There are a number of fairly recent studies showing the neural effects of THC, the psychoactive compound in marijuana. Many of these focus on the hippocampus and nucleus accumbens. The hippocampus is involved in learning and memory, and nucleus accumbens is part of the limbic system, regulating "hedonistic" behaviors (i.e., sex and drug addiction).
There are effects on synaptic plasticity, or rearrangement of synaptic contacts between cells (measured as long-term potentiation and long-term depression), as reported in these two articles (the first one is available free online, the rest are all available online if you have access via subscription, such as through your library, so I didn't include links because my links won't work for you).
Proc Natl Acad Sci U S A. 1998 Aug 18;95(17):10269-73.
Mesolimbic dopaminergic decline after cannabinoid withdrawal.
Diana M, Melis M, Muntoni AL, Gessa GL.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9707636
J Neurosci. 2003 Jun 15;23(12):4815-20.
Functional tolerance and blockade of long-term depression at synapses in the nucleus accumbens after chronic cannabinoid exposure.
Hoffman AF, Oz M, Caulder T, Lupica CR.
These data demonstrate that long-term exposure to the active ingredient of marijuana blocks synaptic plasticity in the NAc and reduces the sensitivity of GABAergic and glutamatergic synapses to both cannabinoids and opioids.
A paper about to come out (the manuscript is already published online) demonstrates negative effects of smoking marijuana on memory. This focuses on memory
while using marijuana, not long-term effects after stopping or after chronic usage.
Psychopharmacology (Berl). 2004 May 7 [Epub ahead of print]
Effects of marijuana on neurophysiological signals of working and episodic memory.
Ilan AB, Smith ME, Gevins A.
Responses in the WM (working memory) task were slower and less accurate after smoking marijuana, accompanied by reduced alpha band EEG reactivity in response to increased task difficulty. In the EM (episodic memory) task, marijuana was associated with an increased tendency to erroneously identify distracter words as having been previously studied.
And two papers that came out in 2001 both show cross-sensitization by THC to other drugs of abuse including morphine, heroin and amphetamine. Sensitization to drugs is an enhancement of the response to the drug that occurs with episodic rather than regular usage (i.e., stronger effects if you only use on weekends instead of every day). Cross-sensitization is the phenomenon where a drug interacts with the same neural pathway as a different class of drugs such that episodic use of one drug leads to a greater effect the first time a different drug is used than if you had no previous drug exposure of any kind.
The article by Lamarque et al. reported that this effect only occurred in "high responder" rats, ones that have been previously shown to be more vulnerable to drug-taking behaviors and are selected based on higher activity levels in a novel environment than the "low responder" rats. So, they posit the hypothesis that marijuana's role as a gateway drug may occur in similarly vulnerable humans. This still leaves unanswered just
what makes some individuals more vulnerable than others in order to know who should never try it even once and who could safely try it without becoming quickly addicted or cross-sensitized to other drugs of abuse. The cross-sensitization to heroin was fairly long-lasting (still present 41 days after the last injection of THC, which was the last day of testing in this study).
Psychopharmacology (Berl). 2001 Nov;158(3):259-66.
Behavioural sensitization after repeated exposure to Delta 9-tetrahydrocannabinol and cross-sensitization with morphine.
Cadoni C, Pisanu A, Solinas M, Acquas E, Di Chiara G.
Neuropharmacology. 2001 Jul;41(1):118-29.
Chronic treatment with Delta(9)-tetrahydrocannabinol enhances the locomotor response to amphetamine and heroin. Implications for vulnerability to drug addiction.
Lamarque S, Taghzouti K, Simon H.