Professor Pankaj Sah

Contact Information
Building: QBI Building #79
Room: 534
Tel: +61 7 334 66376

Mailing Address

Queensland Brain Institute
The University of Queensland
Brisbane, 4072


Lab Members

Lab Home Page

Short biography

Research directions

Current collaborations

Selected publications


Short biography

Professor Pankaj Sah is renowned for his work in understanding the physiology of excitatory synapses and synaptic plasticity in the amygdala, an area of the brain involved in emotional processing. He is currently Deputy Director (Research) at the Queensland Brain Institute (QBI). Previously he was group leader at the John Curtin School of Medical Research at the Australian National University and moved to The University of Queensland as a founding member of QBI in 2003.

His laboratory continues to study the amygdala using a combination of molecular tools, electrophysiology, anatomical reconstruction and calcium imaging. More recently his laboratory has begun research work on humans doing electrophysiological recordings in patients undergoing electrode implantation for deep brain stimulation for the treatment of movement disorders in Parkinson’s disease, essential tremor and Tourette’s syndrome. He has published over 90 papers in international peer reviewed journals.

Research directions

The amygdala is a part of the limbic system that is involved in assigning emotional significance to cognitive events. In particular, it is involved in the processing of fear producing stimuli. One simple form of learning in which the amygdala is involved, is fear conditioning.

Fear conditioning is the process during which a normally innocuous stimulus such as a flashing light becomes associated with a fear producing stimulus (like an electric shock) so that the innocuous stimulus itself subsequently produces a fear response. It represents a form of learning and involves the storage of 'emotional' memories. Fear conditioning occurs in every species that has been examined from flies to humans and its expression shows a remarkably conserved pattern of symptoms which include increases in heart rate and blood pressure, reduction in salivation and freezing of ongoing movement.

Along with the autonomic symptoms of the fear response there are, in humans, cognitive effects such as feelings of dread and despair. Disorders of the storage or expression of fear related responses are thought to underlie such mental disorders as panic attacks, anxiety and post traumatic stress disorder.

The amygdala is critically involved in assigning emotional significance or value to events through associative learning. Stimulation of the amygdala elicits the same constellation of symptoms as fear, and lesions of the amygdala reduce the acquisition and expression of fear. An understanding of the function of this structure is thus essential in the development of rational therapies for a range of related anxiety disorders. The anatomical organisation of the amygdala is now fairly well understood. However, its physiology is just beginning to be elucidated. Our group is involved in studying the physiology and connection of the amygdala. We use a range of techniques including whole cell recordings from cells, and single photon and multiphoton imaging of calcium dynamics in the cell body, dendrites and spines.

It is known that the major inputs to the amygdala use glutamate as the principal transmitter. Glutamatergic synapses can undergo a type of plasticity which has been implicated in the storage of memories. In the amygdala, these synapses are likely to be involved in the acquisition of fear conditioning. The amygdala is broadly divided into three main subnuclei: the lateral, basal and central. Sensory and cortical inputs enter the amygdala at the level of the lateral and basal nuclei. The different subnuclei are extensively interconnected and finally project to the central nucleus. Cells within the central nucleus project to brainstem and hypothalamic nuclei responsible for evoking the physiological responses associated with fear.

One project in our group is involved with examining the properties of cells in the input side of the amygdala. We have shown that cells within the lateral and basal nuclei can be divided into two broad categories: pyramidal cells and interneurones. Pyramidal cells form the major type of cell (93%) and are similar to excitatory cells found throughout the cortex. The remaining cells (7%) are interneurons which are inhibitory and form extensive connections with the excitatory cells in the amygdala. Surprisingly we found that the properties of synaptic inputs onto interneurons were quite different from those onto pyramidal cells. These findings indicate that the modulation of inhibitory pathways may be an important control mechanism within the amygdala. We are now examining the properties of these neurons using a combination of electrophysiological and imaging techniques.

Another project is studying the output side of the amygdala - the central nucleus. This structure is divided into two main parts, the medial and lateral. It has recently been shown that cells in the lateral division are inhibitory and make local circuits while cells in the medial division project out of the amygdala. We have been examining the effects of a class of drugs called benzodiazepines (eg diazepam or valium). These drugs are widely used as anxiolytics and their role in the amygdala is of great interest. These drugs are thought to work by potentiating the actions of the major inhibitory transmitter in the brain, gamma amino butyric acid (GABA). We have found that the central nucleus also contains a second type of GABA receptor which is inhibited by benzodiazepines. This finding may have therapeutic implications as a potential target for new classes of drugs. 

