Cerebellum Purkinje GABA cell

- - CB - - PRINC - purkinje - - gaba
Properties are:  Present   Absent 
Input Receptors
Intrinsic Currents
Output Transmitters
Distal equivalent dendrite
Stellate Cell terminals (T) GabaA
Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites (Vigot R and Batini C, 19971 ).
Parallel Fiber terminals (T) Glutamate
Ionophoretic glutamate applied to dendrites depolarizes Purkinje cells. Glu is released from parallel fibers of granule cells
GabaB
found evidence for the presence of GABAB receptors on cell dendrites. Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites. Therefore, the GABA released by stellate cells modulates Purkinje cells activity through two inhibitory mechanisms (Vigot R and Batini C, 19971 ). The cellular localization of GABAB binding was investigated using lesion techniques. It was suggested that the majority of cerebellar molecular layer GABAB binding sites are located on Purkinje cell dendrites. During development binding in the molecular layer peaks between postnatal day 14 and postnatal day 28 and then decreases to adult levels (Turgeon SM and Albin RL, 19932 ).
I Na,t
I K,Ca
Increased conductance may follow Ca impulses (Llinas and Walton 1998).
I L high threshold
reviewed in McCormick 1998).
I A
(Midtgaard J et al, 1993 [turtle]11 ).
I K
Increased conductance may follow Ca impulses (Llinas and Walton 1998).
I p,q
Intradendritic recordings show Ca-dependent plateau potentials and Ca impulses (Llinás R and Sugimori M, 1980 [rat]8 ).
I Potassium
Macropatch clamp and intracellular recordings in guinea pigs suggested that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current (Etzion Y and Grossman Y, 199812 ).
I Calcium
The presence of Calcium channels was directly demonstrated by imaging studies (Lev-Ram V et al, 199213 ).
Middle equivalent dendrite
Climbing Fiber terminals (T) and Parallel Fiber terminals (T) Glutamate
Ionophoretic glutamate applied to dendrites depolarizes Purkinje cells. Glu is released from parallel fibers of granule cells
Stellate Cell terminals (T) GabaA
Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites (Vigot R and Batini C, 19971 ).
GabaB
found evidence for the presence of GABAB receptors on cell dendrites. Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites. Therefore, the GABA released by stellate cells modulates Purkinje cells activity through two inhibitory mechanisms (Vigot R and Batini C, 19971 ). The cellular localization of GABAB binding was investigated using lesion techniques. It was suggested that the majority of cerebellar molecular layer GABAB binding sites are located on Purkinje cell dendrites. During development binding in the molecular layer peaks between postnatal day 14 and postnatal day 28 and then decreases to adult levels (Turgeon SM and Albin RL, 19932 ).
I Na,t
I L high threshold
reviewed in McCormick 1998).
I K
Increased conductance may follow Ca impulses (Llinas and Walton 1998).
I K,Ca
Increased conductance may follow Ca impulses (Llinas and Walton 1998).
I p,q
Intradendritic recordings show Ca-dependent plateau potentials and Ca impulses (Llinás R and Sugimori M, 1980 [rat]8 ).
I Potassium
Macropatch clamp and intracellular recordings in guinea pigs suggested that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current (Etzion Y and Grossman Y, 199812 ).
I Calcium
The presence of Calcium channels was directly demonstrated by imaging studies (Lev-Ram V et al, 199213 ).
Proximal equivalent dendrite
Climbing Fiber terminals (T) Glutamate
Ionophoretic glutamate applied to dendrites depolarizes Purkinje cells. Glu is released from parallel fibers of granule cells
Stellate Cell terminals (T) GabaA
Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites (Vigot R and Batini C, 19971 ).
