:07:07

dosing, and it faded over minutes.

98

: 00:07:11

The same pattern appeared

in stressed mice.

99

: 00:07:15

And so the conclusions were that these

were robust findings and persisted even

100

: 00:07:20

in mice that had a different resting state

of stress or the depression equivalent

101

: 00:07:26

markers that have been developed

for animal studies of this nature.

102

: 00:07:32

I'm gonna show Figure 1 here, and again,

links to extended data from Figure 1

103

: 00:07:36

will be in the show notes for people

who are interested in that detail.

104

: 00:07:42

For listeners, here's a visual cue in

terms of what the images are representing.

105

: 00:07:47

You wanna imagine a gentle wave

that's rising in the prefrontal

106

: 00:07:50

cortex, which is the adenosine

surge after ketamine was given.

107

: 00:07:56

Now the question arises does

adenosine cause the improvement

108

: 00:08:00

in the depression model that the

researchers found in these mice.

109

: 00:08:05

So really there were two tests

that have to be met in order

110

: 00:08:09

to justify these conclusions.

111

: 00:08:11

The first test is that of necessity.

112

: 00:08:14

Okay, so removing adenosine's

two key locks, if you will.

113

: 00:08:18

So with neurotransmitters, it's

basically a chemical that nests inside

114

: 00:08:22

of a receptor that acts as a lock

and key in order to change the degree

115

: 00:08:28

to which these pathways are active

116

: 00:08:30

or not.

117

: 00:08:31

And so the A1 and A2A receptors for

adenosine, those were the key receptors

118

: 00:08:37

in terms of the adenosine being the

key and the receptors being the lock.

119

: 00:08:41

The two locks, if you will,

are the A1 and A2A receptors.

120

: 00:08:45

So if you remove the adenosine key

or if you block those receptors with

121

: 00:08:51

drugs and ketamine no longer improves

the mouse behavior in standard tests,

122

: 00:08:57

which is the correlate to improvement

in mood, then, um, that's related to

123

: 00:09:03

the importance of a necessity factor

in terms of showing these, uh, results

124

: 00:09:08

that the researchers have published.

125

: 00:09:10

The second one is sufficiency.

126

: 00:09:12

So the data has to be necessary and

sufficient in order to support conclusions

127

: 00:09:17

around commonalities of neurophysiological

correlates of therapeutic benefit.

128

: 00:09:23

And so the second factor sufficiency is

that those receptors have to be turned on.

129

: 00:09:29

So if you, in other words, if you're

able to turn on those receptors without

130

: 00:09:33

ketamine, and you can mimic the rapid

benefit, then again, you can show that the

131

: 00:09:39

activation of those receptors is in some

way sufficient in order to account for the

132

: 00:09:44

change that correlates with improvement

in the mood model of those animals.

133

: 00:09:49

So they found that the A1

receptor produced a longer

134

: 00:09:52

lasting piece, out to 24 hours.

135

: 00:09:56

And again, the extended data

on that from figure 4 is gonna

136

: 00:09:59

be linked to in the show notes.

137

: 00:10:01

Now whereabouts in the brain that

they found this is important.

138

: 00:10:04

So the medial prefrontal cortex, uh, a

key area in terms of regulating mood.

139

: 00:10:10

We know that.

140

: 00:10:11

So local adenosine, there.

141

: 00:10:13

the surrounding glial cells, local

astrocytes to release the adenosine

142

: 00:10:17

seem to improve the behavior.

143

: 00:10:19

That would be the correlate of the

mood improvement in the mouse model.

144

: 00:10:23

Now, if you're knocking the

A1 and A2A receptors out only

145

: 00:10:27

in that region, the systemic

ketamine appeared to stop working.

146

: 00:10:32

Again, so that reinforces this idea

that this is a critical system in terms

147

: 00:10:37

of how ketamine helps to alleviate

depression rapidly in people with

148

: 00:10:42

treatment refractory depression.

149

: 00:10:47

Now, one question that's interesting is

how does the ketamine raise the adenosine

150

: 00:10:51

without overstimulating the brain?

151

: 00:10:53

Because when we're looking at altering

natural neurochemical pathways.

152

: 00:10:59

We also have to be careful

that we're not overshooting and

153

: 00:11:02

causing potential side effects.

154

: 00:11:04

So at antidepressant doses, ketamine

does not cause things like seizure-like

155

: 00:11:09

overactivity either in current treatment

settings, it's pretty well known.

156

: 00:11:14

that's been carefully researched

and the dosing is recommended at

157

: 00:11:17

the levels that it order to achieve

a balance between effectiveness and

158

: 00:11:21

minimization of side effect risk.

