Biomedical subjects

Sachin S Talathi

Publications and source records attributed to Sachin S Talathi.

3 recordsLinked to original sources

PubMed2006

Neural circuitry for recognizing interspike interval sequences.

Sensory systems present environmental information to central nervous system as sequences of action potentials or spikes. How do animals recognize these sequences carrying information about their world? We present a biologically inspired neural circuit designed to enable spike pattern recognition. This circuit is capable of training itself on a given interspike interval (ISI) sequence and is then able to respond to presentations of the same sequence. The essential ingredients of the recognition circuit are (a) a tunable time delay circuit, (b) a spike selection unit, and (c) a tuning mechanism using spike timing dependent plasticity of inhibitory synapses. We have investigated this circuit using Hodgkin-Huxley neuron models connected by realistic excitatory and inhibitory synapses. It is robust in the presence of noise represented as jitter in the spike times of the ISI sequence.

Action Potentials↗

PubMed2005

Synaptic plasticity with discrete state synapses.

Experimental observations on synaptic plasticity at individual glutamatergic synapses from the CA3 Shaffer collateral pathway onto CA1 pyramidal cells in the hippocampus suggest that the transitions in synaptic strength occur among discrete levels at individual synapses [C. C. H. Petersen, Proc. Natl. Acad. Sci. USA 85, 4732 (1998); O'Connor, Wittenberg, and Wang, D. H. O'Connor, Proc. Natl. Acad. Sci. USA (to be published); J. M. Montgomery and D. V. Madison, Trends Neurosci. 27, 744 (2004)]. This happens for both long term potentiation (LTP) and long term depression (LTD) induction protocols. O'Connor, Wittenberg, and Wang have argued that three states would account for their observations on individual synapses in the CA3-CA1 pathway. We develop a quantitative model of this three-state system with transitions among the states determined by a competition between kinases and phosphatases shown by D. H. O'Connor, to be determinant of LTP and LTD, respectively. Specific predictions for various plasticity protocols are given by coupling this description of discrete synaptic alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor ligand gated ion channel conductance changes to a model of postsynaptic membrane potential and associated intracellular calcium fluxes to yield the transition rates among the states. We then present various LTP and LTD induction protocols to the model system and report the resulting whole cell changes in AMPA conductance. We also examine the effect of our discrete state synaptic plasticity model on the synchronization of realistic oscillating neurons. We show that one-to-one synchronization is enhanced by the plasticity we discuss here and the presynaptic and postsynaptic oscillations are in phase. Synaptic strength saturates naturally in this model and does not require artificial upper or lower cutoffs, in contrast to earlier models of plasticity.

Action Potentials↗

PubMed2004

Dynamical model of birdsong maintenance and control.

The neuroethology of song learning, production, and maintenance in songbirds presents interesting similarities to human speech. We have developed a biophysical model of the manner in which song could be maintained in adult songbirds. This model may inform us about the human counterpart to these processes. In songbirds, signals generated in nucleus High Vocal center (HVc) follow a direct route along a premotor pathway to the robust nucleus of the archistriatum (RA) as well as an indirect route to RA through the anterior forebrain pathway (AFP): the neurons of RA are innervated from both sources. HVc expresses very sparse bursts of spikes having interspike intervals of about 2 ms. The expressions of these bursts arrive at the RA with a time difference DeltaT approximately equal to 50+/-10 ms between the two pathways. The observed combination of AMPA and NMDA receptors at RA projection neurons suggests that long-term potentiation and long-term depression can both be induced by spike timing plasticity through the pairing of the HVc and AFP signals. We present a dynamical model that stabilizes this synaptic plasticity through a feedback from the RA to the AFP using known connections. The stabilization occurs dynamically and is absent when the RA-->AFP connection is removed. This requires a dynamical selection of DeltaT. The model does this, and DeltaT lies within the observed range. Our model represents an illustration of a functional consequence of activity-dependent plasticity directly connected with neuroethological observations. Within the model the parameters of the AFP, and thus the magnitude of DeltaT, can also be tuned to an unstable regime. This means that destabilization might be induced by neuromodulation of the AFP.

Action Potentials↗