Dopamine-mediated actions of ephedrine in the rat substantia nigra

  title={Dopamine-mediated actions of ephedrine in the rat substantia nigra},
  author={Adam C. Munhall and Steven W. Johnson},
  journal={Brain Research},

Tyramine excites rat subthalamic neurons in vitro by a dopamine-dependent mechanism

D1‐ and D2‐like dopamine receptors regulate signaling properties of group I metabotropic glutamate receptors in the rat globus pallidus

Data reveal that specific roles of group I mGluRs in the GP depend on the activity of D1‐like and D2‐like dopamine receptors, further corroborating the importance of dopamine in maintaining proper glutamatergic neurotransmission in the BG.

Exploring the neuromechanism of chronic ephedrine addiction in rhesus monkeys: A behavioural and brain resting-state fMRI study

Common Responses in Gene Expression by Ephedra herba in Brain and Heart of Mouse

The brain and heart responded commonly to Ephedra herba with a temporally reciprocal pattern of gene expression, which was associated with neural disease‐related functions, such as the Parkinson's disease pathway, in both the brain and the heart.

Neurotoxicity following chronic intravenous use of “Russian Cocktail”

It is believed that manganese with the possible contribution of methcathinone caused the neurological impairments in three teenagers following chronic intravenous use of a mixture known as “Russian Cocktail”.

Effect of Ephedra altissima stems extract on behavior in the mouse

It can be concluded that Ephedra altissima extract may have a central depression, antidepressant-like activity with no effect as anxiolytic like mood.

Plant-Derived Alkaloids



Alpha1‐adrenergic Effects on Dopamine Neurons Recorded Intracellularly in the Rat Midbrain Slice

It is concluded that stimulation of α1‐adrenergic receptors depolarizes principal (dopamine) neurons by reducing membrane conductance for potassium, but this effect is modulated by the increase in frequency of spontaneous inhibitory postsynaptic potentials evoked by stimulation of β‐ad Renergic receptors located on local interneurons.

Dopamine acts on D2 receptors to increase potassium conductance in neurones of the rat substantia nigra zona compacta.

It is concluded that dopamine acts on D2 receptors on neurones of the rat substantia nigra pars compacta to increase the membrane potassium conductance.

Dopamine selectively reduces GABAB transmission onto dopaminergic neurones by an unconventional presynaptic action

An unconventional presynaptic, D1 and D2 independent action of DA on the GABAB IPSP is described, which might have a principal role in determining therapeutic/side effects of l‐DOPA and antipsychotics and could be also involved in drug abuse.

The mechanism of amphetamine‐induced inhibition of rat substantia nigra compacta neurones investigated with intracellular recording in vitro

It is suggested that the inhibition of substantia nigra compacta neurones by amphetamine is mainly due to the release of endogenous dopamine.

Dopamine D1 receptors facilitate transmitter release

It is concluded that dopamine acts tonically at presynaptic D1 receptors on the terminals of afferent GABA neurons to facilitate selectively GABAB-mediated neurotransmission in the midbrain.

Cocaine inhibits GABA release in the VTA through endogenous 5-HT

  • D. CameronJ. Williams
  • Biology, Psychology
    The Journal of neuroscience : the official journal of the Society for Neuroscience
  • 1994
Using intracellular recordings from midbrain dopamine neurons in a brain slice preparation, it is concluded that cocaine acts to modulate the GABA input to A10 dopamine neurons via inhibition of the 5- HT transporter, increasing the concentration of 5-HT at presynaptic5-HT1D receptors.

Presynaptic dopamine D2‐like receptors inhibit excitatory transmission onto rat ventral tegmental dopaminergic neurones

The results suggest that afferent glutamatergic fibres which terminate on VTA dopaminergic neurones possess presynaptic D2‐like receptors, activation of which inhibits glutamate release by reducing Ca2+ influx.