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1 tter release and rhythmic firing activity of dopamine neurons.
2 fundamental static and dynamic properties of dopamine neurons.
3 ing the wide range of signals transmitted by dopamine neurons.
4 ables are organized across the population of dopamine neurons.
5 resultant grafts contain a small fraction of dopamine neurons.
6 e and accelerated spontaneous firings of VTA dopamine neurons.
7 observed both in vivo and in vitro in rodent dopamine neurons.
8 on of alpha-synuclein pathology in implanted dopamine neurons.
9 ease with walking was particularly strong in dopamine neurons.
10 ntained in the pattern of firing across many dopamine neurons.
11 or were abolished in mice lacking AdipoR1 in dopamine neurons.
12  regions or how it regulates the activity of dopamine neurons.
13 irectly or indirectly via tuberoinfundibular dopamine neurons.
14 ptic regulation that control the activity of dopamine neurons.
15 and reinstated by optogenetically activating dopamine neurons.
16 ced reduction of GABAergic inhibition in VTA dopamine neurons.
17 ion leading to disinhibition of mesostriatal dopamine neurons.
18 DAT-mediated increases in firing activity of dopamine neurons.
19 ibitory pauses in subpopulations of midbrain dopamine neurons.
20 PA receptor (AMPAR)/NMDAR ratios in midbrain dopamine neurons.
21 X6 to be required for development of gastric dopamine neurons.
22 decreases the normal chronic activity of the dopamine neurons.
23 bution of these receptors in living midbrain dopamine neurons.
24 tablished that RPEs are signaled by midbrain dopamine neurons.
25 5-HT2B receptors are expressed by mesolimbic dopamine neurons.
26 t extracellular recordings of identified VTA dopamine neurons.
27 als with pluripotent stem cell (PSC)-derived dopamine neurons.
28 f how intrinsic conductances shape pauses in dopamine neurons.
29 euron subtypes locally inhibited neighboring dopamine neurons.
30 ice in which Synaptotagmin-1 is removed from dopamine neurons.
31 racterized by alpha-synuclein aggregation in dopamine neurons.
32 s, particularly ventral tegmental area (VTA) dopamine neurons.
33 lozapine-n-oxide to bidirectionally modulate dopamine neurons.
34 r the physiological function and survival of dopamine neurons.
35 ology, boosts VGluT2 expression in surviving dopamine neurons.
36 roduction and positioning of periventricular dopamine neurons.
37 ng reduces presynaptic calcium transients in dopamine neurons, a finding consistent with reciprocal c
38 e in which RIMs are selectively removed from dopamine neurons, action potentials failed to evoke sign
39 e that adiponectin can directly modulate VTA dopamine neuron activity and anxiety behavior, and that
40 ses the restraint stress-induced increase in dopamine neuron activity and anxiety behavior.
41 lutamate neurotransmission in modulating VTA dopamine neuron activity and behavioral reinforcement.
42 ificantly impair postingestive-dependent VTA dopamine neuron activity and food seeking, whereas optog
43                            Unexpectedly, VTA dopamine neuron activity in high alcohol drinking (HAD)
44 establish a necessary role of vagus-mediated dopamine neuron activity in postingestive-dependent food
45 ingestive sucrose sensing and vagus-mediated dopamine neuron activity in the ventral tegmental area (
46                                              Dopamine neuron activity in vivo deviated from single-sp
47 During oestrus, ventral tegmental area (VTA) dopamine neuron activity is enhanced and drives post tra
48 c drugs have been shown previously to reduce dopamine neuron activity through action on D(2) autorece
49 d cotransmission convey discrete patterns of dopamine neuron activity to striatal neurons.
50 onoylglycerol (2-AG) in midbrain, increasing dopamine neuron activity via disinhibition.
51  demonstrate that serotonin neurons modulate dopamine neuron activity via glutamate co-transmission a
52   It is unclear whether aripiprazole reduces dopamine neuron activity via inhibition or, as seen foll
53 l modulators of ventral tegmental area (VTA) dopamine neuron activity, but how this metabotropic sign
54 us nerve neurons significantly increases VTA dopamine neuron activity.
55 nal interaction between DAT and Kv2.1 affect dopamine neuron activity.
56  the vHipp-mPFC pathway, normalized aberrant dopamine neuron activity.
57 cocaine potency are driven by alterations in dopamine neuron activity.
