I looked into this further, looked at a couple of studies. Take it what you will. I provide one study that concludes there is no long-term neurological damage from the moderate use of cannabis. On the other hand, I cite another study that the disruption of the endocannabinoid system as a consequence ofcannabis abuse may alter neurochemical systems contributing to the development of emotional disorders.

I'm citing the conclusions and if you want to look at how the study is done I provided a link.

"Adolescence is a time of particular vulnerability for brain
maturation. During this period many individuals experiment
with illicit substance use and sometimes quite frequently.
Some adolescents who abuse cannabis
subsequently develop chronic serious psychiatric symptoms,
such as schizophrenia (e.g. [22]) and also cognitive
deficits [23-25]. However, it has never been shown consistently
that cannabis has direct effects on brain development
and there are no known reports using more
advanced imaging technology such as DTI to examine
white matter integrity. Thus the current study was an initial
evaluation to determine whether any indication of
cortical atrophy or white matter abnormalities could be
detected applying these current MRI methods.
Although differences were observed between subjects who
used cannabis during adolescence and those who did not, no finding indicated pathological change. Regions of
higher ADC, putative evidence of atrophy, were not
present, although regions of significantly lower ADC
were. While low FA would be indicative of less white matter
integrity, particularly with respect to fiber direction, all
FA differences in this study were higher values in cannabis
users than non-users.
However, one limitation of the current study is its crosssectional
evaluation of subjects reporting on their own
former adolescent cannabis use, rather than a longitudinal
design following adolescents into adulthood to
observe how the brain changes over time or alternatively
a cross-sectional study of current cannabis-using adolescents.
Pathological effects from prior frequent use may be
less detectable in adulthood after time has passed and
other changes have taken place to compensate for possible
earlier effects of cannabis.
In addition, although we suggest here that the ADC indicates
the amount of CSF in extracellular tissue and ventricular
space, we have not yet validated this assumption
by direct comparisons and thus this view, while logical,
remains speculative at present.
Thus, these data lead to the likely conclusion that cannabis
use, in at least moderate amounts, during adolescence
does not appear to be neurotoxic, although we cannot
exclude any adverse effects of heavier amounts than that
used by the current subjects. These data are preliminary
and need replication with larger numbers of subjects,
although they do have implications for refuting the hypothesis that cannabis alone can cause a psychiatric disturbance
such as schizophrenia by directly producing
brain pathology."

http://www.pubmedcentral.nih.gov/pic...3&blobtype=pdf

"During the last few years, the increasing interest in the
link between the endocannabinoid system and emotional responses
has led to a number of interesting data derived from
animal studies. These results may contribute to understand
the complex scenario of cannabinoid effects in humans, and
to clarify the mechanisms underlying associations between
cannabis abuse and mental disorders. Results obtained from
transgenic mice lacking CB1 receptors and by using CB1 receptors
selective antagonists and inhibitors of endocannabinoids
inactivation suggest the existence of an intrinsic endocannabinoid
tone which contributes to the regulation of
stress responses and anxiety. An adequate endocannabinoid
function appears to be necessary for adaptive extinction
of aversive memories. The endocannabinoid system might
play a pivotal role in maintaining homeostasis, notably with
regard to physiological and behavioral responses to acute
and prolonged stress. Certain forms of endocannabinoiddependent
synaptic plasticity have been proposed as crucial
mechanisms subserving these phenomena. Throughout this
review, we have focused on the endocannabinoid system as
a major player in the modulation of synaptic transmission
and plasticity considering solely interneural communication.
However, the critical functional role of glial cells in maintaining
a correct brain function and their implications in
diverse neuropathological conditions are now clearly recognized.
The new concept of the tripartite synapse in which the
glial cell (notably astrocytes) plays an active role in the modulation
of neurotransmission has recently emerged [125].
Expression of cannabinoid CB1 receptors and endocannabinoid
synthesis and release have been observed in different
types of glial cells [126, 127]. This â??glial endocannabinoid
systemâ? may have important physiological and pathological
implications [128, 129] and it would be interesting to explore
a possible role in the expression of synaptic plasticity in limbic
and extra-limbic regions related to stress, fear, and anxiety
responses.
Disregulation ormalfunctioning of the endocannabinoid
system might contribute to the aetiology of anxiety-related
disorders and to certain symptoms of melancholic depression.
In turn, the endocannabinoid system might constitute
an interesting pharmacological target for the development of
anti-anxiety and antidepressant therapies. The involvement of the endocannabinoid system in the
regulation of anxiety and its participation in the modulation
of behavioral and physiological responses to aversive situations
have other obvious implications. Cannabis abuse may
be one of the causes disrupting the necessary balance for an
appropriate function of the system. There are functional interactions
between the endocannabinoid system and other
monoaminergic and peptidergic systems also involved in the
regulation of emotional responses [113, 130]. Thus, the disruption
of the endocannabinoid system as a consequence of
cannabis abuse may alter these other neurochemical systems
contributing to the development of emotional disorders. In
addition to acute aversive emotional reactions to cannabis,
the chronic use of this addictive drug may result in mental
disturbances and neuropsychiatric disorders. In particular,
there are data suggesting that exposure to cannabis derivatives
is associated with a higher risk of schizophrenia, depression,
and anxiety [68â??72, 131, 132]. In this review, we have
highlighted the importance of endocannabinoid-based neuroplasticity
phenomena in the regulation of neuroendocrine
and neurochemical systems implicated in the modulation of
emotional responses and extinction of perseverative behaviors
and inadaptative aversive memories. Consequently, it is
likely that impairment of endocannabinoid-mediated synaptic
transmission and plasticity contribute to the expression of
at least some aspects of these psychiatric illnesses.

http://www.pubmedcentral.nih.gov/pic...7&blobtype=pdf