159

: 00:11:24

and in this study they indeed, they

showed does not cause seizure-like

160

: 00:11:28

overactivity in these models, the

mouse model, that the calcium activity

161

: 00:11:33

in excitatory and inhibitory cells,

they found actually decreased.

162

: 00:11:38

And the extended data there from figure

6 that'll be linked to in the show notes.

163

: 00:11:44

So essentially what the researchers

found here is that the ketamine is

164

: 00:11:47

acting like a gentle metabolic brake.

165

: 00:11:50

So it's slowing down lowering

the ATP/ADP ratio inside cells.

166

: 00:11:57

Which favors the adenosine

moving out through so-called

167

: 00:12:00

ENT-1 and ENT-2 transporters.

168

: 00:12:03

And so by blocking those transporters,

then the adenosine surge shrinks,

169

: 00:12:08

which is in figure 3, that will

be shown for viewers and also

170

: 00:12:12

linked to in the show notes.

171

: 00:12:14

And so in isolated mouse brain

mitochondria, ketamine dampens part

172

: 00:12:18

of the TCA cycle, which links ketamine

directly to energy handling in neurons

173

: 00:12:24

and as well upstream to the adenosine

rise that was, that was found.

174

: 00:12:29

And again, from figure 3

extended data in figure 7.

175

: 00:12:34

So that's a lot of jargon, but in plain

English, what it really means is that

176

: 00:12:38

ketamine appears to set off a short

energy shift, which releases adenosine.

177

: 00:12:44

The adenosine flips A1 and A2A

receptors in the prefrontal cortex,

178

: 00:12:49

allowing mood circuits to reset

and providing symptomatic relief.

179

: 00:12:57

Now can this research potentially guide

development of better medications?

180

: 00:13:02

Well, using this adenosine surge as

a screening readout, the team found

181

: 00:13:07

analogs, especially deschloroketamine,

that creates stronger, longer adenosine

182

: 00:13:14

signals and worked at lower doses with

less hyper locomotion in the mice.

183

: 00:13:20

So the hyper locomotion would

be a proxy to motor stimulation

184

: 00:13:24

as a potential side effect.

185

: 00:13:27

This is shown in figure 4

with extended data in figure 8

186

: 00:13:30

that'll be linked to as well.

187

: 00:13:32

Now notably adenosine released did

not track with NMDA receptor blockade.

188

: 00:13:37

So that's a glutamate NMDA

receptor block across compounds.

189

: 00:13:41

And the hint there was that we can

decouple the potential that there was

190

: 00:13:46

benefit from classic side effects via that

glutamate and MDA receptor modulation and

191

: 00:13:54

the extended data from there is figure

9 again linked to in the show notes.

192

: 00:13:58

So what about ECT?

193

: 00:13:59

Let's bring ECT into the discussion.

194

: 00:14:01

So ECT, electroconvulsive therapy, what

the researchers found is that during

195

: 00:14:06

ECT, adenosine in the prefrontal cortex

spikes in a similar size relation

196

: 00:14:13

to ketamine, but more quickly in and

out, and the A1 and A2A receptors

197

: 00:14:17

were again, required for this benefit.

198

: 00:14:20

This is shown in figure 5.

199

: 00:14:23

This research team also tried acute

intermittent hypoxia, which involved

200

: 00:14:28

short controlled dips to 9% oxygen with

normal air breaks, and they saw adenosine

201

: 00:14:34

rise and behavior improve in a adenosine

dependent way In the mouse model.

202

: 00:14:39

Extended data for this is in figure 10.

203

: 00:14:42

Now important to note and just as a

background, so this is a lab protocol

204

: 00:14:46

in animals, it's not, you know,

hypoxia is definitely not recommended

205

: 00:14:50

as a DIY treatment for people.

206

: 00:14:52

And the other thing I really wanna

emphasize is that all of this animal

207

: 00:14:55

research is done with very strict research

ethics, board approval, and supervision.

208

: 00:15:00

So what about caffeine?

209

: 00:15:02

'cause we know that caffeine blocks

adenosine as well, and that's part of

210

: 00:15:06

how it helps to keep, uh, people alert.

211

: 00:15:08

Now what's the implication

for this research?

212

: 00:15:11

Well, here's the practical headline.

213

: 00:15:13

So the paper shows that ketamine's

rapid effects to treat depression

214

: 00:15:17

depend on adenosine A1 and A2A receptors

in the medial prefrontal cortex.

215

: 00:15:24

Now, as far as stimulating those

receptors, now caffeine is a

216

: 00:15:28

non-selective antagonist or

blocker at those same receptors.

217

: 00:15:33

So the thought is that if cath, so the

thought is that if caffeine is on board.

218

: 00:15:38

At the wrong time.