58 ine system, which may be utilized to protect dopamine neurons against Parkinson's disease pathology.
59  we showed that chemogenetic manipulation of dopamine neurons alters cocaine consumption in a manner
60 quired for adiponectin-induced inhibition of dopamine neurons and anxiolytic effects.
61 ert a primary inhibitory drive onto midbrain dopamine neurons and are excited by a variety of aversiv
62 n severe motor impairment, selective loss of dopamine neurons and increased astrocyte activation, whe
63 es neuroprotection for substantia nigra (SN) dopamine neurons and increases BDNF in the nigrostriatal
64 ficantly attenuated the MPTP-induced loss of dopamine neurons and motor behavioral deficits.
65                        Because loss of adult dopamine neurons and motor impairments are features of P
66 able in the pre-outcome activity of midbrain dopamine neurons and of medial prefrontal cortical neuro
67  neuron-derived IGF-1 acts as a regulator of dopamine neurons and regulates dopamine-mediated behavio
68 focused on sex differences in the anatomy of dopamine neurons and relative dopamine levels between ma
69 slocalized to the nucleus in PD iPSC-derived dopamine neurons and repressed genes early in the diseas
70  administration protected against loss of SN dopamine neurons and striatal dopamine levels, reduced a
71 ate intracellular target for amphetamines in dopamine neurons and support a model in which distinct p
72 gical alpha-syn conformers in human midbrain dopamine neurons and tested their contribution to the ag
73 rs control subtype-specific mesodiencephalic dopamine neurons and their appropriate axon innervation.
74         Together with the topography between dopamine neurons and their projections, this specializat
75         Substantia nigra pars compacta (SNc) dopamine neurons and their targets are involved in addic
76 n of expression of the transgene in midbrain dopamine neurons and validation of its effectiveness in
77  (sucralose + optogenetic stimulation of VTA dopamine neurons) and found that nesfatin-1 fully abolis
78 cts were countered by inhibition of midbrain dopamine neurons, and by activation of PV interneurons i
79 s, that this requires activation of midbrain dopamine neurons, and can be ameliorated by activating P
80 ling in setting the functional properties of dopamine neurons, and indicate that dopaminergic dysfunc
81  of striatal dopamine terminals, SNc loss of dopamine neurons, and motor-behavior defects.
82 echanism of manganese-induced dysfunction of dopamine neurons, and reveal a potential therapeutic tar
83 a large majority of BA projectors (>95%) are dopamine neurons, and that BA projectors become activate
84 cleus sends glutamatergic projections to VTA dopamine neurons, and that stimulation of this circuit p
85 ibitory postsynaptic currents (IPSCs) in VTA dopamine neurons, and these effects were mediated by a p
86 ed that substantia nigra pars compacta (SNc) dopamine neurons are a key node in the circuitry that dr
87  in vivo firing patterns of ventral midbrain dopamine neurons are controlled by afferent and intrinsi
88                                     Midbrain dopamine neurons are crucial for many behavioral and cog
89                                        These dopamine neurons are especially susceptible to Parkinson
90 ve strategy for Parkinson's disease in which dopamine neurons are generated by direct conversion of a
91                                     Midbrain dopamine neurons are known to encode reward prediction e
92 xamine whether RPE signals coded by midbrain dopamine neurons are modulated by the cost paid to obtai
93                                              Dopamine neurons are proposed to signal the reward predi
94                                              Dopamine neurons are sensitive to stress and critical fo
95                                              Dopamine neurons are thought to encode novelty in additi
96 d that many VTA neurons, among them putative dopamine neurons, are excited by footshocks, and acquire
97             Our data implicate senescence of dopamine neurons as a contributing factor in the patholo
98 genetically stimulated or inhibited midbrain dopamine neurons as rats performed a skilled reaching ta
99 ion of O-GlcNAcylation importantly regulates dopamine neurons at the molecular, synaptic, cellular, a
100                 Correcting the SV content in dopamine neuron axon terminals by impairing anterograde
101 s drives axonal outgrowth and contributes to dopamine neuron axonal plasticity in the postlesional br
102 erneurons, which drive dopamine release from dopamine neuron axons by activation of nicotinic acetylc
103 ne signals evoked by stimulation of midbrain dopamine neuron axons.
