Neuroscience

Neuroscience and Neuropharmacology study the basic functions of the brain, spinal cord, sensory systems and peripheral nerves with the aim to reveal mechanisms of neurological disorders and new approaches for their treatment. The Department of Pharmacology has a long and distinguished history in Neuroscience and Neuropharmacology research, with active research and training programs studying receptor, transporter and ion channel biology, cellular signaling and synaptic plasticity, sensory mechanisms in hearing and pain, the neurobiology of addiction, and mechanisms of nerve injury, protection and repair.

Neuroscience and Neuropharmacology

The complexity of the nervous system represents a great challenge for scientists trying to understand the causes of neurological disease. Conditions such as depression, schizophrenia, neurodegenerative disease (Alzheimer’s or Parkinson’s), anxiety disorders, insomnia and chronic pain impose great burdens on individuals, their families and society as a whole.

Neuroscience research in the Department of Pharmacology ranges from single molecule studies on neurotransmitter receptors, ion channels and transporters, to cellular studies on isolated nerve cells and circuits, and systems and behavioral approaches in models of disease. This research aims to understand the basic mechanisms of neuronal function, how these mechanisms are changed in disease, and how pharmacological agents interfere with these changes.

Yale University has an active and diverse Neuroscience community with collaborations and training opportunities across multiple Departments and Programs. Faculty in the Department also undertake outside collaborations with academic and industrial partners to support drug development and novel therapeutic approaches. Students and Postdoctoral Researchers trained in Neuroscience and Neuropharmacology have embarked on successful careers in academic, industrial research and other professional careers.

Research in the Department focuses on the following areas:

Neuroscience Image Gallery

Mouse cerebellar purkinje cellS stained for Acetylcholine receptors (Red) and nucleus(DNA) stained with Sytox (Green)

Current elicited with a 1 ms (*a*) or 4 s (*b*) application of 1 mM glutamate from an excised membrane patch containing hundreds of recombinant GluN1/GluN2A receptors. *c,* responses to two 1 ms pulses of 1 mM glutamate (arrowheads) applied at an interval of 300 ms. *d*, /Left/, results from a paired-pulse protocol using 2-s applications of 1 mM glutamate. The peak current evoked by the second application recovers mono-exponentially (solid line). /Right/, early phase of recovery on an expanded time scale. *e*, two groups of consecutive records obtained from a patch containing just one GluN1/GluN2A channel in response to 1 ms applications of 1 mM glutamate (arrowheads). The different mean open times (MOT) during each set of records are indicative of modal gating and result in activations of different durations and ensemble averages that decay with different time-courses. Image from the Howe Lab.

Activation of Protein Kinase C recruits Cav2.1 calcium channels to the plasma membrane at the distal tips of neurites. Left, Localization of actin (blue), tubulin (red) and Cav2.1 channels (green) in the growth cone of an unstimulated neuron (from a collaboration between the Kaczmarek and Forscher laboratories). Right. Live imaging of Cav2.1 channels (red) and tubulin (green) in a single neuronal growth cone before and after activation of protein kinase C. In response to activation of the enzyme, the channels move to the distal edge of the neurite where they are inserted into the plasma membrane (from Zhang et al., J. Neurosci. 28: 2601-2612, 2008).