Current collaborations

Selected publications

Power, J. M. and Sah, P.  2005.  Intracellular calcium store filling by an L-type calcium current in the basolateral amygdala at subthreshold membrane potentials. Journal of Physiology 562, 439-453.

Faber, E. S. L., Delaney, A. J., Sah, P.  2005.  SK channels regulate excitatory synaptic transmission and plasticity in the lateral amygdala. Nature Neuroscience 8, 635-641. 

Faber, E. S. L. and Sah, P.  2005.  Independent roles of calcium and voltage dependent potassium currents in controlling spike frequency adaptation in lateral amygdala pyramidal neurons.  European Journal of Neuroscience 22, 1627-1835.

Faber, E. S. L., Sedlak, P., Vidovic, M. and Sah, P. 2006.  Synaptic activation of TRPC channels by metabotropic glutamate receptors in the lateral amygdala. Neuroscience 137, 781-794. 

Graham, B. A., Schofield, P. R., Walker, S., Sah, P., Margrie, T. W. and Callister, R. J. 2006.  Distinct physiological mechanisms underlie altered glycinergic synaptic transmission in the murine mutants, spastic, spasmodic and oscillator. Journal of Neuroscience  26, 4880-4890.

Woodruff, A. Monyer, H. and Sah, P. 2006.  GABAergic excitation in the basolateral amygdala. Journal of Neuroscience  26, 11881-11887. 

Lopez de Armentia, M. and Sah, P.  2007.  Bidirectional synaptic plasticity at nociceptive afferents in the rat central amygdala.  Journal of Physiology 581: 961-970.

Woodruff, A and Sah, P.  2007.   Networks of parvalbumin-positive interneurons in the basolateral amygdala. Journal of Neuroscience 27:553–563

Power, J. M. and Sah, P. 2007.  Distribution of IP3-mediated calcium responses and their role in nuclear signalling in the rat basolateral amygdala.  Journal of Physiology  580, 835-857.

Woodruff, A. R. and Sah, P.  2007. Inhibition and  synchronization of basal amygdala principal neuron spiking by parvalbumin-positive interneurons.  Journal of Neurophysiology  98, 2956-2961.

Gunnersen, J. M, Kim, M. H., Fuller, S. J., De Silva, M., Britto, J. M., Hammond, V. E., Davies, P. J., Petrou, S., Faber, E. S. L.,  Sah, P.  and Tan, S-S..  2007. Sez-6 proteins affect dendritic arborization patterns and excitability of cortical pyramidal neurons.  Neuron 56,  621-639.

Delaney, A., Crane, J. and Sah, P.  2007.  Noradrenaline modulates transmission at a central synapse by a novel presynaptic mechanism Neuron 56, 880-892.

Coulson, EJ, May, LM, Osborne S, Reid, K, Underwood, CK, Meunier, FA,  Bartlett, PF and  Sah, P .  2008.  p75 neurotrophin receptor mediates neuronal cell death by activating GIRK channels through phosphatidylinositol 4,5-bisphosphate. Journal of Neuroscience 28: 315-324.

Power, J. M. and Sah, P.  2008.  Competition between calcium activated K channels determines cholinergic action on firing properties of basolateral amygdala projection neurons. Journal of Neuroscience  28: 3209-3220.

Walker, T. L., White, A., Black, D. M., Turnbull, G., Wallace, R. H., Sah, P., and Bartlett, P. F.  2008.  Latent stem cells in the hippocampus are activated by neural excitation.  Journal of Neuroscience 28:5240-5247. 

Faber, E.S.L., Delaney, A., Power, J. M., Sedlak, P. L. Crane, J. and  Sah, P.  2008.  Modulation of SK channel trafficking by beta adrenoceptors enhances synaptic transmission and plasticity in the amygdala. Journal of Neuroscience  28, 10803-10813.

Esmaeli, A., Lynch, J.  and Sah, P.  2009. GABAA receptors containing gamma1 subunits contribute to inhibitory transmission in the central amygdala.  Journal of Neurophysiology 101, 341-349.

Crane, J., Windels, F. and Sah, P.  2009.  Oscillations in the basolateral amygdala: aversive stimulation is state dependent and resets the oscillatory phase. Journal of Neurophysiology, 102 1379-1387.

Crane. J., Baiquni, G., Sullivan, RKP, Lee, JD, Sah, P, Taylor, SM, Noakes, RG, Woodruff, T. 2009. The C5a anaphylatoxin receptor CD88 is expressed in presynaptic terminals of hippocampal mossy fibres.  Journal of Neuroinflammation 16: 34-40.