GabaB
found evidence for the presence of GABAB receptors on cell dendrites. Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites. Therefore, the GABA released by stellate cells modulates Purkinje cells activity through two inhibitory mechanisms (Vigot R and Batini C, 19971 ). The cellular localization of GABAB binding was investigated using lesion techniques. It was suggested that the majority of cerebellar molecular layer GABAB binding sites are located on Purkinje cell dendrites. During development binding in the molecular layer peaks between postnatal day 14 and postnatal day 28 and then decreases to adult levels (Turgeon SM and Albin RL, 19932 ).
I Na,t
Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon. Outside-out patches excised from the soma and dendrites up to about 100um revealed a channel density decreasing with distance from the soma. (Stuart G and Häusser M, 19943 ). However, in guinea pigs, a combination of high-speed imaging and simultaneous intracellular recordings showed that direct depolarization of the soma or dendrites never caused dendritic [Na+]i increases, suggesting that the climbing fiber-activated [Na+]i changes in the dendrites are due to Na+ entry through ligand-gated channels (Callaway JC and Ross WN, 1997 [guinea pig]4 ). NaV1.2 is substantially present throughout the dendrites, NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell (Ahn HS et al, 20115 ). (Schaller KL and Caldwell JH, 20036 ). (Dib-Hajj SD et al, 20107 ).
I K,Ca
Increased conductance may follow Ca impulses (Llinás R and Sugimori M, 1980 [rat]8 ). Llinas and Walton 1990).
I p,q
Intradendritic recordings show Ca-dependent plateau potentials and Ca impulses (Llinás R and Sugimori M, 1980 [rat]8 ).
I K
Increased conductance may follow Ca impulses (Llinas and Walton 1998).
I L high threshold
(Llinás R and Sugimori M, 1980 [rat]8 ). reviewed in Llinas and Walton, 1990).
I Potassium
Macropatch clamp and intracellular recordings in guinea pigs suggested that the pattern of Ca2+ spike firing in the dendrites of Purkinje cells is dynamically modulated by a highly aminopyridine-sensitive K+ current, and probably also by a Ca2+-activated potassium current (Etzion Y and Grossman Y, 199812 ).
I Calcium
The presence of Calcium channels was directly demonstrated by imaging studies (Lev-Ram V et al, 199213 ).
Soma
Basket Cell terminals (T) Gaba
Basket cell activation elicits IPSPs in Purkinje cells for review see Llinas and Walton 1998).
GabaA
Recordings in slices showed that GABA inhibition was mediated by GABA(B) receptors in the dendrites and GABA(A) receptors in the soma and dendrites (Vigot R and Batini C, 19971 ).
I Na,p
Sensitive to TTX. This plateau potential underlies impulse bursting (Llinás R and Sugimori M, 1980 [guinea pig]10 ).
I A
Probably.
I Na,t
Sensitive to TTX. This generates the impulses that propagate into the axon (Llinás R and Sugimori M, 1980 [guinea pig]10 ). Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon (Stuart G and Häusser M, 19943 ). The kinetics properties of this current were studied using whole-cell recording from dissociated neurons. Unlike other cells, recovery from inactivation was accompanied by a sizeable ionic current. It was suggested that the current flowing during this recovery may depolarize the cells immediately after an AP, promoting the typical high-frequency firing of these neurons (complex spike) (Raman IM and Bean BP, 20019 ). NaV1.1 is present in the soma and proximal dendrites, NaV1.6 is robustly present in cell bodies and dendrites, and NaV1.7 is absent from the cell (Ahn HS et al, 20115 ). (Schaller KL and Caldwell JH, 20036 ). (Dib-Hajj SD et al, 20107 ).
I K,Ca
(Llinás R and Sugimori M, 1980 [guinea pig]10 ). reviewed in Llinas and Walton, 1990).
I K
a fast voltage activated potassium current that generates the afterhyperpolarization following a fast spike." (data from (Llinás R and Sugimori M, 1980 [guinea pig]10 ). quote from the review in Llinas and Walton 1990).
I T low threshold
Suggested.
