http://www.back-in-business-physiotherapy.com/images/files/DescendingControl.pdf

Descending control of pain.

Working memory performance is influenced by dopamine activation of D1 family dopamine receptors in the prefrontal cortex; working memory performance is maximal at moderate stimulation of D1 family receptors and is reduced by either higher or lower levels of D1 stimulation. The neuronal mechanisms that underlie this complex relationship are not yet understood. Previous work from this laboratory has demonstrated that the D1 family receptors, D1 and D5, are located in different compartments of pyramidal cells. Here we use an antibody specific to the D1receptor and double-label immunohistochemistry at the light and electron microscopic level to demonstrate that D1-like immunoreactivity (D1-LIR) is also present in interneurons. D1 receptor is prevalent in parvalbumin-containing interneurons and is less common in calretinin-containing interneurons. At the ultrastructural level, D1-LIR is found associated with the Golgi apparatus and endoplasmic reticulum in the soma, with the membranes of vesicles in proximal dendrites, and with the plasma membrane on distal dendrites, where it is often located near asymmetric synapses. In addition, D1-LIR is also seen in presynaptic axon terminals, which give rise to symmetric synapses onto dendritic shafts and soma. These results raise the possibility that the circuit basis of working memory in the prefrontal cortex involves a D1-mediated inhibitory component.

https://www.jneurosci.org/content/jneuro/18/24/10553.full.pdf

D1 Receptor in Interneurons of Macaque Prefrontal Cortex: Distribution and Subcellular Localization

The aging respiratory system--pulmonary structure, function and neural control.

The present experiments were designed to further examine the hypothesis that receptor subtype determines the direction of dopamine's (DA) ability to modulate neostriatal neuronal responses. We have reported that DA potentiates responses mediated by activation of N-methyl-d-aspartate (NMDA) receptors, but attenuates responses mediated by activation of non-NMDA receptors in neocortex [Cepeda et al. (1992b) Synapse, 11:330-341] and neostriatum [Cepeda et al. (1993) Proc. Natl. Acad. Sci. U.S.A., 90:9576-9580]. In these studies, responses to excitatory amino acids (EAAs) were evoked by microphoretic application of agonists. The present studies examined whether this differential modulation also applies to components of synaptic responses evoked by electrical stimulation of neostriatal afferents and mediated by activation of specific subtypes of EAA receptors. Using brain slices, the actions of DA and its receptor specific agonists on components of neostriatal synaptic responses that were mediated either by NMDA or non-NMDA receptors were assessed. Responses mediated by NMDA receptors were potentiated by DA while those mediated by non-NMDA receptors were attenuated. These findings provide further support for the hypothesis that the direction of modulatory action of DA is determined by the specific subtype of EAA receptor activated. In addition, the enhancement of NMDA receptor-mediated responses was mimicked by application of SKF 38393, a D1 receptor agonist. Quinpirole, a D2 receptor agonist, consistently attenuated responses mediated by activation of non-NMDA receptors. Thus, the complex modulatory actions of DA are dependent upon combinations of co-activation of specific subtypes of EAA and DA receptors. These findings are of clinical relevance since the actions of DA and EAAs have been implicated in neurological and affective disorders.

Neuromodulatory actions of dopamine on synaptically-evoked neostriatal responses in slices

The effects of methylenedioxymethamphetamine (MDMA, "Ecstasy") on monoaminergic neurotransmission in the central nervous system.

In cultured embryonic chick motoneurons, glutamate-activated currents rise quickly and then decay rapidly to relatively small steady-state current levels. Dopaminergic modulation of these receptors was studied using patch-clamp recording techniques. At concentrations > or = 10 nM, dopamine enhanced glutamate-activated currents by about 200%. This enhancement was diminished by the nonspecific dopamine receptor antagonist S(+)-apomorphine and the more specific D1 receptor antagonist SCH23390, and it was mimicked by the D1 partial agonist SKF38393. Glutamate receptor desensitization rate was not altered in the presence of dopamine. Enhancement was specific to the kainate component. Current-variance analysis indicated that in the presence of dopamine the conductances of glutamate-activated channels were not altered but that the relative fraction of kainate-type channels activated by glutamate increased. Intracellular cAMP levels increased by 33% following exposure to 100 microM dopamine. The effects of elevated cAMP or protein kinase A (PKA) were tested by including 100 microM cAMP or PKA, respectively, in the recording pipette solution. This increased the kainate-activated currents specifically. Dopaminergic enhancement was not observed when a PKA inhibitor was in the pipette. mRNA encoding D1 was detected in the spinal cord by a reverse transcription, polymerase chain-reaction amplification procedure. Thus, dopamine is acting most probably on an avian homolog of the D1 receptor family. We conclude that dopamine causes cAMP to increase, which results in increased activation of kainate-gated channels during glutamate-mediated transmission.

https://www.jneurosci.org/content/jneuro/15/5/3905.full.pdf

Dopamine enhances glutamate-activated currents in spinal motoneurons

Acetylcholinesterase (AChE) specific activity was assayed using diaphragm muscles obtained from mature adult (10 months) and aged (25– 27 months) rats. Biochemical assays indicated significant age-related increases in the AChE specific activity of both noninnervated and innervated tissue. The different molecular forms of AChE were separated by velocity sedimentation and were further assayed. The age-related increase was manifest primarily in the 10S (G4) form in both noninnervated and innervated tissue and also the 16S (A12) form of the noninnervated samples. To ascertain more conclusively whether AChE activity in the end-plate junctional region of innervated tissue changed in the older rats, miniature end-plate currents (m.e.p.c.s) were recorded under voltage-clamp conditions before and after AChE inhibition. When AChE activity was inhibited by 10 microM echothiopate or 1 mM methanesulfonyl fluoride, m.e.p.c. amplitudes and decay time constants increased in both age groups. The magnitude of these increases was larger in the older animals. However, calculations of the relative change in m.e.p.c. amplitudes after AChE inhibition indicated that less ACh was hydrolyzed by AChE in the older animals. Inhibition of AChE did not affect mean channel open time, which was estimated from spectral analyses of ACh-induced membrane noise. These data indicate that the prolonged decay times in the older rats following AChE inhibition is quite likely due to an expanded field of postsynaptic ACh receptors and not exclusively to a change in junctional AChE.

https://www.jneurosci.org/content/jneuro/8/8/3011.full.pdf

Biochemical and physiological consequences of an age-related increase in acetylcholinesterase activity at the rat neuromuscular junction

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Dopamine enhances glutamate-activated currents in spinal motoneurons

Biochemical and physiological consequences of an age-related increase in acetylcholinesterase activity at the rat neuromuscular junction