In JoVE (3)
Other Publications (2)
Articles by Zana R. Majeed in JoVE
Proprioception and Tension Receptors in Crab Limbs: Student Laboratory Exercises Zana R. Majeed1,2, Josh Titlow1,2, H. Bernard Hartman3, Robin Cooper1,2 1Department of Biology, University of Kentucky, 2Center of Muscle Biology, University of Kentucky, 3Oregon Institute of Marine Biology, University of Oregon Physiological and anatomical techniques are demonstrated to address function and structure for joint proprioceptors and muscle tension receptors in crustacean walking limbs.
Neural Circuit Recording from an Intact Cockroach Nervous System Josh S. Titlow1, Zana R. Majeed1,2, H. Bernard Hartman3, Ellen Burns1, Robin L. Cooper1 1Department of Biology, University of Kentucky, 2Department of Biology, University of Salahaddin, 3Oregon Institute of Marine Biology, University of Oregon This article describes the cockroach ventral nerve cord dissection and extracellular recordings from the cercal nerve and connectives. Evoked responses are generated by electrical stimulation of the cercal nerve or direct mechanical stimulation of the cerci.
Intracellular Recording, Sensory Field Mapping, and Culturing Identified Neurons in the Leech, Hirudo medicinalis Josh Titlow1, Zana R. Majeed1,2, John G Nicholls3, Robin L. Cooper1 1Department of Biology, University of Kentucky, 2Department of Biology, College of Science, University of Salahaddin, Iraq, 3Department of Neurobiology and Cognitive Neuroscience, SISSA, Italy This article describes three nervous system preparations using leeches: intracellular recording from neurons in ventral ganglia, culturing neurons from ventral ganglia, and recording from a patch of innervated skin to map sensory fields.
Other articles by Zana R. Majeed on PubMed
DREADDs in Drosophila: a Pharmacogenetic Approach for Controlling Behavior, Neuronal Signaling, and Physiology in the Fly Cell Reports. Sep, 2013 | Pubmed ID: 24012754 We have translated a powerful genetic tool, designer receptors exclusively activated by designer drugs (DREADDs), from mammalian systems to Drosophila melanogaster to selectively, rapidly, reversibly, and dose-dependently control behaviors and physiological processes in the fly. DREADDs are muscarinic acetylcholine G protein-coupled receptors evolved for loss of affinity to acetylcholine and for the ability to be fully activated by an otherwise biologically inert chemical, clozapine-N-oxide. We demonstrate its ability to control a variety of behaviors and processes in larvae and adults, including heart rate, sensory processing, diurnal behavior, learning and memory, and courtship. The advantages of this particular technology include the dose-responsive control of behaviors, the lack of a need for specialized equipment, and the capacity to remotely control signaling in essentially all neuronal and nonneuronal fly tissues.
5-HT Stimulation of Heart Rate in Drosophila Does Not Act Through CAMP As Revealed by Pharmacogenetics Journal of Applied Physiology (Bethesda, Md. : 1985). Oct, 2013 | Pubmed ID: 24092690 The fruit fly, Drosophila melanogaster, is a good experimental organism to study the underlying mechanism of heart rate (HR) regulation. It is already known that many neuromodulators (serotonin, dopamine, octopamine, acetylcholine) change the HR in Drosophila melanogaster larvae. In this study, we investigated the role of cAMP-PKA signaling pathway in HR regulation and 5-HT positive chronotropic action. In order to obtain insight into the 5-HT mechanism of action in larvae cardiomyocytes, genetic and pharmacological approaches were used. We used transgenic flies that expressed the hM4Di receptor (designer receptors exclusively activated by designer drugs; DREADDs) as one tool. Our previous results showed that activation of hM4Di receptors (modified muscarinic acetylcholine receptors) decreases or arrests the heart from beating. In this study, it was hypothesized that the positive chronotropic effect of serotonin (5-Hydroxytryptamine, 5-HT) are mediated by serotonin receptors coupled to the adenylyl cyclase pathway and downstream cAMP and PKA activity. Activation of hM4Di by clozapine-N-oxide (CNO) was predicted to block the effects of serotonin by inhibiting adenylyl cyclase activity through Gαi pathway activation. Interestingly, we found here that manipulation of adenylyl cyclase activity and cAMP levels had no significant effect on HR. The ability of hM4Di receptor activation to slow or stop the heart is therefore likely mediated by activation of GIRK channels to produce hyperpolarization of cardiomyocytes, and not through inhibition of adenylyl cyclase.