scholarly journals Lateral habenula projections to dopamine and GABA neurons in the rat ventral tegmental area

2009 ◽  
Vol 30 (7) ◽  
pp. 1239-1250 ◽  
Author(s):  
Natalia Omelchenko ◽  
Roland Bell ◽  
Susan R. Sesack
Keyword(s):  
Ventral Tegmental Area ◽  
Lateral Habenula ◽  
Gaba Neurons ◽  
Ventral Tegmental

A-type K+ Current of Dopamine and GABA Neurons in the Ventral Tegmental Area

2006 ◽  
Vol 96 (2) ◽  
pp. 544-554 ◽  
Author(s):  
Susumu Koyama ◽  
Sarah B. Appel
Keyword(s):  
Ventral Tegmental Area ◽  
Current Density ◽  
Drugs Of Abuse ◽  
Physiological Role ◽  
Firing Frequency ◽  
Membrane Hyperpolarization ◽  
Gaba Neurons ◽  
Type K ◽  
Voltage Dependent ◽  
Ventral Tegmental

A-type K+ current ( IA) is a rapidly inactivating voltage-dependent potassium current which can regulate the frequency of action potential (AP) generation. Increased firing frequency of ventral tegmental area (VTA) neurons is associated with the reinforcing effects of some drugs of abuse like nicotine and ethanol. In the present study, we classified dopamine (DA) and GABA VTA neurons, and investigated IA properties and the physiological role of IA in these neurons using conventional whole cell current- and voltage-clamp recording. DA VTA neurons had a mean firing frequency of 3.5 Hz with a long AP duration. GABA VTA neurons had a mean firing frequency of 16.7 Hz with a short AP duration. For IA properties, the voltage-dependence of steady-state IA activation and inactivation was similar in DA and GABA VTA neurons. IA inactivation was significantly faster and became faster at positive voltages in GABA neurons than DA neurons. Recovery from inactivation was significantly faster in DA neurons than GABA neurons. IA current density at full recovery was significantly larger in DA neurons than GABA neurons. In DA and GABA VTA neurons, latency to the first AP after the recovery from membrane hyperpolarization (repolarization latency) was measured. Longer repolarization latency was accompanied by larger IA current density in DA VTA neurons, compared with GABA VTA neurons. We suggest that IA contributes more to the regulation of AP generation in DA VTA neurons than in GABA VTA neurons.

scholarly journals Functional evidence for a direct excitatory projection from the lateral habenula to the ventral tegmental area in the rat

2016 ◽  
Vol 116 (3) ◽  
pp. 1161-1174 ◽  
Author(s):  
P. Leon Brown ◽  
Paul D. Shepard
Keyword(s):  
Ventral Tegmental Area ◽  
Dopamine Neurons ◽  
Lateral Habenula ◽  
Aversive Stimuli ◽  
Rat Pups ◽  
Tegmental Nucleus ◽  
Fasciculus Retroflexus ◽  
Ventral Tegmental ◽  
Midbrain Dopamine ◽  
Midbrain Dopamine Neurons

The lateral habenula, a phylogenetically conserved epithalamic structure, is activated by aversive stimuli and reward omission. Excitatory efferents from the lateral habenula predominately inhibit midbrain dopamine neuronal firing through a disynaptic, feedforward inhibitory mechanism involving the rostromedial tegmental nucleus. However, the lateral habenula also directly targets dopamine neurons within the ventral tegmental area, suggesting that opposing actions may result from increased lateral habenula activity. In the present study, we tested the effect of habenular efferent stimulation on dopamine and nondopamine neurons in the ventral tegmental area of Sprague-Dawley rats using a parasagittal brain slice preparation. Single pulse stimulation of the fasciculus retroflexus excited 48% of dopamine neurons and 51% of nondopamine neurons in the ventral tegmental area of rat pups. These proportions were not altered by excision of the rostromedial tegmental nucleus and were evident in both cortical- and striatal-projecting dopamine neurons. Glutamate receptor antagonists blocked this excitation, and fasciculus retroflexus stimulation elicited evoked excitatory postsynaptic potentials with a nearly constant onset latency, indicative of a monosynaptic, glutamatergic connection. Comparison of responses in rat pups and young adults showed no significant difference in the proportion of neurons excited by fasciculus retroflexus stimulation. Our data indicate that the well-known, indirect inhibitory effect of lateral habenula activation on midbrain dopamine neurons is complemented by a significant, direct excitatory effect. This pathway may contribute to the role of midbrain dopamine neurons in processing aversive stimuli and salience.

Responses of ventral tegmental area GABA neurons to brain stimulation reward

2001 ◽  
Vol 906 (1-2) ◽  
pp. 190-197 ◽  
Author(s):  
Scott C Steffensen ◽  
Rong-Sheng Lee ◽  
Sarah H Stobbs ◽  
Steven J Henriksen
Keyword(s):  
Ventral Tegmental Area ◽  
Brain Stimulation ◽  
Brain Stimulation Reward ◽  
Gaba Neurons ◽  
Ventral Tegmental

scholarly journals nNOS-expressing neurons in the ventral tegmental area and substantia nigra pars compacta

2018 ◽  
Author(s):  
Eleanor J Paul ◽  
Eliza Kalk ◽  
Kyoko Tossell ◽  
Elaine E. Irvine ◽  
Dominic J. Withers ◽  
...  
Keyword(s):  
Substantia Nigra ◽  
Ventral Tegmental Area ◽  
Brain Regions ◽  
Substantia Nigra Pars Compacta ◽  
Neuron Activity ◽  
Potential Candidate ◽  
Gaba Neurons ◽  
Local Interneurons ◽  
Ventral Tegmental ◽  
Oxide Synthase

