Sensitivity to interstimulus interval due to calcium interactions in the Purkinje cell spines
Introduction
In classical conditioning, memory storage depends on the order as well as the timing of the conditioned and unconditioned stimuli. A commonly used experimental paradigm is conditioning of the rabbit nictitating membrane response [3]. A tone is used as the conditioned stimulus and an air puff to the eyes as the unconditioned stimulus. The cerebellum, which is crucial to memory storage, receives information about the tone from parallel fibres (PF) and receives information about the airpuff from climbing fibres (CF). Both PF and CF stimulation lead to Ca2+ increases in the Purkinje cell spines and dendrites, the former through inositol trisphosphate (IP3) induced Ca2+ release (IICR) while CF activation causes dendritic Ca2+ spikes.
As part of identifying the PF and CF interactions leading to memory formation, a PF and CF stimulation protocol in a slice preparation using pulses, , followed by 3 CF pulses, , has been developed [9]. The resulting PSD found is a Ca2+ as well as PKC dependent process [2]. The aim of the present study is to analyze the interaction between the PF and CF induced Ca2+ transients, using stimulation protocols similar to those in [9].
Section snippets
Methods
PF activation of mGluR receptors leads to activation of G protein, phospholipase C and production of IP3 [14], [13]. Calcium concentration in the spine is determined by IICR [6], buffers [5], and diffusion from the shaft:where:Purkinje cell data were used to adjust the parameters [5]. a
Results and discussion
Fig. 1 illustrates the amount of IP3 and Ca2+ produced from 1, 8 or pulses given at . IP3, but not calcium, is linearly related to the number of PF pulses [11]. One PF leads to an insignificant increase in Ca2+ (see inset); pulses increase Ca2+ to . The amount of IP3 produced by pulses, [1], is the threshold for producing significant IICR in experiments [1], [5], [10]. Sixteen PF pulses produces a suprathreshold IP3 concentration; rapid calcium release causes buffer
Jeanette Hellgren Kotaleski received a M.S. in Medical Sciences from Umeå University in 1989, a M.S. in Engineering Physics from Kungliga Tekniska Högskolan in 1991 and a Ph.D. in Computer Science in 1998 on work focusing on modeling bursting mechanisms and coordination in motor systems. She is now a postdoc at the Krasnow Institute working on modeling biochemical pathways underlying classical conditioning.
References (14)
- et al.
Equations for InsP3 receptor-mediated [Ca2+]i oscillations derived from a detailed kinetic modela Hodgkin–Huxley like formalism
J. Theor. Biol.
(1994) - et al.
Supralinear Ca2+ signaling by cooperative and mobile Ca2+ buffering in Purkinje neurons
Neuron
(1999) - et al.
The role of protein kinase C in the biochemical pathway of classical conditioning
Neurocomputing
(2001) - et al.
Local calcium signalling by inositol-1,4,5-trisphosphate in Purkinje cell dendrites
Nature
(1998) - et al.
Pairing-specific long-term depression prevented by blockade of PKC or intracellular Ca2+
NeuroReport
(1998) - et al.
Twenty years of classical conditioning research with the rabbit
Prog. Psychobiol. Physiol. Psych.
(1983) - et al.
Inositol 1,4,5-trisphosphate (InsP3) and calcium interact to increase the dynamic range of InsP3 receptor-dependent calcium signaling
J. Gen. Physiol.
(1997)
Cited by (0)
Jeanette Hellgren Kotaleski received a M.S. in Medical Sciences from Umeå University in 1989, a M.S. in Engineering Physics from Kungliga Tekniska Högskolan in 1991 and a Ph.D. in Computer Science in 1998 on work focusing on modeling bursting mechanisms and coordination in motor systems. She is now a postdoc at the Krasnow Institute working on modeling biochemical pathways underlying classical conditioning.
Kim T. Blackwell received a B.S. in Biomedical Engineering from Boston University in 1981 and a V.M.D. in Veterinary Medicine in 1986, a M.S. in Systems Engineering in 1987, and a Ph.D. in Bioengineering in 1988 from the University of Pennsylvania. From 1988 to 1996, she was a senior research scientist at ERIM. Since 1996, she has been at George Mason University as an associative professor for Computational Sciences and Informatics, and affiliated with the Krasnow Institute. She is currently studying biological mechanisms of classical conditioning using computer modeling and biophysical techniques.