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pten is essential for both , central nervous system ( cns ) development and maintenance of cns circuit structure and function .
the generation of conditional mutant animals has allowed exquisite control over temporal and spatial patterns of pten expression and delineated specific roles for pten at each developmental stage . during early embryonic development , pten deletion in proliferating neural stem / progenitor cells results in increased cell proliferation , and severe defects in cortical , hippocampal and cerebellar lamination .
pten also inhibits cell proliferation of adult born neural stem cells , controlling self - renewal in the olfactory bulb and dentate gyrus .
after neurons become post - mitotic , pten deletion or knock - down has dramatic effects on neuronal growth , highlighting the importance of pten for controlling post - mitotic neuronal development .
deletion of pten in differentiated postmitotic cortical and hippocampal neurons leads to progressive somatic and dendritic hypertrophy , and the growth of ectopic dendritic branches . 

pten deletion also leads to progressive growth of axonal arbors , which is most readily observed in the hippocampal mossy fiber pathway where deletion also leads to enlargement of presynaptic terminals and increased vesicle numbers .
indeed , pten is enriched in the axonal compartment and the growth cones during axonal extension , coupling semaphorins ( sema3a ) to growth cone collapse .
the effects of pten deletion on spine density and morphology are more complex and likely depend on neuronal identity and the differences in spine classification .
recent studies in basolateral amygdala and dentate gyrus granule neurons suggest that pten deletion does not change overall dendritic protrusion density , but induces a shift in protrusion morphology from thin spines to mushroom spines .
rapamycin , the mtorc1 inhibitor prevents somatic , dendritic , and axonal growth induced by pten deletion , and reverses some but not all these anatomical abnormalities if rapamycin is administered after these changes have already occurred .
pten deletion in adult excitatory cortical neurons using -camk2-cre conditional deletion of floxed - pten , reveals that pten is not only necessary for proper cortical development , but also exerts profound control over dendritic growth in adulthood . by using two - photon imaging of the same cortical dendritic arbors over weeks ,
chow et al . show that apical dendrites of l2/3 pyramidal neurons that underwent deletion of pten in adulthood , demonstrate dramatic and progressive growth .
importantly , treatment of these mice with the mtorc1 inhibitor , rapamycin , halts dendritic growth , and reduces spine density on the newly grown segments .
adult deletion of pten in l5 neurons has no effects on apical dendritic arbors , suggesting that pten exerts distinct effects on different cortical layers in adulthood .
these structural changes are accompanied by profound alterations in synaptic function . in the dentate gyrus ,
consistent with the increase in the proportion of mature dendritic spines , pten knockdown or deletion increases the frequency of excitatory ( miniature and spontaneous ) postsynaptic currents . to dissect the presynaptic and postsynaptic contributions to altered functional connectivity in excitatory and inhibitory neurons , weston and colleagues have carried out studies in autaptic dentate granule cell and striatal cultures .
they find that pten deletion increases evoked synaptic release onto both inhibitory and excitatory neurons , mainly by increasing the number of vesicles available for release .
these effects are counterbalanced by impaired vesicle fusion induced by hyperactive mtor signaling , although the prevailing overall effect was an increase in functional connectivity . in the dentate gyrus ,
these physiological changes have dramatic effects on neuronal synchronization , as loss of pten in as few as 9% of dentate granule cells lead to development of spontaneous seizures .
loss of pten in auditory cortical neurons enhances the strength of long - range connections inputs from both the contralateral auditory cortex and the thalamus , as well as from local inputs .
this hyperconnectivity may constitute a physiological basis for asd phenotypes associated with problems in processing and integration of complex sensory information .
in addition to changes in basal synaptic transmission , pten is also intimately involved in the mechanisms underlying synaptic plasticity .
activity - induced long - term potentiation ( ltp ) and long - term depression ( ltd ) of synaptic transmission are two types of enduring changes in neuronal connections that underlie learning and memory functions .
conditional alpha - camk2-cre dependent deletion of pten in mature differentiated ca1 neurons demonstrated that pten deletion leads to deficits in both major forms of synaptic plasticity ( ltp and ltd ) before the onset of anatomical abnormalities , suggesting that pten controls structural synaptic growth and synaptic plasticity through independent mechanisms .
acute blockade of pi3k impairs ltp in hippocampal ca1 synapses , which reflects the importance of pi3k / pten balance in synaptic plasticity .
the precise mechanism through which pten controls synaptic plasticity is not completely understood . during ltd ,
this interaction anchors pten to the postsynaptic membrane , eventually depressing ampa receptor - mediated synaptic responses .