104            Conditioned by these experiences, dopamine neurons begin to fire upon the earliest present
105 llular senescence transcriptional program in dopamine neurons both in human stem cell-derived dopamin
106                                           In dopamine neurons, both variants can act as autoreceptors
107 in somatic regions of ventral tegmental area dopamine neurons, but did not activate ROS production in
108 iation of gamma-aminobutyric acid (GABA) and dopamine neurons, but not glutamate neurons, relies on q
109          G(q) and G(s) stimulation activated dopamine neurons, but only G(q) stimulation robustly enh
110 h after induction of depolarization block of dopamine neurons by acute haloperidol treatment (0.6 mg/
111  both dopamine and glutamate transporters in dopamine neurons by increasing activation of the small G
112 nce in this trade-off, and identify a single dopamine neuron called DAN-i1 that can do so.
113 cell transcriptomic analyses of iPSC-derived dopamine neurons carrying the GBA-N370S PD risk variant,
114 sc1 and constitutive activation of mTORC1 in dopamine neurons causes somatodendritic hypertrophy, red
115 ons not only in dopamine release but also in dopamine neuron connectivity, cotransmission, modulation
116 tors to improve their derivation and predict dopamine neuron content after engraftment.
117                  Distinct populations of VTA dopamine neurons contribute to components of the impulse
118 ndent expectation signal that influences how dopamine neurons convey reward prediction errors to guid
119 on-dependently increased the excitability of dopamine neurons, decreased the amplitude of action pote
120  of cell-replacement therapies that comprise dopamine neurons derived from human pluripotent stem cel
121                     These data identify that dopamine neuron-derived IGF-1 acts as a regulator of dop
122         In addition, conditional deletion of dopamine neuron-derived IGF-1 in adult mice leads to dec
123 plicated in psychiatric disorders, including dopamine neuron differentiation and innate immune respon
124         During memory expression, subsets of dopamine neurons directly and indirectly modulate the ac
125            Inhibiting ventral tegmental area dopamine neurons disrupted the tendency for reward-paire
126 terozygous (cHET) reduction of Gls1 in their dopamine neurons, dopamine neuron survival and transmiss
127 show that this enhanced VGluT2 expression in dopamine neurons drives axonal outgrowth and contributes
128                       Stromalin knockdown in dopamine neurons during a critical developmental period
129 ationship between mitochondrial function and dopamine neuron dysfunction and death using C. elegans m
130                                     Midbrain dopamine neuron dysfunction contributes to various psych
131 f VTA GABA neurons to increase inhibition of dopamine neurons, eliciting real-time and learned avoida
132 ENT This project serves to determine whether dopamine neurons encode differences in cued approach beh
133  navigated in a virtual-reality environment, dopamine neurons encoded an array of sensory, motor and
134        Ablation of AdipoR1 specifically from dopamine neurons enhances neuronal and anxiogenic respon
135 g 5-HT2B receptors totally or exclusively in dopamine neurons exhibit heightened cocaine-induced loco
136 ices, but it has been unclear whether or how dopamine neurons factor it into their teaching signal.
137  highlight the key role of netrin-1 in adult dopamine neuron fate, and the therapeutic potential of t
138                                 Although all dopamine neurons fire action potentials in a pacemaker p
139  endogenous opioid nociceptin that regulates dopamine neuron firing and acts uniquely to gate motivat
140 nectin haploinsufficiency leads to increased dopamine neuron firing and anxiety behavior under basal
141 mine content in the striatum and deficits in dopamine neuron firing and causes reduced spontaneous lo
142 mework for the biophysical implementation of dopamine neuron firing patterns in the intact brain.
143 brane potential events that cause changes in dopamine neuron firing patterns remain unknown.
144 scales, from subsecond phasic release due to dopamine neuron firing to tonic release responsible for
145 Antipsychotic failure coincided with reduced dopamine neuron firing, which was not observed during an
146 nstitution experiments that Kenyon cells and dopamine neurons from axoaxonic reciprocal synapses.
147 lens to record the activity of more than 300 dopamine neurons from the ventral tegmental area of the
148 in Parkinson disease (PD) is not uniform, as dopamine neurons from the ventral tier are lost more rap
149                    Given the similarities in dopamine neuron function across the animal kingdom, this
150  impact of regional astrocyte differences on dopamine neuron function and susceptibility to degenerat
151 vHipp activity and downstream alterations in dopamine neuron function in the MAM rodent model.