219

: 00:15:39

It might blunt the very signaling that

ketamine is trying to accomplish via

220

: 00:15:44

these adenosine pathways in order to

help create the antidepressant response.

221

: 00:15:50

So these researchers explicitly

flagged dietary caffeine as a

222

: 00:15:54

potential interference in clinical

applications with ketamine, and

223

: 00:15:59

that future clinical trials should

consider controlling for that variable.

224

: 00:16:05

I just wanted to highlight two additional

mechanistic notes from this paper.

225

: 00:16:09

to help this all make sense.

226

: 00:16:11

So the estimated adenosine levels during

ketamine and/or ECT sat around the 100

227

: 00:16:19

nM range, which is exactly where the high

affinity A1 and A2A receptors are engaged,

228

: 00:16:26

and the low affinity subtypes were not.

229

: 00:16:29

But those are the receptors

that caffeine blocks.

230

: 00:16:33

Second is that when researchers blocked

these A1 and A2A adenosine receptors with

231

: 00:16:38

selective antagonists in mice, ketamine's,

antidepressant-like effects vanished.

232

: 00:16:44

The side effect of hyper locomotion

did not, however, and that seemed

233

: 00:16:49

to be the worst trade off, less

benefit without fewer side effects.

234

: 00:16:54

So what does this mean for people

and ketamine clinics or ECT programs?

235

: 00:16:59

Well, this is preclinical work in mice.

236

: 00:17:01

Again, it's very important

to emphasize that.

237

: 00:17:03

So of course we do need human

studies, but this lays the

238

: 00:17:07

groundwork for those studies.

239

: 00:17:09

The sensible interim step would be

to consider treating caffeine like a

240

: 00:17:12

variable to standardize around ketamine

research and even ECT research.

241

: 00:17:19

As a sidebar, it's interesting because in

ECT, both research and clinical practice,

242

: 00:17:23

sometimes in order to make a seizure

more likely to occur or to lengthen

243

: 00:17:28

the duration of seizures, if they're

too short and not as effective, it is

244

: 00:17:32

sometimes part of practice to administer

a dose of caffeine before ECT and see if

245

: 00:17:38

that can help to improve the quality of

seizures and/or the duration of seizures,

246

: 00:17:42

although there's some controversy

around whether or not that's actually

247

: 00:17:46

evidence-based in terms of practice,

but it has been done and sometimes will

248

: 00:17:50

continue to be done and the response

tends to be more or less variable.

249

: 00:17:54

But it is sometimes a strategy

that is employed with ECT now.

250

: 00:17:59

there's potential now re-analysis of that

practice because it that that pre ECT

251

: 00:18:04

caffeine that was previously thought to

perhaps improve the quality and or length

252

: 00:18:08

of ECT seizures in order to improve the

therapeutic benefit of those seizures

253

: 00:18:14

may actually be counterproductive because

the caffeine might actually be blocking

254

: 00:18:18

the adenosine pathways that the ECT is

trying in a therapeutic way to achieve

255

: 00:18:23

improvement in depressive symptoms.

256

: 00:18:26

So the researchers basically consider that

the intake of dietary caffeine should be

257

: 00:18:32

treated like a variable to standardize

around, when either using ketamine or

258

: 00:18:37

ECT clinically or when designing clinical

trials with those therapeutic modalities.

259

: 00:18:44

So the recommendations were to be

documenting the amount of caffeine

260

: 00:18:49

intake, the timing of caffeine intake,

trying to keep it consistent visit to

261

: 00:18:54

visit, to avoid some fluctuation in that

potential variable or even considering

262

: 00:18:58

an abstinence on your discussions

with your own care providers at either

263

: 00:19:03

ketamine clinic or ECT program, clinical

trials, especially the authors felt

264

: 00:19:09

that should be controlling for caffeine

intake so that it doesn't muddy the

265

: 00:19:12

results and confuse things for everyone.

266

: 00:19:17

So because ketamine's rapid effect uses

adenosine receptors, the same ones that

267

: 00:19:22

caffeine blocks, it's important to think

about standardizing caffeine intake

268

: 00:19:26

around treatments, so your results aren't

in some way diluted by the potential

269

: 00:19:31

for caffeine to be interfering with

the positive effect of ketamine or ECT.

270

: 00:19:37

Now, importantly, again, a caveat,

this is animal studies, right?

271

: 00:19:40

So the paper does not test acute caffeine

intake plus ketamine effect in humans.

272

: 00:19:45

So until trials answer this question

directly, think more of it in terms of

273

: 00:19:49

control and consistency, not as caffeine

as very likely to either inhibit or

274

: 00:19:55

augment response to ketamine or ECT.

275

: 00:20:00

So to wrap up, let's look at a

few quick questions in summary.

276

: 00:20:03

So first is adenosine the whole story?