pten may also exert effects on ltp through the hormone leptin , which phosphorylates and inactivates pten , increasing the membrane expression of glur1 and thus , the synaptic density of glur2-lacking ampa receptors in adult hippocampus . in dentate granule cells ,
conditional pten ablation inhibits metabotropic glutamate receptor ( mglur ) and protein synthesis - dependent ltd .
drebrin is a protein highly enriched in dendrites , and modulates synaptic plasticity by affecting the spine morphology and by regulating neuronal transmission .
clustering of drebrin is regulated by ampa receptor activity and drebrin regulates the synaptic targeting of nmda receptors .
pten negatively regulates drebrin phosphorylation , and neuronal activity induces a dissociation of the pten / drebrin complex .
the reduced levels of drebrin observed in patients with alzheimer s disease suggest an important role of pten / drebrin interaction in synaptic plasticity .
changes in voltage or calcium - gated conductances which modulate the intrinsic excitability of neurons can sculpt how neuronal networks respond to changes in synaptic weights .
these changes can occur at the level of single dendrites , within the somatic compartment , or even in the axon initial segment , and fine tune the way input is integrated , maintaining the dynamic range of the neuron .
there is increasing evidence that pten and mtor - related proteins can regulate the expression of intrinsic ion channels , modulating the intrinsic excitability of the cell .
the first evidence for this modulation was demonstrated in hippocampal neurons where the mtor inhibitor rapamycin increased dendritic translation of the potassium channel kv1.1 . in the hypothalamus ,
aging increases mtor signaling in the pro - opiomelanocortin ( pomc ) , elevating atp activated potassium ( k ( atp ) ) channel activity , ultimately resulting in obesity . in the cerebellum , neuregulin-1 and neuritin increase the density of kv4.2 channels by engaging the mtor pathway .
our own work demonstrates that single - copy loss of pten in the mature visual cortex significantly decreases intrinsic excitability of l2/3 excitatory visual cortical neurons without changing dendritic branching .
as calcium activated conductances play a large role in setting the amplitude of the ahp , we tested whether blockade of these conductances could normalize the firing properties and the spike ahp in the pten mutants .
blockade of sk channels ( but not bk channels ) rescued the intrinsic firing properties and ahp of pten deficient neurons .
in addition , we found an increased protein expression of the sk2 channel subunit in visual cortex .
finally , we asked whether these changes in the intrinsic firing patterns affected the way about how visual information is processed in vivo .
we found that loss of pten decreased the magnitude of the visually evoked action potential discharges , without altering the orientation selectivity of the neurons .
therefore , single copy loss of pten , through changes in sk channel expression levels , decreases the responsiveness of excitatory visual cortical neurons .
these physiological changes are especially relevant as de novo or inherited mutations in pten are emerging as one of the most validated causes of autism spectrum disorder , intellectual disability and extreme macrocephaly .
these disorders add to the already well - established role of pten mutations in causing the pten hamartoma tumor syndromes which include cowden , bannayan - riley - ruvalcaba , lhermitte duclos , and proteus syndromes . in the future
, it will be essential to determine which of the complex structural and physiological changes induced by pten deficits can be reversed or ameliorated by mtor inhibition , and which changes will necessitate other interventions to normalize intrinsic excitability , synaptic connectivity , and plasticity.(fig .
( a ) left : a drawing representing dendritic and axonal growth caused by loss of pten .
( b ) an illustration demonstrating the potential role of pten in synaptic long - term depression ( ltd ) and long term potentiation ( ltp ) . c. a schematic illustrating that loss of pten leads to increased expression of calcium - activated potassium channels and decreased intrinsic excitability
pten ( phosphatase and tensin homolog on chromosome ten ) is a dual protein / lipid phosphatase that dephosphorylates pip3 , thereby inhibiting the akt / mtor pathway . 
 this inhibition ultimately decreases protein translation , cell proliferation and cell growth . in the central nervous system , inhibition of pten 
 leads to increased stem cell proliferation , somatic , dendritic and axonal growth , accelerated spine maturation , diminished synaptic plasticity , and altered intrinsic excitability . in agreement with these findings , 
 patients carrying single - copy inactivating mutations of pten suffer from autism , macrocephaly , mental retardation , and epilepsy.1 - 9 understanding the mechanisms through which pten modulates the structure , function , and plasticity of cortical networks is a major focus of study . 
 preventing and reversing the changes induced by loss of pten in model animals will pave the way for treatments in humans .