152 mentary refers to 'O-GlcNAcylation regulates dopamine neuron function, survival and degeneration in P
153 nized role for NAPE-PLD in the regulation of dopamine neuron function, which may be linked to the con
154            Here, we bidirectionally modulate dopamine neuron G-protein signaling with DREADDs (design
155                           Hyperactivation of dopamine neurons generates behavioral pathologies.
156 nd synaptic stimulation in subpopulations of dopamine neurons grouped according to their axonal proje
157 rol cellular survival and death) in midbrain dopamine neurons has led to the identification of the Bc
158                           This suggests that dopamine neurons have access to a wider variety of infor
159                             Substantia nigra dopamine neurons have been implicated in the initiation
160                                     Midbrain dopamine neurons have been proposed to signal prediction
161 ordings from large populations of individual dopamine neurons have not been performed in a behavioura
162                 Thus, preserving or rescuing dopamine neuron health and function is of paramount impo
163 observed Lewy pathology in healthy embryonic dopamine neurons implanted into the striatum of patients
164     Genetic deletion of GABAB receptors from dopamine neurons in adult mice did not affect general or
165 st paid to obtain rewards, by recording from dopamine neurons in awake behaving monkeys during perfor
166 mer driven by optical activation of midbrain dopamine neurons in DAT-cre mice.
167 ctive, immunocytochemically-defined midbrain dopamine neurons in isoflurane-anaesthetized adult mice.
168 ersely, LHb activation selectively inhibited dopamine neurons in lateral VTA, which were unaffected b
169 crease in the number of spontaneously active dopamine neurons in MAM rats but not in controls.
170  adaptive coding has been linked to midbrain dopamine neurons in nonhuman primates, and evidence in s
171  elicit a beneficial effect on nigrostriatal dopamine neurons in PD.
172 mine and glutamatergic signaling in midbrain dopamine neurons in response to acute administration of
173 ons.SIGNIFICANCE STATEMENT A small subset of dopamine neurons in the adult, healthy brain expresses v
174 ncentive cues, support an important role for dopamine neurons in the attribution of incentive salienc
175 ressive correspondence between the firing of dopamine neurons in the mammalian midbrain and the rewar
176         There is increased appreciation that dopamine neurons in the midbrain respond not only to rew
177  signal in the SN is a proxy for function of dopamine neurons in the nigrostriatal pathway.
178  main pathological features of PD is loss of dopamine neurons in the nigrostriatal pathway.
179                                              Dopamine neurons in the substantia nigra (SN) pars compa
180 t these symptoms arise following the loss of dopamine neurons in the substantia nigra has been known
181 mers produce a small but significant loss of dopamine neurons in the substantia nigra pars compacta (
182                                              Dopamine neurons in the substantia nigra pars compacta a
183 toms accompanied by the preferential loss of dopamine neurons in the substantia nigra pars compacta.
184 kinson's disease is characterized by loss of dopamine neurons in the substantia nigra(1).
185           Here, we show that, in contrast to dopamine neurons in the substantia nigra, vagal motoneur
186 ced striatal dopamine signaling, and loss of dopamine neurons in the substantia nigra.
187 sociated with decreased neural activities of dopamine neurons in the ventral tegmental area (DA(VTA)
188                                              Dopamine neurons in the ventral tegmental area (VTA) are
189                            Here we show that dopamine neurons in the ventral tegmental area (VTA) exp
190 lasticity, at least in part by disinhibiting dopamine neurons in the ventral tegmental area.
191                            Here we show that dopamine neurons in the VTA that project to the basal am
192 ral to cellular senescence in SATB1 knockout dopamine neurons in vitro and in vivo.
193 ient direct lineage reprogramming to induced dopamine neurons in vitro and in vivo.
194    Here, we develop a biophysical model of a dopamine neuron incorporating ion channel stochasticity
195                          The activity of VTA dopamine neurons increases significantly after administr
196 t-induced internalization of D2 receptors on dopamine neurons indicate a purposefully regulated local
197 ing differentiation into cultures containing dopamine neurons, induced pluripotent stem cells from pa
198 wn by increased survival of substantia nigra dopamine neurons, integrity of striatal dopaminergic fib
199                    D2R-mediated signaling in dopamine neurons is involved in the presynaptic regulati
200 hese fundamental properties, the activity of dopamine neurons is regulated and underlies the wide-ran
201 te the complexity of inputs, the output from dopamine neurons is remarkably homogeneous and robust.