277

: 00:20:05

Well, based on this research, it

does look very central as far as

278

: 00:20:09

playing a role in the therapeutic

benefit of both ketamine and ECT.

279

: 00:20:13

And there's also a very high

likelihood that the adenosine

280

: 00:20:17

pathway changes trigger other

plasticity players like brain derived

281

: 00:20:21

neurotropic factor or BDNF or mTOR.

282

: 00:20:25

So maybe think of it as adenosine

as like the starter pistol that is

283

: 00:20:29

triggering a cascade of downstream

effects that improve depressive symptoms.

284

: 00:20:34

Does this research of approaches

to ECT or even require some change

285

: 00:20:39

to ECT practices these days?

286

: 00:20:41

No, not at all.

287

: 00:20:43

ECT has been around for decades.

288

: 00:20:44

Obviously.

289

: 00:20:45

It's very well established as a

very effective treatment for severe

290

: 00:20:49

treatment refractory depression,

particularly with psychotic features.

291

: 00:20:53

So no, but understanding the relevance

in terms of things like ECT's

292

: 00:20:58

adenosine spike, as they showed in

figure 5, could inform approaches to

293

: 00:21:04

providing ECT to improve effectiveness

and decreased side effects.

294

: 00:21:08

For example, tweaking stimulation

parameters, uh, or perhaps considering

295

: 00:21:14

how combination strategies could

be more effective for patients in

296

: 00:21:18

clinical practice future studies.

297

: 00:21:21

So what's the bottom line on caffeine?

298

: 00:21:23

Well, mechanistically caffeine could

potentially dampen ketamine's effect

299

: 00:21:27

by blocking the adenosine A1 and A2A

receptors during the critical adenosine

300

: 00:21:33

window, but until we have human data to

standardize that, it's a bit difficult

301

: 00:21:38

to extrapolate from this research.

302

: 00:21:40

However, it is very interesting.

303

: 00:21:43

So if adenosine is indeed the shared

messenger of these rapid antidepressant

304

: 00:21:47

effects, the future seems to lie in things

like smarter timing, cleaner drugs, better

305

: 00:21:54

targeted neurostimulation, and maybe

even thoughtful caffeine control around

306

: 00:21:59

intake or taking breaks on treatment days.

307

: 00:22:03

The figures, as I've been mentioning

and extended data from the

308

: 00:22:06

study, I'll link to those in the

show notes if you wanna dig in.

309

: 00:22:10

and you have more specific interest.

310

: 00:22:12

I wanted to also emphasize that

this episode summarizes preclinical

311

: 00:22:16

research in mice, and again is

for educational information only.

312

: 00:22:19

It's not medical advice.

313

: 00:22:21

So treatments like ketamine, ECT,

other non-invasive neurostimulation or

314

: 00:22:26

particularly controlled oxygen necessarily

translate from this research into clinical

315

: 00:22:30

practice and any of those should really

only be considered in regulated clinical

316

: 00:22:34

settings under qualified supervision.

317

: 00:22:51

Thanks again for joining me today

on the Neurostimulation Podcast.

318

: 00:22:54

I hope that you enjoyed this exploration

into the fascinating world of

319

: 00:22:59

neuroscience, clinical neurostimulation,

ketamine induced improvements in treatment

320

: 00:23:05

refractory depression as much as I did.

321

: 00:23:08

If you found today's episode

interesting, don't forget to like

322

: 00:23:10

and subscribe to the podcast.

323

: 00:23:12

It's the best way to make sure that you

don't miss a future episode, and it helps

324

: 00:23:16

us to reach more curious minds like yours.

325

: 00:23:19

Again, if you think that today's

episode might resonate with a

326

: 00:23:22

friend, a family member, or a

colleague, please share it with them.

327

: 00:23:26

Knowledge is better when it's shared

and you never know who might find

328

: 00:23:29

this information helpful or inspiring.

329

: 00:23:32

For details about the research that

we've been talking about, please

330

: 00:23:35

check out the links in the show notes.

331

: 00:23:37

You'll find everything that you

need to understand more about this

332

: 00:23:39

study and associated topics, and

I'd love to hear your thoughts.

333

: 00:23:43

Please do join in the conversation

in the comment section below.

334

: 00:23:48

Your questions, ideas, and feedback

really do make this podcast better.

335

: 00:23:53

Finally, don't forget to

tune into the next episode.

336

: 00:23:55

It's gonna be another exciting journey

into the cutting edge of neuroscience.

337

: 00:23:59

Clinical neurostimulation and

interventional mental health.

338

: 00:24:03

Thanks again for listening.

339

: 00:24:04

Take care, be well, stay curious,

and I'll see you next time on

340

: 00:24:08

the Neurostimulation Podcast.