AbstractGABA neurons in the ventral tegmental area (VTA) and substantia nigra pars compact (SNc) play key roles in reward and aversion through their local inhibitory control of dopamine neuron activity and through long-range projections to several target regions including the nucleus accumbens. It is not clear if some of these GABA neurons are dedicated local interneurons or if they all collateralize and send projections externally as well as making local synaptic connections. Testing between these possibilities has been challenging in the absence of interneuron-specific molecular markers. We hypothesised that one potential candidate might be neuronal nitric oxide synthase (nNOS), a common interneuronal marker in other brain regions. To test this, we used a combination of immunolabelling (including antibodies for nNOS that we validated in tissue from nNOS-deficient mice) and cell-type-specific virus-based anterograde tracing in mice. We show that nNOS-expressing neurons in the parabrachial pigmented (PBP) part of the VTA and the SNc are GABAergic local interneurons, whereas nNOS-expressing neurons in the Rostral Linear Nucleus (RLi) are mostly glutamatergic and project to a number of regions, including the lateral hypothalamus, the ventral pallidum, and the median raphe nucleus. Taken together, these findings indicate that nNOS is expressed by neurochemically- and anatomically-distinct neuronal sub-groups in a sub-region-specific manner in the VTA and SNc.

scholarly journals Ventral Tegmental Area GABA, glutamate, and glutamate-GABA neurons are heterogenous in their electrophysiological and pharmacological properties

2020 ◽  
Author(s):  
Jorge Miranda-Barrientos ◽  
Ian Chambers ◽  
Smriti Mongia ◽  
Bing Liu ◽  
Hui-Ling Wang ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Viral Vectors ◽  
Ex Vivo ◽  
Glutamate Transporter ◽  
Receptor Activation ◽  
Firing Frequency ◽  
Dopamine Neurons ◽  
Gaba Neurons ◽  
Double Transgenic Mouse ◽  
Ventral Tegmental

AbstractThe ventral tegmental area (VTA) contains dopamine neurons intermixed with GABA-releasing (expressing vesicular GABA transporter, VGaT), glutamate-releasing (expressing vesicular glutamate transporter, VGluT2), and co-releasing (co-expressing VGaT and VGluT2) neurons. By delivering INTRSECT viral vectors into VTA of double vglut2-Cre/vgat-Flp transgenic mice, we targeted specific VTA cell populations for ex vivo recordings. We found that VGluT2+ VGaT− and VGluT2+ VGaT+ neurons on average had relatively hyperpolarized resting membrane voltage, greater rheobase, and lower spontaneous firing frequency compared to VGluT2− VGaT+ neurons, suggesting that VTA glutamate-releasing and glutamate-GABA co-releasing neurons require stronger excitatory drive to fire than GABA-releasing neurons. In addition, we detected expression of Oprm1mRNA (encoding μ opioid receptors, MOR) in VGluT2+ VGaT− and VGluT2− VGaT+ neurons, and their hyperpolarization by the MOR agonist DAMGO. Collectively, we demonstrate the utility of the double transgenic mouse to access VTA glutamate, glutamate-GABA and GABA neurons, and show some electrophysiological heterogeneity among them.Impact StatementSome physiological properties of VTA glutamate-releasing and glutamate-GABA co-releasing neurons are distinct from those of VTA GABA-releasing neurons. μ-opioid receptor activation hyperpolarizes some VTA glutamate-releasing and some GABA-releasing neurons.

scholarly journals Ventral tegmental area GABA neurons mediate stress-induced anhedonia

2020 ◽  
Author(s):  
Daniel C. Lowes ◽  
Linda A. Chamberlin ◽  
Lisa N. Kretsge ◽  
Emma S. Holt ◽  
Atheir I. Abbas ◽  
...  
Keyword(s):  
Ventral Tegmental Area ◽  
Low Frequency ◽  
Potential Mechanism ◽  
Gaba Neurons ◽  
Reward Seeking ◽  
Seeking Behavior ◽  
Stressful Experiences ◽  
Ventral Tegmental ◽  
Necessary And Sufficient ◽  
Depressive Episodes

AbstractStressful experiences frequently precede depressive episodes1. Depression results in anhedonia, or disrupted reward-seeking, in most patients2. In humans3,4 and rodents5,6, stress can disrupt reward-seeking, providing a potential mechanism by which stress can precipitate depression7-9. Yet despite decades investigating how stress modulates dopamine neuron transmission between the ventral tegmental area (VTA) and nucleus accumbens (NAc), the underpinnings of the stress-anhedonia transition remain elusive10-13. Here we show that during restraint stress, VTA GABA neurons drive low frequency NAc LFP oscillations, rhythmically modulating NAc firing rates. The strength of these stress-induced NAc oscillations predict the degree of impaired reward-seeking upon release from restraint. Inhibiting VTA GABA neurons disrupts stress-induced NAc oscillations and reverses the effect of stress on reward-seeking. By contrast, mimicking these oscillations with rhythmic VTA GABA stimulation in the absence of stress blunts subsequent reward-seeking. These experiments demonstrate that VTA GABA inputs to the NAc are both necessary and sufficient for stress-induced decreases in reward seeking behavior, elucidating a key circuit-level mechanism underlying stress-induced anhedonia.

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