202            Rapid phasic activity of midbrain dopamine neurons is thought to signal reward prediction
203 gic input to NAc shell arising from midbrain dopamine neurons, it alters fundamental properties of th
204 ediction errors have been mapped to midbrain dopamine neurons, it is unclear how the brain represents
205 ved by distinct subtypes of mesodiencephalic dopamine neurons located in the substantia nigra pars co
206 on's disease (PD) and results in age-related dopamine neuron loss and locomotor dysfunction in Drosop
207  moderately high-amino acid diet also blocks dopamine neuron loss and motor deficits in Drosophila th
208 athologically characterized by nigrostriatal dopamine neuron loss and the postmortem presence of Lewy
209 movement impairments but did not protect the dopamine neuron loss.
210 tia nigra (SN) to produce degeneration of SN dopamine neurons, loss of striatal dopamine levels, and
211  decades of research, it remains unclear how dopamine neurons make this calculation.
212  has suggested that the firing of mesolimbic dopamine neurons may activate nodes of the salience netw
213 nt mice, revealing that beta2* nAChRs on VTA dopamine neurons mediate nicotine's conditioned aversive
214 luence the functional properties of midbrain dopamine neurons, midbrain inflammation may play a role
215                        Results show that VTA dopamine neurons modulate numerous distinct aspects of c
216                                              Dopamine neuron morphology, excitability, and dopamine r
217 n for diversity among ventral tegmental area dopamine neurons, much less is known regarding functiona
218                           Whether individual dopamine neurons multiplex several variables, or whether
219                                              Dopamine neurons of the hypothalamic arcuate nucleus (AR
220 on and voltammetry, we address this issue in dopamine neurons of the neuroendocrine system, which fac
221 mine metabolism that accumulates with age in dopamine neurons of the substantia nigra (SN).
222                                              Dopamine neurons of the ventral tegmental area (VTA) reg
223 ne-induced inhibitory synaptic plasticity in dopamine neurons of the ventral tegmental area (VTA).
224  used with optofluidic delivery to stimulate dopamine neurons of the ventral tegmental area of freely
225 J mice suggest that manganese accumulates in dopamine neurons of the VTA and substantia nigra via nif
226                                     We found dopamine neurons of the VTA encode strength of incentive
227                       Finally, silencing VTA dopamine neurons, or their axon terminals in the BA duri
228  phasic and slowly ramping dopamine signals: dopamine neurons perform a derivative-like computation o
229  signaling and not recapitulated by NAcSh or dopamine neuron photostimulation.
230         The implications of this finding for dopamine neuron physiology are discussed.SIGNIFICANCE ST
231                                              Dopamine neurons played a causal role only after outcome
232 ontaneous tonic discharge activity of nigral dopamine neurons plays a fundamental role in dopaminergi
233 c AdipoRon in wild-type mice decreases basal dopamine neuron population activity and firing rate and
234 suggest that MS-mediated changes in midbrain dopamine neuron population activity could be one mechani
235 FC or LHb in normal rats potently suppressed dopamine neuron population activity, but in unique patte
236 egmental area and decreased substantia nigra dopamine neuron population activity.
237 show for the first time that the activity of dopamine neurons precisely represents the impulse vector
238 found that NAc inputs synapsed directly onto dopamine neurons, preferentially activating GABAB recept
239 discovered that chemogenetic manipulation of dopamine neurons produced rapid, bidirectional modulatio
240  to identify predictive markers expressed in dopamine neuron progenitors that correlate with graft ou
241                                    Thus, VTA dopamine neurons projecting to the BA contribute to fear
242 Induced pluripotent stem cell (iPSC)-derived dopamine neurons provide an opportunity to model Parkins
243 hese data provide evidence that ensembles of dopamine neurons provide highly specific teaching signal
244                             However, the way dopamine neurons receive information about reward outcom
245 he pattern of firing across a small group of dopamine neurons recorded in rats signals the identity o
246                           Here, we show that dopamine neurons recorded in rats that had self-administ
247                                     Midbrain dopamine neurons recorded in vivo pause their firing in
248 ese areas provide critical input to midbrain dopamine neurons regarding expected outcomes, suggesting
249       Optogenetic studies have revealed that dopamine neurons release dopamine in a synaptic signal m
250                    We now find that midbrain dopamine neurons release glutamate and dopamine with dif
251 ite decades of research, the function of VTA dopamine neurons remains controversial.