I Calcium
The presence of Calcium channels was directly demonstrated by imaging studies (Lev-Ram V et al, 199213 ).
Axon hillock
Basket Cell terminals (T) Gaba
Basket cell activation elicits IPSPs in Purkinje cells for review see Llinas and Walton 1998).
I K
I Na,t
Simultaneous whole-cell recordings, made from the soma and dendrites rat brain slices, showed that AP evoked by either current pulses or synaptic stimulation of parallel or climbing fibers, always occurred first at the soma and decreased in amplitude with increasing distance into the dendrites. Simultaneous somatic and axonal recordings showed that these action potentials were initiated in the axon (Stuart G and Häusser M, 19943 ). The kinetics properties of this current were studied using whole-cell recording from dissociated neurons. Unlike other cells, recovery from inactivation was accompanied by a sizeable ionic current. It was suggested that the current flowing during this recovery may depolarize the cells immediately after an AP, promoting the typical high-frequency firing of these neurons (complex spike) (Raman IM and Bean BP, 20019 ).
Axon fiber
I Na,t
Axon terminal
I N
Gaba
(Ito M et al, 196414 ).
Classical References: first publications on each compartmental property; search PubMed for complete list
1.  Vigot R and Batini C. (1997) GABA(B) receptor activation of Purkinje cells in cerebellar slices. Neurosci Res 29:151-60.
2.  Turgeon SM and Albin RL. (1993) Pharmacology, distribution, cellular localization, and development of GABAB binding in rodent cerebellum. Neuroscience 55:311-23.
3.  Stuart G and Häusser M. (1994) Initiation and spread of sodium action potentials in cerebellar Purkinje cells. Neuron 13:703-12.
4.  Callaway JC and Ross WN. (1997) Spatial distribution of synaptically activated sodium concentration changes in cerebellar Purkinje neurons. J Neurophysiol 77:145-52 [Journal] .
5.  Ahn HS, Black JA, Zhao P, Tyrrell L, Waxman SG and Dib-Hajj SD. (2011) Nav1.7 is the predominant sodium channel in rodent olfactory sensory neurons. Mol Pain 7:32 [Journal] .
6.  Schaller KL and Caldwell JH. (2003) Expression and distribution of voltage-gated sodium channels in the cerebellum. Cerebellum 2:2-9 [Journal] .
7.  Dib-Hajj SD, Cummins TR, Black JA and Waxman SG. (2010) Sodium channels in normal and pathological pain. Annu Rev Neurosci 33:325-47 [Journal] .
8.  Llinás R and Sugimori M. (1980) Electrophysiological properties of in vitro Purkinje cell dendrites in mammalian cerebellar slices. J Physiol 305:197-213.
9.  Raman IM and Bean BP. (2001) Inactivation and recovery of sodium currents in cerebellar Purkinje neurons: evidence for two mechanisms. Biophys J 80:729-37 [Journal] .
10.  Llinás R and Sugimori M. (1980) Electrophysiological properties of in vitro Purkinje cell somata in mammalian cerebellar slices. J Physiol 305:171-95.
11.  Midtgaard J, Lasser-Ross N and Ross WN. (1993) Spatial distribution of Ca2+ influx in turtle Purkinje cell dendrites in vitro: role of a transient outward current. J Neurophysiol 70:2455-69 [Journal] .
12.  Etzion Y and Grossman Y. (1998) Potassium currents modulation of calcium spike firing in dendrites of cerebellar Purkinje cells. Exp Brain Res 122:283-94.
13.  Lev-Ram V, Miyakawa H, Lasser-Ross N and Ross WN. (1992) Calcium transients in cerebellar Purkinje neurons evoked by intracellular stimulation. J Neurophysiol 68:1167-77 [Journal] .
14.  Ito M, Yoshida M and Obata K. (1964) Monosynaptic inhibition of the intracerebellar nuclei induced rom the cerebellar cortex. Experientia 20:575-6.