252  role of glutamatergic input as a whole onto dopamine neurons remains unclear.
253 arget SNL GABA neurons, and CeA->SNL and SNL dopamine neurons respond similarly to salient stimuli.
254                                              Dopamine neurons respond to errors in predicting value-n
255                                              Dopamine neuron responses to cues predicting reward and
256 t into behavioral reinforcement via midbrain dopamine neuron responses.
257 duces DCC cleavage and a significant loss of dopamine neurons, resulting in motor deficits.
258 olocomotion, while optogenetic activation of dopamine neurons reverses this hypolocomotor phenotype.
259                           We discovered that dopamine neurons secrete IGF-1 from the cell bodies foll
260 behavior; most critically, it indicates that dopamine neurons selectively modulate signal reception p
261 redictable, with smaller grafts, enriched in dopamine neurons, showing appropriate integration and ac
262                                     Midbrain dopamine neurons signal reward prediction error (RPE), o
263                      Regional differences in dopamine neuron signaling are likely to be differentiall
264                                   Inhibiting dopamine neurons spared the suppressive effect of reward
265                           This suggests that dopamine neurons specifically in the VTA encode motivati
266 edge about whether and how activation of VTA dopamine neurons specifically influences regional or glo
267 ist transcript was significantly enriched in dopamine neurons, suggesting tight regulation of X-linke
268 reduction of Gls1 in their dopamine neurons, dopamine neuron survival and transmission were unaffecte
269 Egln1, Kcnj6, Spen, and Uchl1) implicated in dopamine neuron survival and/or Parkinson's disease.
270 the detrimental effect of these mutations on dopamine neuron survival.
271  not only in a signaling role at a subset of dopamine neuron synapses, but also in mediating vesicula
272                                              Dopamine neuron synaptic actions vary across the striatu
273 tion level dopaminergic activation to select dopamine neurons that predict behavioral choice in Droso
274                                We identified dopamine neurons that uniquely coexpress the Onecut3 and
275  show that, during lactation, neuroendocrine dopamine neurons, the "TIDA" cells that control prolacti
276 urons exert inhibitory control over midbrain dopamine neurons, the activity of which are suppressed d
277  SV pool size without altering the number of dopamine neurons, their axons, or synapses.
278 erized the cell-specific connectivity of VTA dopamine neurons, their mRNA translational profile, and
279                  However, afferents onto SNc dopamine neurons themselves appear insensitive to drugs
280 al patterns emerge from this synthesis: that dopamine neurons themselves calculate reward prediction
281 and critical role for positive feedback onto dopamine neurons through reciprocal connections with Ken
282 contribution of ventral tegmental area (VTA) dopamine neurons to auditory-cued fear learning in male
283 ative afferents bidirectionally modulate VTA dopamine neurons to enable temporally precise vocal lear
284        How cocaine exposures act on midbrain dopamine neurons to precipitate addiction-relevant chang
285                    Independent discharges of dopamine neurons (tonic or pacemaker firing) determine t
286 C-matching increases the survival of grafted dopamine neurons (tyrosine hydroxylase: TH+).
287 se data indicate that the features that make dopamine neurons unique are highly concordant and not a
288               Finally, ablation of KORs from dopamine neurons using AAV-TH-cre in KOR(loxP) mice prev
289 onin neurons activate ventral tegmental area dopamine neurons via glutamate co-transmission and that
290                                 To evaluate, dopamine neurons were recorded from male rats performing
291                                     Midbrain dopamine neurons, which can be regulated by neuropeptide
292  type-specific Tsc1 deletion to test whether dopamine neurons, which modulate cognitive, motivational
293 and Ca(2+) homeostasis in G2019S LRRK2 human dopamine neurons, which potentially contributes to the p
294 uA1 subunits in ventral tegmental area (VTA) dopamine neurons, which subsequently enhance the motivat
295  action potential firing rate in vivo in VTA dopamine neurons, which was blocked by rolipram pretreat
296 sive alpha-synucleinopathies earlier than SN dopamine neurons while exhibiting milder cell loss in PD
297 periments where we optogenetically activated dopamine neurons while rats were learning associative re
298 nce between excitation and inhibition in VTA dopamine neurons, while PDE4 inhibition reestablishes th
299                    Treatment of iPSC-derived dopamine neurons with HDAC4-modulating compounds upregul
300 terogeneity in the basic organization of VTA dopamine neurons with regard to sex.

 
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